Nur Atik
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Research Interests
Nur Atik has a total of 205 co-authors. Here are the top co-authors by number of shared publications:
- Astrid Feinisa Khairani
Department of Biomedical Sciences, Faculty of Medicine, Universitas Padjadjaran, Sumedang, West Java, Indonesia
6 shared publications - Akihiro Harada
Department of Cell Biology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan
5 shared publications Cep Juli
Department of Neurology, Faculty of Medicine, Universitas Padjadjaran, Bandung, West Java, Indonesia
5 shared publicationsMasataka Kunii
Department of Cell Biology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan
4 shared publicationsTomohiko Iwano
Department of Anatomy and Cell Biology, Graduate School of Medicine, University of Yamanashi, Yamanashi, Japan 3
4 shared publicationsAchadiyani Achadiyani
Department of Biomedical Sciences Division of Cell Biology Faculty of Medicine Universitas Padjadjaran Jalan Raya Bandung -Sumedang Km. 21 Jatinangor Sumedang INDONESIA
3 shared publications
Latest Publications
- Open Access
- 1 November 2026
- Published by Taylor & Francis in Clinical, Cosmetic and Investigational Dermatology
- Vol. ume 19, 1-17
Temporal Dynamics of hTERT and Tumor Suppressor Gene Expression During Replicative Senescence in Human Dermal Fibroblasts: A High-Resolution Longitudinal Study
- 1 November 2026
- Published by Taylor & Francis in Clinical, Cosmetic and Investigational Dermatology
- Vol. ume 19, 1-17
Open AccessTemporal Dynamics of hTERT and Tumor Suppressor Gene Expression During Replicative Senescence in Human Dermal Fibroblasts: A High-Resolution Longitudinal Study
- Open Access
- 27 July 2026
- Published by Wiley in Journal of Cosmetic Dermatology
- Vol. 25 (8) , e71094
Impact of Oral Herbal Supplementation on Human Skin Aging: A Systematic Review of Clinical Trials
Background: Skin aging, characterized by wrinkles, decreased elasticity, and dryness, is both a public health and esthetic issue, affecting most adults and leading to lowered quality of life and higher healthcare costs. While topical treatments are common, systemic approaches are gaining interest for their potential to enhance skin hydration, elasticity, and barrier function. Nonetheless, the effects of oral herbal supplements remain less examined. Aim: This systematic review evaluated the effectiveness of oral herbal supplements in reducing skin aging in humans, focusing on elasticity, hydration, wrinkle depth, and antioxidant activity. Methods: Randomized controlled trials (RCTs) were identified through structured database searches (March–August 2025). Twelve RCTs published between 2020 and 2025 met the inclusion criteria, involving adults who received oral herbal supplements versus placebo or standard care. Outcomes measured included skin elasticity, hydration, wrinkle depth, smoothness, antioxidant capacity, and inflammatory markers. Quality assessment using the Cochrane RoB 2 tool indicated that all 12 RCTs were judged as having some concerns of bias. Results: Interventions included Glycine max , bilberry, cranberry, Hydrangea serrata, Pycnogenol, and others. Most studies reported significant improvements in dermatological outcomes. Proposed mechanisms involve antioxidant activity, anti‐inflammatory effects, collagen synthesis, barrier restoration, photoprotection, DNA repair, and microbiome modulation. Conclusion: In conclusion, oral herbal supplements show promising potential in improving skin aging outcomes by targeting multiple biological pathways. Further research with larger populations, longer durations, and biomarker‐based endpoints is needed to confirm efficacy and support standardized use in dermatology and esthetic medicine.
