Nora F. Ghanem

This research aimed to examine the impact of synthesized chitosan nanoparticles (ChN) on streptozotocin (STZ)-induced diabetic rats through metabolic, antioxidant, histopathological, histochemical, ultrastructural and immunohistochemical analyses. ChN were analyzed through Scanning Electron Microscopy (SEM), X-ray diffraction (XRD), and Fourier Transform Infrared (FTIR). Rats were allocated into the following groups: control, ChN (0.5mg/kg body weight), diabetics induced by streptozotocin (STZ, 65mg/kg body weight), and STZ-ChN (0.5 mg/kg body weight). SEM results indicated that ChN exhibited a uniform spherical morphology. Treatment with ChN led to a significant increase in insulin levels and a decrease in glucose and HbA1c, in contrast to the STZ group. ChN treatment significantly reduced the lipid profile. Significant increase in superoxide dismutase and nitric oxide levels, alongside a reduction in malondialdehyde levels was seen after ChN treatment. ChN therapy improved the histopathological changes of pancreatic islets, increasing β-cell density and insulin immunostaining expression. Pancreatic collagen deposition and TGF-β1 immunostaining were also decreased. Ultrastructural studies confirmed the protective effects of ChN on pancreatic cells (α, β, δ). These findings indicated that ChN may function as a potential therapeutic agent for diabetes mellitus management, emphasizing its role in modulating metabolic, antioxidant, and hypoglycemic disturbances while protecting pancreatic tissue.

Tartrazine, a coal tar-derived azo color, is utilized in food, drinks, cosmetics, and pharmaceuticals. Its azo group catabolizes in the gut, poisoning the liver. This study investigated the efficacy of melatonin, an endogenous antioxidant from the pineal gland against hepatotoxicity in tartrazine-intoxicated rats. Thirty-two adult male wistar albino rats were allocated into four groups: control group, melatonin group (10 mg/kg), tartrazine-treated group (7.5 mg/kg), and tartrazine + melatonin-treated group (7.5 mg/kg tartrazine + 10 mg/kg melatonin). Doses were taken daily for 4 weeks. Melatonin's influence on hepatotoxicity was assessed by monitoring liver enzyme activity, antioxidant state, apoptotic and inflammatory markers, DNA fragmentation, histological and ultrastructural changes. Rats exposed to tartrazine exhibited elevated liver enzymes, oxidant-antioxidant imbalance, and elevated hepatic inflammatory markers (TNF-α, IL-6). Tartrazine also damaged DNA and induced histological and ultrastructural alterations in liver tissue, as shown by the comet assay. Alpha-fetoprotein (AFP) and proliferating cell nuclear antigen (PCNA) were strongly expressed in immunohistochemistry. In rats, melatonin significantly reduced all tartrazine effects. Conversely, melatonin treatment significantly alleviated all aforementioned effects induced by tartrazine in rats by decreasing liver enzymes, elevating antioxidant enzymes, and reducing hepatic inflammatory markers. Enhanced histological assessment and the ultrastructure of the liver was detected following melatonin use. The use of melatonin may safeguard against tartrazine-induced hepatic DNA damage. In conclusion, the current findings indicate that tartrazine administration has detrimental health effects and deleterious impacts on liver function and structure. Melatonin mitigated tartrazine-induced liver damage via antioxidant, anti-inflammatory, and anti-apoptotic pathways.

Background: Cryptosporidium, a global intestinal protozoan parasite, induces mild to severe diarrhea in several vertebrate hosts, potentially resulting in life-threatening sickness. This study aimed to assess the efficacy of biosynthesized nano-zinc oxide using cellulose nanocrystals and Zingiber officinale extract (Bio-ZnNPs) in the treatment of experimentally infected mice with cryptosporidiosis. Methods: A total of 20 male mice were allocated into four experimental groups (G1-G4), with triplicates. G1 (Control); non-infected, non-treated, G2 (Inf); infected with Cryptosporidium parvum, G3 (Bio-ZnNPs); infected- treated with Bio-ZnNPs at 200 mg/kg B.W. and G4 (NTZ) infected- treated with nitazoxanide (NTZ) at 100 mg/kg B.W. Mice were inoculated with 3000 oocysts of C. parvum. All treatments commenced on the initial day of oocyst shedding and persisted for five continuous days for all groups, excluding the negative control one. Oocysts count was assessed daily from the 1st to the 5th day post-treatment. Hematological analyses, blood biochemistry, immunoglobulin level assessments and histopathological evaluations were performed on day 5 post-treatment. Result: The Bio-ZnNPs treated group exhibited the highest percentage reduction in C. parvum oocyst excretion. Furthermore, Bio-ZnNPs treatment resulted in notable enhancements in hematological parameters, liver enzymes and immunoglobulin levels, including immunoglobulin G and immunoglobulin M using Bio-ZnNPs. Additionally, a significant improvement in intestinal lesions with no intraluminal oocysts was noted in the Bio-ZnNPs treated group. Taken all together, this work demonstrated the promising performance of nanocomposites composed of cellulose nanocrystals and zinc oxide nanoparticles as an effective drug delivery strategy to enhance the efficacy of Zingiber officinale extract against experimental infected mice with C. parvum.

