Significant Increase In GSH Levels Research Articles

Effects of long-term Tai Chi vs. aerobic exercise on antioxidant activity and cognitive function in individuals with Parkinson’s disease

An imbalance between the generation of reactive oxygen species and the body’s antioxidant defense mechanisms is closely related to the development and progression of Parkinson’s disease (PD). Considering that physical exercise is a potential therapeutic intervention for modulating oxidative stress markers and cognitive function in PD, the primary purpose of this study was to compare the effects of different long-term exercise modalities on antioxidants and cognitive performance in patients with PD. In addition, the secondary purpose was to explore whether changes in the levels of these biochemical markers are associated with alterations in cognitive performance pre- and post-intervention. In all, 61 participants were randomly divided into the aerobic exercise (AE, n=20), Tai Chi exercise (TCE, n=21), or control (n=20) group. Blood samples were collected before and after a 12-week intervention period for the analysis of antioxidant markers [leukocyte 8-hydroxydeoxyguanosine (8-OHdG), catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-Px), oxidized glutathione (GSSG), superoxide dismutase (SOD), and uric acid (UA)]. Cognitive function was evaluated using the Mini-Mental State Examination (MMSE). Although no significant changes were observed in the activity of 8-OhdG, GSH-Px, GSSG, GSH:GSSG ratio, SOD, and cognitive performance in the AE and TCE groups, the 12-week AE intervention led to a significant increase in CAT and GSH levels, along with a significantly decrease in UA levels among individuals with PD. Conversely, the TCE intervention resulted in a significant increase in GSH levels. However, SOD activity and MMSE scores were significantly decreased after 12 weeks in the control group. The correlations between changes in MMSE scores and changes in the levels of GSH and UA prior to and after the intervention reached significance in the AE group. Thus, long-term AE and TCE might serve as effective strategies for reducing oxidative damage and preserving cognitive function in PD, with AE exhibiting greater benefits compared with TCE. These findings hold potential clinical relevance as complementary measures to standard medical treatments and alternative therapies, such as antioxidant supplements and dietary adjustments, particularly for individuals in the early stages of PD.

Abstract Tu138: Tandem Mass Tagging (TMT)-based Identification of Proteome Signatures for Ischemia-Reperfusion Injury in Swine

Background: The composition of proteins in blood plasma mirrors the physical changes occurring in the course of disease pathogenesis. Currently available clinical markers are insufficient to predict the actual damage and the redox changes in response to ischemia. Hence, we identified novel redox markers for ischemia/reperfusion (I/R) in swine using TMT-proteomics. Methodology: We employed TMT-10plex isobaric labeling-based quantitative proteomics to track the plasma proteome in Sus Scorfa pigs subjected to surgical I/R at different time points. Plasma samples were collected before ischemia, at 1-hr after ischemia (baseline), and 4-hr, 24-hrs, and 7 days following reperfusion. Results: An average of 4853 spectra and a total of 457 proteins were identified, ensuring a 1% false discovery rate for peptides and proteins with at least two distinct peptides. Pre-ischemia plasma samples served as the control group in all the analyses. TMT analysis revealed temporal changes in the plasma proteome with a prominent shift at 4 hours after I/R insult. To investigate the significantly changed proteins (>1.5 fold), a temporal analysis was carried out. Notably, endopin-1, a serpin protein family member, and fibronectin B were detectable in the plasma following 4 hours of ischemia-reperfusion, indicating the release of these proteins in the circulation during the ischemia-reperfusion. A positive correlation was observed between the redox proteins (i.e., catalase and glutathione peroxidase) with the serpin proteins in the plasma. Biochemical analysis of circulating glutathione, a small-molecular antioxidant, revealed a reductive redox after 60 minutes of Ischemia (hypoxic condition) but this was shifted to an oxidative milieu at 4hrs following reperfusion (hyperoxia) in the adult pigs subjected to I/R insult. Interestingly, we noticed a significant increase in GSH levels and a decrease in catalase levels at 24 hours following I/R, suggesting a compensatory biochemical response in association with repair after I/R insult/injury in the heart. These results correlated with the increased circulating LDH levels indicating the rate of tissue damage following I/R. Conclusion: The present study reveals the presence of a previously unexplored Serpin protein member, endopin-1, during I/R. Understanding the kinetics of endopin-1 expression along with the shift in redox state can help unravel its role in the progression and resolution phases of I/R injury.

Effects of Different Therapeutic Approaches on Redox Balance in Psoriatic Patients.