- 27 July 2026
- Published by Wiley in Journal of Cosmetic Dermatology
- Vol. 25 (8) , e71094
Open AccessImpact of Oral Herbal Supplementation on Human Skin Aging: A Systematic Review of Clinical Trials
Background: Skin aging, characterized by wrinkles, decreased elasticity, and dryness, is both a public health and esthetic issue, affecting most adults and leading to lowered quality of life and higher healthcare costs. While topical treatments are common, systemic approaches are gaining interest for their potential to enhance skin hydration, elasticity, and barrier function. Nonetheless, the effects of oral herbal supplements remain less examined. Aim: This systematic review evaluated the effectiveness of oral herbal supplements in reducing skin aging in humans, focusing on elasticity, hydration, wrinkle depth, and antioxidant activity. Methods: Randomized controlled trials (RCTs) were identified through structured database searches (March–August 2025). Twelve RCTs published between 2020 and 2025 met the inclusion criteria, involving adults who received oral herbal supplements versus placebo or standard care. Outcomes measured included skin elasticity, hydration, wrinkle depth, smoothness, antioxidant capacity, and inflammatory markers. Quality assessment using the Cochrane RoB 2 tool indicated that all 12 RCTs were judged as having some concerns of bias. Results: Interventions included Glycine max , bilberry, cranberry, Hydrangea serrata, Pycnogenol, and others. Most studies reported significant improvements in dermatological outcomes. Proposed mechanisms involve antioxidant activity, anti‐inflammatory effects, collagen synthesis, barrier restoration, photoprotection, DNA repair, and microbiome modulation. Conclusion: In conclusion, oral herbal supplements show promising potential in improving skin aging outcomes by targeting multiple biological pathways. Further research with larger populations, longer durations, and biomarker‐based endpoints is needed to confirm efficacy and support standardized use in dermatology and esthetic medicine.
- Open Access
- 25 May 2025
- Published by Veterinary World in Veterinary World
- Vol. 18 (5) , 1313-1321
A comparative study of collagen morphology and joint strength in anterior cruciate ligament repair and reconstruction models in rabbits
Background and Aim: Anterior cruciate ligament (ACL) repair offers several theoretical advantages over reconstruction, including preservation of native proprioception and reduced donor-site morbidity. However, the current experimental models are predominantly limited to ACL reconstruction, leaving a critical gap in ACL repair research. This study introduces a novel rabbit model to evaluate osteointegration and mechanical strength at the tendon/ligament-bone interface following ACL repair and reconstruction. Materials and Methods: Six male New Zealand White rabbits (Oryctolagus cuniculus), aged 90 ± 0 days and weighing 2.50 ± 0.20 kg, were randomly assigned to two groups: ACL reconstruction (n = 3) using the extensor digitorum longus tendon graft and ACL repair (n = 3) using the Krackow suture technique at the femoral attachment. Specimens were collected 6 weeks postoperatively for histological evaluation of Sharpey’s-like fibers, immunohistochemical analysis of types I and III collagen, and biomechanical tensile testing. Results: All surgical procedures were completed without complications. Histological analysis showed greater numbers of Sharpey’s-like fibers in the reconstruction group (6.33 ± 0.58%) compared to the repair group (5.67 ± 1.6%), though not statistically significant (p > 0.05). Type I collagen fibers were significantly longer in the reconstruction group in both longitudinal (3.10 ± 0.05 μm vs. 2.97 ± 0.04 μm) and transverse (1.94 ± 0.09 μm vs. 1.81 ± 0.05 μm) dimensions (p < 0.05). Type III collagen dimensions did not differ significantly. The mean tensile failure load was higher in the reconstruction group (105.96 ± 63.37 N) than in the repair group (62.56 ± 20.11 N), though this difference was not statistically significant (p > 0.05). Conclusion: This study establishes a reproducible and cost-effective ACL repair model in rabbits and confirms that tendon-bone osteointegration occurs in both ACL repair and reconstruction. Superior biomechanical strength and enhanced type I collagen integration in the reconstruction group underscore current clinical outcomes favoring reconstruction. This model offers a valuable platform for exploring biological augmentation strategies to enhance ACL repair efficacy. Keywords: anterior cruciate ligament repair, biomechanics, osteointegration, rabbit model, type I collagen.