Background: Cryptosporidiosis poses several health risks, particularly due to its potential severity and the populations it can affect. Comprehending these hazards is crucial for efficient prevention and treatment. This study was to investigate the efficiency of cellulose nanocrystals (CNC), nitazoxanide (NTZ) and nitazoxanide-cellulose nanocrystals (NTZ-CNC) in treating experimental infected mice of cryptosporidiosis. Methods: A total of 75 male swiss albino mice were allocated into eight groups (5 mice/ group) with triplicates of each group. Infection with cryptosporidiosis was conducted with 3000 Cryptosporidium parvum oocysts. All treatments commenced on the initial day of oocyst emergence and persisted for five succeeding days across all groups, except for the negative control group. Oocysts shedding was estimated daily from 1st till 20 days post treatment. Hematological and blood biochemical analysis, immunoglobulins levels as well as histopathological studies were performed. Result: It was detected that NTZ-CNC group had the lowest Cryptosporidium oocysts shedding. Also, these treatments induced significant improvements in hematological, blood biochemical, immunoglobulins levels including immunoglobulin G and immunoglobulin M with best improvements recorded in NTZ-CNC treated groups. A remarkable amelioration of the intestinal histopathological lesions was observed, especially in NTZ-CNC treated group. In conclusion, this study reported that CNC could significantly enhance the therapeutic effects of NTZ, making it a promising treatment for cryptosporidiosis due to its potent anti-parasitic and anti-inflammatory capabilities.

Environmental and occupational exposure to hexavalent chromium (CrVI) is mostly renowned as a possible hepatotoxic in mammals.Echinacea purpurea(L.) Moench, a phenolic-rich plant, is recurrently used for its therapeutic properties. Therefore, this investigation was done to explore whetherE. purpurea(EP) root extract would have any potential health benefits against an acute dose of CrVI-induced oxidative damage and hepatotoxicity. Results revealed that GC–MS analysis of EP root extract has 26 identified components with a significant amount of total phenolic and flavonoid contents. Twenty-four Male Wistar rats were divided into four groups: control, EP (50 mg/kg BW/day for 21 days), CrVI (15 mg/kg BW as a single intraperitoneal dosage), and EP + CrVI, respectively. Rats treated with CrVI displayed a remarkable rise in oxidative stress markers (TBARS, H₂O₂, PCC), bilirubin, and lactate dehydrogenase activity, and a marked decrease in enzymatic and non-enzymatic antioxidants, transaminases, and alkaline phosphatase activities, and serum protein level. Also, CrVI administration induced apoptosis and inflammation in addition to histological and ultrastructural abnormalities in the liver tissue. The examined parameters were improved significantly in rats pretreated with EP and then intoxicated with CrVI. Conclusively, EP had a potent antioxidant activity and could be used in the modulation of CrVI-induced hepatotoxicity.

Aluminum (Al) is an important factor in the environment as it is used in agriculture and several industries leading to hazardous effects via oxidative stress. Bromelain is a cheap extract from the byproduct waste of Ananas comosus stem. It has been used in several biological and therapeutic applications. So, this study was undertaken to assess the hepatoprotective potential of bromelain versus oxidative stress induced by aluminum chloride in rats. Results revealed that administration of AlCl₃ reduced the body and liver weights and increased Al concentration in the blood and liver tissue. Also, AlCl₃ caused valuable changes in hematological parameters and increased TBARS and H₂O₂ concentrations in rat liver. Enzymatic (SOD, CAT, GPx, GR, and GST) and nonenzymatic (GSH) antioxidants and protein content were significantly decreased. Furthermore, alterations in liver biomarkers such as bilirubin level and enzyme activities in both serum and liver homogenate (LDH, ALP, AST, and ALT) were detected. AlCl₃ also caused inflammation as indicated by upregulation of the inflammation‐related genes [interleukin 1 beta (IL‐1β)], tumor necrosis factor‐alpha (TNF‐α), as well as matrix metalloproteinase (MMP9), and downregulation of nuclear factor erythroid 2 (Nrf2) expression. In addition, histopathological examination showed significant variations in the liver that confirms the biochemical results. Otherwise, bromelain intake alone slumped lipid peroxidation and gotten better antioxidant status significantly. Moreover, supplementation with bromelain before AlCl₃ intoxication restores enzymatic and nonenzymatic antioxidants as well as biochemical indices and tissue architecture with respect to the AlCl₃ group. In conclusion, bromelain proved its remarkable protective power to abolish AlCl₃ toxicity. So, it might represent a new strategy in the therapy of metal toxicity by its antioxidant capacity.

