Serpil Aygörmez
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Serpil Aygörmez has a total of 74 co-authors. Here are the top co-authors by number of shared publications:
- Mustafa Makav
Kafkas University
13 shared publications - Mushap Kuru
Department of Obstetrics and Gynecology, Faculty of Veterinary Medicine, Kafkas University, Kars, Turkey
12 shared publications - Yusuf Umut Batı
Kafkas Üniversitesi
10 shared publications - Enes Akyüz
Kafkas Üniversitesi
9 shared publications - Erol Aydın
Kafkas Üniversitesi
9 shared publications - Kübra Kaya
Department of Physiology, Veterinary Faculty, Kafkas University, Kars 36000, Turkey
9 shared publications
Latest Publications
- Open Access
Molecular Detection of Bacterial Abortion Agents and Assessment of Serum MDA and GSH Levels in Aborting Small Ruminants in Siirt Province
Abortions in sheep and goat farming cause significant economic losses and a severe decline in productivity. The aim of this study was to detect the presence of Chlamydia abortus, Coxiella burnetii, Listeria spp., Listeria monocytogenes, and Campylobacter spp.—pathogens responsible for abortion cases in small ruminants—and to evaluate certain serum oxidative stress parameters. A total of 215 vaginal swab samples (sheep = 158; goats = 57) were examined using the Polymerase Chain Reaction (PCR) method. To evaluate the impact of the predominant bacterial agent, serum malondialdehyde and glutathione levels were analyzed in a focused subset (n = 140) comprising Campylobacter spp.-positive animals (n = 70) and pathogen-negative aborting controls (n = 70). PCR analysis revealed an overall positivity rate of 34.41% (n = 74), with Campylobacter spp. detected in 32.55% (70/215) and Chlamydia abortus in 1.86% (4/215) of samples, while no other targeted agents (Coxiella burnetii and Listeria spp.) were detected. In the Campylobacter spp.-positive group, serum malondialdehyde levels (32.14 ± 0.89) were significantly higher and glutathione levels (32.92 ± 3.25) were markedly lower compared to controls (9.30 ± 2.33 and 103.12 ± 1.63, respectively; p < 0.001; effect size r = 0.86), showing significant intra-species differences (p < 0.05) but no inter-species variation between infected sheep and goats (p > 0.05). In conclusion, Campylobacter spp. may play a significant role in small ruminant abortions in Siirt, which might be accompanied by cellular oxidative stress.
Open AccessMolecular Detection of Bacterial Abortion Agents and Assessment of Serum MDA and GSH Levels in Aborting Small Ruminants in Siirt Province
Abortions in sheep and goat farming cause significant economic losses and a severe decline in productivity. The aim of this study was to detect the presence of Chlamydia abortus, Coxiella burnetii, Listeria spp., Listeria monocytogenes, and Campylobacter spp.—pathogens responsible for abortion cases in small ruminants—and to evaluate certain serum oxidative stress parameters. A total of 215 vaginal swab samples (sheep = 158; goats = 57) were examined using the Polymerase Chain Reaction (PCR) method. To evaluate the impact of the predominant bacterial agent, serum malondialdehyde and glutathione levels were analyzed in a focused subset (n = 140) comprising Campylobacter spp.-positive animals (n = 70) and pathogen-negative aborting controls (n = 70). PCR analysis revealed an overall positivity rate of 34.41% (n = 74), with Campylobacter spp. detected in 32.55% (70/215) and Chlamydia abortus in 1.86% (4/215) of samples, while no other targeted agents (Coxiella burnetii and Listeria spp.) were detected. In the Campylobacter spp.-positive group, serum malondialdehyde levels (32.14 ± 0.89) were significantly higher and glutathione levels (32.92 ± 3.25) were markedly lower compared to controls (9.30 ± 2.33 and 103.12 ± 1.63, respectively; p < 0.001; effect size r = 0.86), showing significant intra-species differences (p < 0.05) but no inter-species variation between infected sheep and goats (p > 0.05). In conclusion, Campylobacter spp. may play a significant role in small ruminant abortions in Siirt, which might be accompanied by cellular oxidative stress.