- 25 May 2025
- Published by Veterinary World in Veterinary World
- Vol. 18 (5) , 1313-1321
Open AccessA comparative study of collagen morphology and joint strength in anterior cruciate ligament repair and reconstruction models in rabbits
Background and Aim: Anterior cruciate ligament (ACL) repair offers several theoretical advantages over reconstruction, including preservation of native proprioception and reduced donor-site morbidity. However, the current experimental models are predominantly limited to ACL reconstruction, leaving a critical gap in ACL repair research. This study introduces a novel rabbit model to evaluate osteointegration and mechanical strength at the tendon/ligament-bone interface following ACL repair and reconstruction. Materials and Methods: Six male New Zealand White rabbits (Oryctolagus cuniculus), aged 90 ± 0 days and weighing 2.50 ± 0.20 kg, were randomly assigned to two groups: ACL reconstruction (n = 3) using the extensor digitorum longus tendon graft and ACL repair (n = 3) using the Krackow suture technique at the femoral attachment. Specimens were collected 6 weeks postoperatively for histological evaluation of Sharpey’s-like fibers, immunohistochemical analysis of types I and III collagen, and biomechanical tensile testing. Results: All surgical procedures were completed without complications. Histological analysis showed greater numbers of Sharpey’s-like fibers in the reconstruction group (6.33 ± 0.58%) compared to the repair group (5.67 ± 1.6%), though not statistically significant (p > 0.05). Type I collagen fibers were significantly longer in the reconstruction group in both longitudinal (3.10 ± 0.05 μm vs. 2.97 ± 0.04 μm) and transverse (1.94 ± 0.09 μm vs. 1.81 ± 0.05 μm) dimensions (p < 0.05). Type III collagen dimensions did not differ significantly. The mean tensile failure load was higher in the reconstruction group (105.96 ± 63.37 N) than in the repair group (62.56 ± 20.11 N), though this difference was not statistically significant (p > 0.05). Conclusion: This study establishes a reproducible and cost-effective ACL repair model in rabbits and confirms that tendon-bone osteointegration occurs in both ACL repair and reconstruction. Superior biomechanical strength and enhanced type I collagen integration in the reconstruction group underscore current clinical outcomes favoring reconstruction. This model offers a valuable platform for exploring biological augmentation strategies to enhance ACL repair efficacy. Keywords: anterior cruciate ligament repair, biomechanics, osteointegration, rabbit model, type I collagen.
- Open Access
- 1 May 2025
- Published by Taylor & Francis in Journal of Experimental Pharmacology
- Vol. ume 17, 239-247
Aaptamine Alters Vimentin Expression and Migration Capability of Triple-Negative Breast Cancer Cells
Purpose: This study aimed to explore the effect of Aaptamine, an alkaloid derived from marine sponges, on the vimentin expression in both mRNA and protein levels and the migration capacity of breast cancer cells. Methods: The triple-negative breast cancer cell line MDA-MB-231 was used for in vitro experiments. Low-cytotoxicity concentrations of Aaptamine (12.5 to 50 μM) were given to MDA-MB-231 cells. The vimentin mRNA and protein expression were evaluated using RT-qPCR and immunofluorescence, respectively, 72 h after Aaptamine treatment. The migration scratch assay was conducted for 48 hours. Results: Aaptamine treatment in three different doses did not affect the expression of vimentin at the mRNA level while significantly lowering vimentin protein expression at the concentration of 12.5 μM. In addition, Aaptamine significantly inhibited breast cancer cell migration in a dose-dependent manner. Conclusion: Aaptamine inhibits vimentin protein expression and demonstrates anti-migration activity in the sub-cytotoxic dose.
- 1 May 2025
- Published by Taylor & Francis in Journal of Experimental Pharmacology
- Vol. ume 17, 239-247
Open AccessAaptamine Alters Vimentin Expression and Migration Capability of Triple-Negative Breast Cancer Cells
Purpose: This study aimed to explore the effect of Aaptamine, an alkaloid derived from marine sponges, on the vimentin expression in both mRNA and protein levels and the migration capacity of breast cancer cells. Methods: The triple-negative breast cancer cell line MDA-MB-231 was used for in vitro experiments. Low-cytotoxicity concentrations of Aaptamine (12.5 to 50 μM) were given to MDA-MB-231 cells. The vimentin mRNA and protein expression were evaluated using RT-qPCR and immunofluorescence, respectively, 72 h after Aaptamine treatment. The migration scratch assay was conducted for 48 hours. Results: Aaptamine treatment in three different doses did not affect the expression of vimentin at the mRNA level while significantly lowering vimentin protein expression at the concentration of 12.5 μM. In addition, Aaptamine significantly inhibited breast cancer cell migration in a dose-dependent manner. Conclusion: Aaptamine inhibits vimentin protein expression and demonstrates anti-migration activity in the sub-cytotoxic dose.