Environmental and occupational exposure to chromium compounds, especially hexavalent chromium [Cr(VI)], is widely recognized as a potential nephrotoxic in humans and animals. Its toxicity is associated with the overproduction of free radicals, which induces oxidative damage. Echinacea purpurea (L.) Moench is an herbaceous perennial plant rich in phenolic components and frequently used for its medicinal benefits. The current work evaluated the effectiveness of E. purpurea (EP) against oxidative stress and nephrotoxicity induced by potassium dichromate in male rats. Male Wistar rats were divided into four groups: control, E. purpurea (EP; 50 mg/kg; once daily for 3 weeks), hexavalent chromium (Cr(VI); 15 mg/kg; single intraperitoneal dose), and EP + Cr(VI) where rats were pretreated with EP for 3 weeks before receiving CrVI, respectively. Results revealed that rats exposed to Cr(VI) showed a significant increase in PC, TBARS, and H2O2, kidney function biomarkers (Urea, creatinine, and uric acid), lactate dehydrogenase activity (LDH), TNF-alpha, IL-18, nuclear factor kappa B (NF kappa B), and IGF-1 (Insulin-like growth factor-1) levels as well as a considerable decline in metallothionein (MT), glutathione (GSH) content, enzymatic antioxidants (SOD, CAT, GPx, GR, and GST), alkaline phosphatase (ALP) activities, and protein content. Cr(VI) induced apoptosis in kidney tissues as revealed by upregulation of Bax and caspase 3 and downregulation of Bcl-2. Furthermore, EP treatment ameliorated the Cr(VI)-induced histopathological and ultrastructure variations of kidney tissue, which was confirmed by the biochemical and molecular data. It is clear from the results of this study that EP exerts nephroprotective effects by improving the redox state, suppressing inflammatory reaction and cell apoptosis as well as ameliorating the performance of kidney tissue architecture, which is eventually reflected by the improvement of kidney function in rats.

The present study evaluated the antioxidant capacity and antidiabetic effect of Actinidia deliciosa in diabetic rats. Rats were grouped as follows: control, Actinidia deliciosa aqueous extract (ADAE, 1g/kg, daily and orally), streptozotocin (STZ, 50mg/kg BW, single intraperitoneal dose), and STZ plus ADAE, respectively. Twenty-eight components were detected by GC-MS analysis with high phenolic contents and high DPPH scavenging activity. In vivo results revealed that rats treated with STZ showed a highly significant elevation in blood glucose and a decrease in insulin hormone levels. Thiobarbituric acid-reactive substances and hydrogen peroxide levels were elevated, while bodyweight, enzymatic, and nonenzymatic antioxidants were significantly decreased. Furthermore, histopathological and immunohistochemical insulin expression, besides ultrastructure microscopic variations (β-cells, α-cells, and -cells), were seen in pancreas sections supporting the obtained biochemical changes. Otherwise, rats supplemented with ADAE alone showed an improved antioxidant status and declined lipid peroxidation. Moreover, diabetic rats augmented with ADAE showed significant modulation in oxidative stress markers and different pancreatic tissue investigations compared to diabetic ones. Conclusively, ADAE has a potent antioxidant and hypoglycemic influence that may be utilized as a health-promoting complementary therapy in diabetes mellitus.

The present research intended to assess the possible protective and hypoglycemic effect of Actinidia deliciosa fruit aqueous extract (ADAE) in diabetic rats. The scavenging antioxidant capabilities of ADAE were evaluated using GC‐MS analysis. In addition, rats were divided into four groups: control, ADAE, streptozotocin‐induced DM (STZ), and STZ‐treated rats + ADAE in an in vivo investigation. GC‐MS analysis of ADAE was shown to include major components with high total phenolic contents and high DPPH scavenging activity. In diabetic rats, significant elevation in blood glucose level, lipid peroxidation, bilirubin, and lactate dehydrogenase activity as well as a change in lipid profile was observed, while insulin, body and liver weights, enzymatic and nonenzymatic antioxidants, liver function biomarkers, and protein content were significantly decreased. Furthermore, changes in the expression of the peroxisome proliferator‐activated receptor (PPAR‐γ), apoptotic, and inflammation‐related genes were found. In addition, histological differences in rat liver tissue architecture were discovered, corroborating the biochemical modifications. However, consuming ADAE alone reduced lipid peroxidation and improved antioxidant status. Furthermore, diabetic rats given ADAE showed significant reductions in oxidative stress indicators and biochemical parameters, as well as improved tissue structure, when compared to the diabetic rats’ group. Also, ADAE supplementation protects diabetic rats’ hepatic tissue by upregulating PPAR‐γ and downregulating apoptotic and inflammatory‐related gene expression. In conclusion, A. deliciosa has beneficial protective effects so, it might be used as a complementary therapy in diabetes mellitus.