- 8 September 2026
- Published by Taylor & Francis in Drug and Chemical Toxicology
- Vol. 49 (6) , 1642-1653
Insights into the protective role of trigonelline in 5-fluorouracil–induced lung injury: targeting oxidative stress, inflammation, and apoptosis
- 8 September 2026
- Published by Taylor & Francis in Drug and Chemical Toxicology
- Vol. 49 (6) , 1642-1653
Insights into the protective role of trigonelline in 5-fluorouracil–induced lung injury: targeting oxidative stress, inflammation, and apoptosis
- Open Access
- 21 July 2026
- Published by Wiley in Journal of Biochemical and Molecular Toxicology
- Vol. 40 (8)
Zingerone Alleviates Acetaminophen‐Induced Liver Damage by Regulating Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy
The aim of this study is to investigate the protective effect of zingerone (ZNG), an antioxidant agent, against acetaminophen (APAP)‐induced liver damage, which is used as an analgesic and antipyretic. For this purpose, twenty‐eight male rats were divided into four groups: control, ZNG, APAP, and APAP + ZNG. ZNG was administered orally for 7 days, followed by a single dose of APAP on the 7th day. At the end of the study, biochemical, molecular, and immunohistochemical analyses were performed on the liver tissue. According to the data obtained, APAP was found to trigger oxidative stress, inflammation, autophagy, apoptosis, endoplasmic reticulum stress, autophagy, and heat shock proteins in liver tissue. On the other hand, it has been observed that after ZNG treatment, the activities of antioxidant enzymes SOD, GPx, and CAT increased, MDA levels, a significant indicator of lipid peroxidation, decreased, and GSH stores were replenished. Following ZNG treatment, apoptosis was attenuated, resulting in decreased mRNA transcript levels of Bax, caspase‐3, and increase in Bcl‐2 levels. ZNG treatment resulted in a decrease in endoplasmic reticulum stress, inflammation, autophagy mRNA transcript levels. In addition, a decrease in heat shock proteins was detected. In conclusion, it has been observed that ZNG may be a significant protective against APAP liver damage.
- 21 July 2026
- Published by Wiley in Journal of Biochemical and Molecular Toxicology
- Vol. 40 (8)
Open AccessZingerone Alleviates Acetaminophen‐Induced Liver Damage by Regulating Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy
The aim of this study is to investigate the protective effect of zingerone (ZNG), an antioxidant agent, against acetaminophen (APAP)‐induced liver damage, which is used as an analgesic and antipyretic. For this purpose, twenty‐eight male rats were divided into four groups: control, ZNG, APAP, and APAP + ZNG. ZNG was administered orally for 7 days, followed by a single dose of APAP on the 7th day. At the end of the study, biochemical, molecular, and immunohistochemical analyses were performed on the liver tissue. According to the data obtained, APAP was found to trigger oxidative stress, inflammation, autophagy, apoptosis, endoplasmic reticulum stress, autophagy, and heat shock proteins in liver tissue. On the other hand, it has been observed that after ZNG treatment, the activities of antioxidant enzymes SOD, GPx, and CAT increased, MDA levels, a significant indicator of lipid peroxidation, decreased, and GSH stores were replenished. Following ZNG treatment, apoptosis was attenuated, resulting in decreased mRNA transcript levels of Bax, caspase‐3, and increase in Bcl‐2 levels. ZNG treatment resulted in a decrease in endoplasmic reticulum stress, inflammation, autophagy mRNA transcript levels. In addition, a decrease in heat shock proteins was detected. In conclusion, it has been observed that ZNG may be a significant protective against APAP liver damage.
- 18 June 2026
- Published by Vizetek Publishing Company
Veteriner Klinik Bilimlerde Seçilmiş Konular Güncel Yaklaşımlar
Veteriner Klinik Bilimlerde Seçilmiş Konular: Güncel Yaklaşımlar başlıklı bu eser, modern veteriner hekimliğin gelişimine yön veren kritik konu başlıklarını, en güncel literatür verileri ve kanıta dayalı bilimsel yaklaşımlarla harmanlayarak sunmaktadır. Kitapta yer alan yedi özgün bölüm; ovaryum hasarının moleküler zeminindeki oksidatif süreçlerden, küçükbaş hayvancılıkta cinsel aktiviteyi doğal yollarla uyaran koç etkisine; embriyo transferi teknolojisinin tüm teknik aşamalarından, anne-yavru bağının etolojik paternlerine kadar üreme bilimini kapsamlıca ele almaktadır. Bununla birlikte, kuzu yaşama gücünün yönetimi ile neonatal kayıpların önlenmesindeki kritik kontrol noktaları ve küçük hayvan ortopedik cerrahisinde doku iyileşmesini destekleyen rejeneratif tıp uygulamaları klinik esaslarıyla paylaşılmaktadır. Hem sahada aktif çalışan veteriner hekimler hem de akademisyenler için başvuru kaynağı niteliğindeki bu eser, klinik bilimlerdeki modern yaklaşımları anlamak isteyen herkese benzersiz bir perspektif sunmaktadır.