- Open Access
- 1 May 2025
- Published by Taylor & Francis in Journal of Multidisciplinary Healthcare
- Vol. ume 18, 2813-2823
Resistance Exercise as a Safe Modality for Quality of Life Improvement in Patients with Coronary Artery Diseases: A Review
Individuals with cardiovascular diseases (CVD) tend to have decreasing cardiorespiratory fitness (CRF), muscle strength, and quality of life (QoL). Because of its multiple benefits, participation in an exercise-based cardiac rehabilitation (CR) program was highly recommended for CVD patients. Currently, there is a trend of increasing the use of resistance exercises (RE) in CR and treatment of CVD, including coronary artery disease (CAD), peripheral arterial disease, and stroke. The application of RE in CVD patients also raises concerns for physicians due to adverse events related to cardiovascular responses. Therefore, this review aimed to explore the effect of RE on cardiovascular responses, cardiovascular risk factors, muscle strength, CRF, and the QoL, including its safety in CAD patients. Articles published in the last ten years were searched using PubMed, Science Direct, Research Gate, and Google Scholar databases using relevant keywords. Studies found that the administration of RE in CAD patients was proven safe when prescribed properly. Some literature showed that RE affected CVD risk factors by improving blood pressure, blood sugar, lipid profile, and body composition. In addition, systemic vascular resistance change led to vasodilatation and reduced blood pressure. Fatal and non-fatal myocardial infarction and mortality also decreased after progressive RE. High-intensity RE was proven to be better at increasing muscle strength compared to low-intensity because it produced a greater increase in the number of myofibrils and neural adaptation. Subsequently, aerobic exercise (AE) combined with RE caused a better increase in CRF. An increase in muscle strength and CRF, as well as diminished symptoms and controlled risk factors obtained from RE administration, increased QoL. To conclude, RE was a safe modality for QoL improvement in CAD patients through controlling risk factors and improving muscle strength and CRF.
- 1 May 2025
- Published by Taylor & Francis in Journal of Multidisciplinary Healthcare
- Vol. ume 18, 2813-2823
Open AccessResistance Exercise as a Safe Modality for Quality of Life Improvement in Patients with Coronary Artery Diseases: A Review
Individuals with cardiovascular diseases (CVD) tend to have decreasing cardiorespiratory fitness (CRF), muscle strength, and quality of life (QoL). Because of its multiple benefits, participation in an exercise-based cardiac rehabilitation (CR) program was highly recommended for CVD patients. Currently, there is a trend of increasing the use of resistance exercises (RE) in CR and treatment of CVD, including coronary artery disease (CAD), peripheral arterial disease, and stroke. The application of RE in CVD patients also raises concerns for physicians due to adverse events related to cardiovascular responses. Therefore, this review aimed to explore the effect of RE on cardiovascular responses, cardiovascular risk factors, muscle strength, CRF, and the QoL, including its safety in CAD patients. Articles published in the last ten years were searched using PubMed, Science Direct, Research Gate, and Google Scholar databases using relevant keywords. Studies found that the administration of RE in CAD patients was proven safe when prescribed properly. Some literature showed that RE affected CVD risk factors by improving blood pressure, blood sugar, lipid profile, and body composition. In addition, systemic vascular resistance change led to vasodilatation and reduced blood pressure. Fatal and non-fatal myocardial infarction and mortality also decreased after progressive RE. High-intensity RE was proven to be better at increasing muscle strength compared to low-intensity because it produced a greater increase in the number of myofibrils and neural adaptation. Subsequently, aerobic exercise (AE) combined with RE caused a better increase in CRF. An increase in muscle strength and CRF, as well as diminished symptoms and controlled risk factors obtained from RE administration, increased QoL. To conclude, RE was a safe modality for QoL improvement in CAD patients through controlling risk factors and improving muscle strength and CRF.
- Open Access
- 10 March 2025
- Published by MDPI AG in Biomolecules
- Vol. 15 (3) , 396
Extracellular Vesicles from Adipose-Derived Mesenchymal Stem Cells Improve Ligament–Bone Integration After Anterior Cruciate Ligament Primary Repair in Rabbit
Backgrounds: In this research, we want to find out whether extracellular vesicles (EVs) from adipose-derived mesenchymal stem cells (MSCs) can improve ligament–bone integration after primary Anterior Cruciate Ligament (ACL) repair by performing immunological and biomechanical tests. Methods: All of the rabbits underwent ACL resection at the proximal attachment to the femur bone, and then were divided into four groups. We performed an ELISA examination from the tissue at the bone–ligament interface of iNOS, CD206, MMP-3, and TIMP-1 to evaluate their levels at the inflammatory stage at the end of the first week. Immunoexpression of type I and III collagen and failure load biomechanical tests were performed at the end of the sixth week. Result: The group that underwent ACL repair with EVs augmentation had significantly higher levels of CD206, significantly lower MMP-3 levels, and significantly higher TIMP-1 levels in the first week. The iNOS levels in the group that underwent ACL repair with EVs augmentation were significantly different compared to the control group that did not receive any. The number of type I collagen fibers and the failure load levels in the group that underwent ACL repair with EVs augmentation were significantly higher. Conclusions: EVs from adipose-derived MSCs can improve the outcome of primary ACL repair in rabbits by regulating the inflammatory process during the healing period.
- 10 March 2025
- Published by MDPI AG in Biomolecules
- Vol. 15 (3) , 396
Open AccessExtracellular Vesicles from Adipose-Derived Mesenchymal Stem Cells Improve Ligament–Bone Integration After Anterior Cruciate Ligament Primary Repair in Rabbit
Backgrounds: In this research, we want to find out whether extracellular vesicles (EVs) from adipose-derived mesenchymal stem cells (MSCs) can improve ligament–bone integration after primary Anterior Cruciate Ligament (ACL) repair by performing immunological and biomechanical tests. Methods: All of the rabbits underwent ACL resection at the proximal attachment to the femur bone, and then were divided into four groups. We performed an ELISA examination from the tissue at the bone–ligament interface of iNOS, CD206, MMP-3, and TIMP-1 to evaluate their levels at the inflammatory stage at the end of the first week. Immunoexpression of type I and III collagen and failure load biomechanical tests were performed at the end of the sixth week. Result: The group that underwent ACL repair with EVs augmentation had significantly higher levels of CD206, significantly lower MMP-3 levels, and significantly higher TIMP-1 levels in the first week. The iNOS levels in the group that underwent ACL repair with EVs augmentation were significantly different compared to the control group that did not receive any. The number of type I collagen fibers and the failure load levels in the group that underwent ACL repair with EVs augmentation were significantly higher. Conclusions: EVs from adipose-derived MSCs can improve the outcome of primary ACL repair in rabbits by regulating the inflammatory process during the healing period.
- Open Access
The Role of SBDP Protein as a Potential Biomarker for Early-Onset Subarachnoid Hemorrhagic
Background and Objectives: Cerebral vasospasm is the most common complication of subarachnoid hemorrhage (SAH) that is related to high mortality and morbidity. Early biomarkers predicting those conditions are still limited. This study aims to analyze spectrin degradation products (SBDPs) as potential biomarkers for SAH patients, which can be used to monitor clinical outcomes. Materials and Methods: We conducted a prospective observational study in acute SAH within 72 h of onset. All patients underwent placement of continuous cerebrospinal drainage, and liquor was taken four times and analyzed using ELISA to measure SBDP150, SBDP145, and SBDP120 levels and analyzed using Friedman test and post hoc Wilcoxon analysis. The relationship between SBDP levels and vasospasm, as well as functional outcomes (using the Glasgow Outcome Scale–Extended, GOSE), was assessed. Results: We enrolled thirty-five patients: thirty patients with lumbar drainage (LD) and five with extra ventricular drainage (EVD). Friedman’s analysis showed significant changes over time for SBDP120 (p = 0.0001) and SBDP145 (p = 0.0001), but not for SBDP150 (p = 0.218). Levels of SBDP120 on day 3 (p = 0.001), SBDP120 on day 5 (p = 0.022), and SBDP145 on day 3 (p = 0.005) in EVD group were higher than in the LD group. SBDP145 on day 5 was significantly higher in patients with vasospasm (p = 0.041 in all patients, p = 0.028 in LD patients), indicating its potential as an early biomarker for vasospasm. SBDP145 on day 7 (p = 0.014) is the strongest predictor of unfavorable GOSE at 90 days in all patients. In LD patients, SBDP145 on day 7 (p = 0.002), SBDP120 on day 7 (p = 0.009), and SBDP120 on day 10 (p = 0.043) were significantly associated with poor GOSE at 90 days. Conclusions: A higher level of SBDP145 on day 5 can predict vasospasm risk, while an elevated level of SBDP145 and SBDP120 on day 7 is a potential predictor of poor functional outcomes. SBDPs may serve as valuable biomarkers for SAH management.