- 18 June 2026
- Published by Vizetek Publishing Company
Veteriner Klinik Bilimlerde Seçilmiş Konular Güncel Yaklaşımlar
Veteriner Klinik Bilimlerde Seçilmiş Konular: Güncel Yaklaşımlar başlıklı bu eser, modern veteriner hekimliğin gelişimine yön veren kritik konu başlıklarını, en güncel literatür verileri ve kanıta dayalı bilimsel yaklaşımlarla harmanlayarak sunmaktadır. Kitapta yer alan yedi özgün bölüm; ovaryum hasarının moleküler zeminindeki oksidatif süreçlerden, küçükbaş hayvancılıkta cinsel aktiviteyi doğal yollarla uyaran koç etkisine; embriyo transferi teknolojisinin tüm teknik aşamalarından, anne-yavru bağının etolojik paternlerine kadar üreme bilimini kapsamlıca ele almaktadır. Bununla birlikte, kuzu yaşama gücünün yönetimi ile neonatal kayıpların önlenmesindeki kritik kontrol noktaları ve küçük hayvan ortopedik cerrahisinde doku iyileşmesini destekleyen rejeneratif tıp uygulamaları klinik esaslarıyla paylaşılmaktadır. Hem sahada aktif çalışan veteriner hekimler hem de akademisyenler için başvuru kaynağı niteliğindeki bu eser, klinik bilimlerdeki modern yaklaşımları anlamak isteyen herkese benzersiz bir perspektif sunmaktadır.
- Open Access
- 10 April 2026
- Published by Wiley in Journal of Applied Toxicology
- Vol. 46 (12) , 4497-4510
Protective Role of Polydatin Against Vancomycin‐Induced Lung Toxicity via Oxidative Stress, Inflammation, Endoplasmic Reticulum Stress, Apoptosis, and Ferroptosis Pathways
This study aimed to evaluate whether polydatin (Poly) could eliminate the harmful effects of vancomycin (VCM) on the lungs of rats. Rats were administered VCM (200 mg/kg) and Poly (50 mg/kg), both separately and in combination, for a duration of 7 days. Following this, various methods were utilized to analyze proteins and pathological changes in lung tissue related to oxidative stress, inflammation, endoplasmic reticulum stress, apoptosis, and ferroptosis. It was found that Poly application significantly enhanced antioxidant enzyme activities and nonenzymatic antioxidants while decreasing VCM‐induced lipid peroxidation. The study showed that VCM elevated the expression of inflammatory cytokines as well as Janus kinase 2 (JAK‐2) and signal transducer and activator of transcription 3 (STAT‐3), whereas Poly treatment inhibited these genes. Furthermore, VCM was found to induce apoptotic markers, but Poly offered protection to lung tissue against the harmful effects of VCM by demonstrating an antiapoptotic effect. Additionally, the increased expression of prostaglandin endoperoxide synthase 2 (PTGS2) and transferrin receptor 1 (TFR1), along with the decreased expression of glutathione peroxidase 4 (GPX4) in lung tissue induced by VCM, showed improvement following Poly administration. VCM was observed to increase, while Poly decreased the expression of endoplasmic reticulum stress markers. Overall, the findings of this study suggest that Poly has therapeutic potential in combating VCM‐induced lung toxicity.
- 10 April 2026
- Published by Wiley in Journal of Applied Toxicology
- Vol. 46 (12) , 4497-4510
Open AccessProtective Role of Polydatin Against Vancomycin‐Induced Lung Toxicity via Oxidative Stress, Inflammation, Endoplasmic Reticulum Stress, Apoptosis, and Ferroptosis Pathways
This study aimed to evaluate whether polydatin (Poly) could eliminate the harmful effects of vancomycin (VCM) on the lungs of rats. Rats were administered VCM (200 mg/kg) and Poly (50 mg/kg), both separately and in combination, for a duration of 7 days. Following this, various methods were utilized to analyze proteins and pathological changes in lung tissue related to oxidative stress, inflammation, endoplasmic reticulum stress, apoptosis, and ferroptosis. It was found that Poly application significantly enhanced antioxidant enzyme activities and nonenzymatic antioxidants while decreasing VCM‐induced lipid peroxidation. The study showed that VCM elevated the expression of inflammatory cytokines as well as Janus kinase 2 (JAK‐2) and signal transducer and activator of transcription 3 (STAT‐3), whereas Poly treatment inhibited these genes. Furthermore, VCM was found to induce apoptotic markers, but Poly offered protection to lung tissue against the harmful effects of VCM by demonstrating an antiapoptotic effect. Additionally, the increased expression of prostaglandin endoperoxide synthase 2 (PTGS2) and transferrin receptor 1 (TFR1), along with the decreased expression of glutathione peroxidase 4 (GPX4) in lung tissue induced by VCM, showed improvement following Poly administration. VCM was observed to increase, while Poly decreased the expression of endoplasmic reticulum stress markers. Overall, the findings of this study suggest that Poly has therapeutic potential in combating VCM‐induced lung toxicity.
- Open Access
- 6 March 2026
- Published by Springer Nature in Naunyn-Schmiedeberg's Archives of Pharmacology
- Vol. 399 (8) , 12799-12800
Correction: Nobiletin reduces 5-FU-induced lung injury with antioxidative, anti-inflammatory and anti-apoptotic activities
- 6 March 2026
- Published by Springer Nature in Naunyn-Schmiedeberg's Archives of Pharmacology
- Vol. 399 (8) , 12799-12800
Open AccessCorrection: Nobiletin reduces 5-FU-induced lung injury with antioxidative, anti-inflammatory and anti-apoptotic activities
- Open Access
- 4 March 2026
- Published by Kocatepe Veteriner Dergisi in Kocatepe Veterinary Journal
- Vol. 19 (1) , 63-73
Morin Reduces Ciprofloxacin-Induced Brain Damage by Regulating Oxidative Stress, Inflammation, and Histopathological Changes
Ciprofloxacin (CPFX), one of the fluoroquinones, is an antibacterial antibiotic that is used in the treatment of urinary tract, respiratory, abdominal and gastrointestinal infections as well as having negative side effects on the central nervous system. Morin, a bioactive flavonoid, is an antioxidant with neuroprotective properties thanks to its many pharmacological properties. The protective effect off Morin against brain damage caused by CPFX, broad spectrum antibiotic, was investigated. Twentyeight female rats were divided into four groups as control, Morin, CPFX, CPFX+Morin. CPFX, Morin was administered once a day for seven days. Oxidative stress and inflammation parameters were analyzed to determine brain tissue damage and histopathological analysis was performed to determine tissue damage and structural changes. According to the findings obtained as a result of the analyses, CPFX increased nuclear factor kappa B (NF-B), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin 1β (IL-1β) and decreased glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) in brain. Co-administration of CPFX with Morin increased GSH and GPx, SOD, CAT and decreased NF-B, MDA, TNF-α, IL-1β levels. According to findings, when evaluated together, it was found that CPFX caused damage in brain tissue by causing oxidative stress and inflammation and Morin as a supportive treatment reduced the damage in brain tissue by bringing these markers closer to normal.
- 4 March 2026
- Published by Kocatepe Veteriner Dergisi in Kocatepe Veterinary Journal
- Vol. 19 (1) , 63-73
Open AccessMorin Reduces Ciprofloxacin-Induced Brain Damage by Regulating Oxidative Stress, Inflammation, and Histopathological Changes
Ciprofloxacin (CPFX), one of the fluoroquinones, is an antibacterial antibiotic that is used in the treatment of urinary tract, respiratory, abdominal and gastrointestinal infections as well as having negative side effects on the central nervous system. Morin, a bioactive flavonoid, is an antioxidant with neuroprotective properties thanks to its many pharmacological properties. The protective effect off Morin against brain damage caused by CPFX, broad spectrum antibiotic, was investigated. Twentyeight female rats were divided into four groups as control, Morin, CPFX, CPFX+Morin. CPFX, Morin was administered once a day for seven days. Oxidative stress and inflammation parameters were analyzed to determine brain tissue damage and histopathological analysis was performed to determine tissue damage and structural changes. According to the findings obtained as a result of the analyses, CPFX increased nuclear factor kappa B (NF-B), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin 1β (IL-1β) and decreased glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) in brain. Co-administration of CPFX with Morin increased GSH and GPx, SOD, CAT and decreased NF-B, MDA, TNF-α, IL-1β levels. According to findings, when evaluated together, it was found that CPFX caused damage in brain tissue by causing oxidative stress and inflammation and Morin as a supportive treatment reduced the damage in brain tissue by bringing these markers closer to normal.