Open AccessThe Role of SBDP Protein as a Potential Biomarker for Early-Onset Subarachnoid Hemorrhagic
Background and Objectives: Cerebral vasospasm is the most common complication of subarachnoid hemorrhage (SAH) that is related to high mortality and morbidity. Early biomarkers predicting those conditions are still limited. This study aims to analyze spectrin degradation products (SBDPs) as potential biomarkers for SAH patients, which can be used to monitor clinical outcomes. Materials and Methods: We conducted a prospective observational study in acute SAH within 72 h of onset. All patients underwent placement of continuous cerebrospinal drainage, and liquor was taken four times and analyzed using ELISA to measure SBDP150, SBDP145, and SBDP120 levels and analyzed using Friedman test and post hoc Wilcoxon analysis. The relationship between SBDP levels and vasospasm, as well as functional outcomes (using the Glasgow Outcome Scale–Extended, GOSE), was assessed. Results: We enrolled thirty-five patients: thirty patients with lumbar drainage (LD) and five with extra ventricular drainage (EVD). Friedman’s analysis showed significant changes over time for SBDP120 (p = 0.0001) and SBDP145 (p = 0.0001), but not for SBDP150 (p = 0.218). Levels of SBDP120 on day 3 (p = 0.001), SBDP120 on day 5 (p = 0.022), and SBDP145 on day 3 (p = 0.005) in EVD group were higher than in the LD group. SBDP145 on day 5 was significantly higher in patients with vasospasm (p = 0.041 in all patients, p = 0.028 in LD patients), indicating its potential as an early biomarker for vasospasm. SBDP145 on day 7 (p = 0.014) is the strongest predictor of unfavorable GOSE at 90 days in all patients. In LD patients, SBDP145 on day 7 (p = 0.002), SBDP120 on day 7 (p = 0.009), and SBDP120 on day 10 (p = 0.043) were significantly associated with poor GOSE at 90 days. Conclusions: A higher level of SBDP145 on day 5 can predict vasospasm risk, while an elevated level of SBDP145 and SBDP120 on day 7 is a potential predictor of poor functional outcomes. SBDPs may serve as valuable biomarkers for SAH management.
- Open Access
- 30 September 2024
- Published by Oriental Scientific Publishing Company in Biomedical and Pharmacology Journal
- Vol. 17 (3) , 1715-1726
Effect of Metformin on Interleukin-6 Expression in Human Fibroblast Cell Aging Model
During skin aging, there is excessive secretion of inflammatory cytokines such as interleukin-6 (IL-6), which can make the ageing process more severe. Metformin has been known to have good anti-inflammatory activity through various pathways, one of which reduces the expression of inflammatory cytokines. This study aimed to analyze the effect of metformin treatment on IL-6 gene expression in an in vitro human fibroblast cell. Human fibroblast cells were obtained through foreskin isolation, and 72 cultured human fibroblast cells were divided into six groups based on cell passages, ranging from the third to the eighth. The expression of IL-6 was assessed in three treatments: negative control (normal cells), metformin 100 µM, and positive control (Vitamin E 50 µM). Treatment and measurement of IL-6 gene expression were carried out using qRT-PCR and calculated using the Livak-Schmittgen method. The results were then compared and analyzed using One-Way Analysis of Variance (ANOVA) and followed by post-hoc analysis. The negative control group had the lowest IL-6 gene expression compared to the metformin group and positive control group. The negative control IL-6 expression showed the highest value at passage 3 (0.166 ± 0.04) and the lowest at passage 6 (0.048 ± 0.04). Meanwhile, the expression of IL-6 positive control passage 4 (5.590 ± 3.34) showed the highest value and passage 7 (0.000 ± 0.00) showed the lowest value. In the metformin group, IL-6 gene expression was highest in passage 5 (0.836 ± 0.15) and lowest in passage 3 (0.078 ± 0.02). Based on treatment, there is a difference in IL-6 gene expression at passage 4 (p-value <0.05) and passage 5 (p-value <0.001). Metformin treatment passage 5 showed a significant difference with negative control (p-value <0.05) and with positive control (p-value <0.05). Our study concluded that the administration of metformin had no effect on IL-6 gene expression in human fibroblasts. However, metformin demonstrated anti-aging potential, as evidenced by a statistically significant difference in IL-6 expression between the negative control and positive control treatment groups.