- 14 February 2026
- Published by Elsevier in The Veterinary Journal
- Vol. 316, 106592
The evaluation of inflammation and oxidative stress following successful non-surgical uterine flushing in Tuj sheep using a Wallace Sure Pro® catheter
- 14 February 2026
- Published by Elsevier in The Veterinary Journal
- Vol. 316, 106592
The evaluation of inflammation and oxidative stress following successful non-surgical uterine flushing in Tuj sheep using a Wallace Sure Pro® catheter
- Open Access
- 20 January 2026
- Published by Springer Nature in Biological Trace Element Research
- Vol. 204 (3) , 2052-2064
Protective Role of Chrysin against Mercury Chloride-Induced Testicular Damage via Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy Pathways
The aim of this research was to examine the potential ameliorative effects of chrysin (CHR) against mercuric chloride (HgCl 2 )-induced testicular damage in rats. For this purpose, rats were divided into four groups: Control, CHR, HgCl 2 and HgCl 2 + CHR. HgCl 2 was administered intraperitoneally at a dose of 1.23 mg/kg, and CHR was administered orally at a dose of 50 mg/kg for 7 days. Biochemical, molecular and immunohistochemical analyses were performed to determine the effect of treatment-mediated changes in the testicular tissue. Based on the results obtained in testicular tissue, administration of HgCl 2 was observed to lower antioxidant markers, elevate malondialdehyde (MDA) levels, and increase inflammatory marker expression in rat testicular tissue. It also led to reduced testosterone levels. Additionally, there was a decrease in the expression of antiapoptotic B-cell lymphoma 2 (Bcl-2) an apoptosis marker while the levels of Caspase-3 and Bcl-2-associated X protein (Bax) were found to be higher. The endoplasmic reticulum stress marker protein kinase R-like ER kinase (PERK) and the autophagy marker Beclin-1 showed strong immunoreactivity. Additionally, HgCl 2 + CHR treatment were found to significantly reduce oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and autophagy processes in testicular tissue. In conclusion, HgCl 2 administration to rats caused testicular tissue damage compared to the other groups, but CHR treatment alleviated this damage. Overall, this demonstrates the potential ameliorative mechanisms of CHR as a possible agent for HgCl 2 -induced testicular damage.
- 20 January 2026
- Published by Springer Nature in Biological Trace Element Research
- Vol. 204 (3) , 2052-2064
Open AccessProtective Role of Chrysin against Mercury Chloride-Induced Testicular Damage via Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy Pathways
The aim of this research was to examine the potential ameliorative effects of chrysin (CHR) against mercuric chloride (HgCl 2 )-induced testicular damage in rats. For this purpose, rats were divided into four groups: Control, CHR, HgCl 2 and HgCl 2 + CHR. HgCl 2 was administered intraperitoneally at a dose of 1.23 mg/kg, and CHR was administered orally at a dose of 50 mg/kg for 7 days. Biochemical, molecular and immunohistochemical analyses were performed to determine the effect of treatment-mediated changes in the testicular tissue. Based on the results obtained in testicular tissue, administration of HgCl 2 was observed to lower antioxidant markers, elevate malondialdehyde (MDA) levels, and increase inflammatory marker expression in rat testicular tissue. It also led to reduced testosterone levels. Additionally, there was a decrease in the expression of antiapoptotic B-cell lymphoma 2 (Bcl-2) an apoptosis marker while the levels of Caspase-3 and Bcl-2-associated X protein (Bax) were found to be higher. The endoplasmic reticulum stress marker protein kinase R-like ER kinase (PERK) and the autophagy marker Beclin-1 showed strong immunoreactivity. Additionally, HgCl 2 + CHR treatment were found to significantly reduce oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and autophagy processes in testicular tissue. In conclusion, HgCl 2 administration to rats caused testicular tissue damage compared to the other groups, but CHR treatment alleviated this damage. Overall, this demonstrates the potential ameliorative mechanisms of CHR as a possible agent for HgCl 2 -induced testicular damage.