- 30 September 2024
- Published by Oriental Scientific Publishing Company in Biomedical and Pharmacology Journal
- Vol. 17 (3) , 1715-1726
Open AccessEffect of Metformin on Interleukin-6 Expression in Human Fibroblast Cell Aging Model
During skin aging, there is excessive secretion of inflammatory cytokines such as interleukin-6 (IL-6), which can make the ageing process more severe. Metformin has been known to have good anti-inflammatory activity through various pathways, one of which reduces the expression of inflammatory cytokines. This study aimed to analyze the effect of metformin treatment on IL-6 gene expression in an in vitro human fibroblast cell. Human fibroblast cells were obtained through foreskin isolation, and 72 cultured human fibroblast cells were divided into six groups based on cell passages, ranging from the third to the eighth. The expression of IL-6 was assessed in three treatments: negative control (normal cells), metformin 100 µM, and positive control (Vitamin E 50 µM). Treatment and measurement of IL-6 gene expression were carried out using qRT-PCR and calculated using the Livak-Schmittgen method. The results were then compared and analyzed using One-Way Analysis of Variance (ANOVA) and followed by post-hoc analysis. The negative control group had the lowest IL-6 gene expression compared to the metformin group and positive control group. The negative control IL-6 expression showed the highest value at passage 3 (0.166 ± 0.04) and the lowest at passage 6 (0.048 ± 0.04). Meanwhile, the expression of IL-6 positive control passage 4 (5.590 ± 3.34) showed the highest value and passage 7 (0.000 ± 0.00) showed the lowest value. In the metformin group, IL-6 gene expression was highest in passage 5 (0.836 ± 0.15) and lowest in passage 3 (0.078 ± 0.02). Based on treatment, there is a difference in IL-6 gene expression at passage 4 (p-value <0.05) and passage 5 (p-value <0.001). Metformin treatment passage 5 showed a significant difference with negative control (p-value <0.05) and with positive control (p-value <0.05). Our study concluded that the administration of metformin had no effect on IL-6 gene expression in human fibroblasts. However, metformin demonstrated anti-aging potential, as evidenced by a statistically significant difference in IL-6 expression between the negative control and positive control treatment groups.
- Open Access
- 1 July 2024
- Published by Taylor & Francis in Infection and Drug Resistance
- Vol. ume 17, 3199-3208
The Roles of Endocytosis and Autophagy at the Cellular Level During Influenza Virus Infection: A Mini-Review
Acute respiratory infections contribute to morbidity and mortality worldwide. The common cause of this deadly disease is a virus, and one of the most commonly found is the influenza virus. Influenza viruses have several capabilities in infection, including utilizing the host’s machinery to survive within cells and replicate safely. This review aims to examine the literature on how influenza viruses use host machinery, including endocytosis and autophagy, for their internalization and replication within cells. This review method involves a literature search by examining articles published in the PubMed and Scopus databases. The keywords used were “Endocytosis” OR “Autophagy” AND “Influenza Virus”. Eighteen articles were included due to inclusion and exclusion criteria. GTPases switch, and V-ATPase plays a key role in the endocytic machinery hijacked by influenza viruses to enter host cells. On the other hand, LC3 and Atg5 facilitate influenza-induced apoptosis via the autophagic pathway. In conclusion, influenza viruses primarily use clathrin-mediated endocytosis to enter cells and avoid degradation during endosomal maturation by exiting endosomes for transfer to the nucleus for replication. It also uses autophagy to induce apoptosis to continue replication. The capability of the influenza viruses to hijack endocytosis and autophagy mechanisms could be critical points for further research. Therefore, we discuss how the influenza virus utilizes both endocytosis and autophagy and the approach for a new strategic therapy targeting those mechanisms.
- 1 July 2024
- Published by Taylor & Francis in Infection and Drug Resistance
- Vol. ume 17, 3199-3208
Open AccessThe Roles of Endocytosis and Autophagy at the Cellular Level During Influenza Virus Infection: A Mini-Review
Acute respiratory infections contribute to morbidity and mortality worldwide. The common cause of this deadly disease is a virus, and one of the most commonly found is the influenza virus. Influenza viruses have several capabilities in infection, including utilizing the host’s machinery to survive within cells and replicate safely. This review aims to examine the literature on how influenza viruses use host machinery, including endocytosis and autophagy, for their internalization and replication within cells. This review method involves a literature search by examining articles published in the PubMed and Scopus databases. The keywords used were “Endocytosis” OR “Autophagy” AND “Influenza Virus”. Eighteen articles were included due to inclusion and exclusion criteria. GTPases switch, and V-ATPase plays a key role in the endocytic machinery hijacked by influenza viruses to enter host cells. On the other hand, LC3 and Atg5 facilitate influenza-induced apoptosis via the autophagic pathway. In conclusion, influenza viruses primarily use clathrin-mediated endocytosis to enter cells and avoid degradation during endosomal maturation by exiting endosomes for transfer to the nucleus for replication. It also uses autophagy to induce apoptosis to continue replication. The capability of the influenza viruses to hijack endocytosis and autophagy mechanisms could be critical points for further research. Therefore, we discuss how the influenza virus utilizes both endocytosis and autophagy and the approach for a new strategic therapy targeting those mechanisms.
- Open Access
- 1 March 2024
- Published by Taylor & Francis in Integrated Blood Pressure Control
- Vol. ume 17, 21-37
Resistance Training in Cardiovascular Diseases: A Review on Its Effectiveness in Controlling Risk Factors
Cardiovascular Disease (CVD), a term encompassing various disorders affecting the heart and blood vessels, includes coronary artery disease (CAD). CAD is primarily due to the development of atherosclerotic plaques that disrupt blood flow, oxygenation, and nutrient delivery to the myocardium. Risk factors contributing to CAD progression include smoking, hypertension, diabetes mellitus (DM), dyslipidaemia, and obesity. While aerobic exercise (AE) has shown promising results in controlling CVD risk factors, the impact of resistance training (RT) has not been extensively investigated. This review aims to describe the effects of RT on CVD risk factors based on studies retrieved from PubMed and Google Scholar databases. Both isometric and isotonic RT have been found to decrease systolic blood pressure (SBP), diastolic blood pressure, or mean arterial pressure, with SBP showing a more significant reduction. Hypertensive patients engaging in RT alongside a calorie-restricted diet demonstrated significant improvements in blood pressure. RT is associated with increased nitric oxide bioavailability, sympathetic modulation, and enhanced endothelial function. In type-2 DM patients, 8– 12 weeks of RT led to improvements in fasting blood glucose levels, insulin secretion, metabolic syndrome risk, and glucose transporter numbers. Combining AE with RT had a more significant impact in reducing insulin resistance and enhancing blood glucose compared to performing exercises separately. It also significantly decreased total cholesterol, triglycerides, and low-density lipoprotein levels while increasing high-density lipoprotein within 12 weeks of application. However, improvements are considered insignificant when lipid levels are already low to normal at baseline. The administration of RT resulted in weight loss and improved body mass index, with more pronounced effects seen when combining AE with RT and a calorie-restricted diet. Considering these results, the administration of RT, either alone or in combination with AE, proves beneficial in rehabilitating CAD patients by improving various risk factors.
- 1 March 2024
- Published by Taylor & Francis in Integrated Blood Pressure Control
- Vol. ume 17, 21-37
Open AccessResistance Training in Cardiovascular Diseases: A Review on Its Effectiveness in Controlling Risk Factors
Cardiovascular Disease (CVD), a term encompassing various disorders affecting the heart and blood vessels, includes coronary artery disease (CAD). CAD is primarily due to the development of atherosclerotic plaques that disrupt blood flow, oxygenation, and nutrient delivery to the myocardium. Risk factors contributing to CAD progression include smoking, hypertension, diabetes mellitus (DM), dyslipidaemia, and obesity. While aerobic exercise (AE) has shown promising results in controlling CVD risk factors, the impact of resistance training (RT) has not been extensively investigated. This review aims to describe the effects of RT on CVD risk factors based on studies retrieved from PubMed and Google Scholar databases. Both isometric and isotonic RT have been found to decrease systolic blood pressure (SBP), diastolic blood pressure, or mean arterial pressure, with SBP showing a more significant reduction. Hypertensive patients engaging in RT alongside a calorie-restricted diet demonstrated significant improvements in blood pressure. RT is associated with increased nitric oxide bioavailability, sympathetic modulation, and enhanced endothelial function. In type-2 DM patients, 8– 12 weeks of RT led to improvements in fasting blood glucose levels, insulin secretion, metabolic syndrome risk, and glucose transporter numbers. Combining AE with RT had a more significant impact in reducing insulin resistance and enhancing blood glucose compared to performing exercises separately. It also significantly decreased total cholesterol, triglycerides, and low-density lipoprotein levels while increasing high-density lipoprotein within 12 weeks of application. However, improvements are considered insignificant when lipid levels are already low to normal at baseline. The administration of RT resulted in weight loss and improved body mass index, with more pronounced effects seen when combining AE with RT and a calorie-restricted diet. Considering these results, the administration of RT, either alone or in combination with AE, proves beneficial in rehabilitating CAD patients by improving various risk factors.