Given that oxidative stress represents an important etiological factor in the pathogenesis of psoriasis, the aim of this study was to assess the effects of different therapeutic approaches, methotrexate, secukinumab, and ustekinumab on systemic oxidative stress biomarkers in psoriatic patients. This study involved 78 psoriatic patients, divided into the group treated with methotrexate (23 patients), secukinumab (28 patients), and ustekinumab (27 patients), and 15 healthy controls. Oxidative stress biomarkers (index of lipid peroxidation measured as TBARS, nitrites (NO2-), superoxide anion radical (O2-), and hydrogen peroxide (H2O2)) and antioxidative defense system (superoxide dismutase (SOD) activity, catalase (CAT) activity, and reduced glutathione (GSH)) were determined spectrophotometrically from the blood before the initiation of therapy in 16th, 28th, and 52nd week. O2- and SOD showed the most prominent changes comparing the psoriatic patients and healthy controls. CAT activity was significantly lower in psoriatic patients, and methotrexate induced a further decline in CAT activity. Ustekinumab induced a significant increase in GSH level after 52 weeks of treatment, while methotrexate reduced GSH. All applied therapeutic options induced a reduction in PASI, BSA, DLQI, and EARP. Biological drugs exert more pronounced antioxidant effects compared to methotrexate, which is most clearly observed in the values of O2- and SOD.

Protective Effect of Silymarin on Attenuating of Rhabdomyolysis -induced Acute Kidney Injury in Animal Models

Acute kidney injury is one of the most serious complications of rhabdomyolysis characterized by an acute loss of renal function. The study aims to investigate the renoprotective effect of silymarin against rhabdomyolysis-induced acute kidney injury in rats. Twenty-four healthy rats were equally divided into three groups: control, induction, and treatment groups. Rats in the control and induction groups received distilled water, while rats in the treatment group received silymarin (50 mg /kg/day p.o) for three consecutive days. On the first day, all rats (except rats of control group) received a single intramuscular injection of glycerol (10 mL/kg, 50% v/v in sterile saline) divided equally into each hind leg for induction of acute kidney injury. On the fourth day of experiment, blood and kidney,s were collected from all rats for biochemical and histopathological assay. Silymarin efficiently attenuated acute kidney injury caused by rhabdomyolysis evidenced by a significant decrease in serum creatinine and blood urea nitrogen(BUN), along with a significant reduction in renal homogenate levels of TNF-α, IL-6, NF-κB, caspase-3, and MDA with a significant increase in GSH level, which was further confirmed by improving renal histological changes when compared to that of induction group. This study found that silymarin has a potential attenuating effect on acute kidney injury due to its antioxidant, anti-inflammatory and antiapoptotic actions.

Nano cerium oxide and cerium/zinc nanocomposites characterization and therapeutic role in combating obesity via controlling oxidative stress and insulin resistance in rat model

BackgroundCeO2NPs and ZnONPs can curb the increase of cholesterol and triglycerides observed in rats with non-alcoholic fatty liver disease. It was suggested that CeO2 NPs could potentially have an insulin-sensitizing effect, specifically on adipose tissue and skeletal muscle. It was reported that ZnONPs combat the increase of insulin resistance observed in obese rats and could be beneficial value in NAFLD. In our previous work, ZnO-NPs manifested valuable anti-obesity effects via lowering body weight gain, oxidative stress, BMI, lipids, and insulin resistance. MethodsIn the present study, cerium oxide nanoparticles (A-1) and cerium/zinc nanocomposites (A-2 and A-3) were synthesized by solgel to investigate their role on oxidative stress, adipocyte hormones, and insulin resistance in an obese rat model. X-ray diffraction, HRTEM, SEM, and XPS were carried out to confirm the crystal structure, the particle size, the morphology of the nanoparticles and the oxidation states. ResultsThe Rietveld refinement has also been executed on A-1 (chi2 = 1.00; average Bragg = 2.92%; R-factor = 2.45%) and on A-2 (Rw = 9.87%, Rex= 9.68%, χ2 = 1.04, GoF = 1.02). The XPS spectra indicated the presence of Ce in + 4 and + 3 oxidation states and Zn as ZnO and ZnO.OH. Cerium oxide and ZnO crystal sizes lie in the range 40.53–45.01 and 40.53–45.01 nm, respectively. The results indicated that treating obese rats with any of the tested nano compounds (5 mg or 10 mg/Kg) lowered plasma cholesterol, triglycerides, LDL, insulin resistance, glucose, and BMI significantly relative to obese group values. On the other hand, HDL increased significantly in obese rats after treatment with either A-2 or A-3 compared to obese rats. The current investigation showed antioxidant activities for A-1, A-2, and A3 as evidenced by the significant increase in GSH level and a significant decrease in MDA. ConclusionIt was found that A-1, A-2, and A-3 have an efficient therapeutic role in treating of obesity-related hyperlipidemia, oxidative stress and insulin resistance. The results of A-2 and A-3 were more pronounced than those of A-1. The use of Zn/Ce nanocomposite (that have positive characteristics) in combating obesity and its complications could be become a new trend in therapeutic application for a management of obesity.

Evaluation of the immunomodulatory, antioxidant, and histopathological effects of Cymbopogon schoenanthus essential oil extract on kidney and spleen in BALB/C Mice

This study aimed to evaluate the impact of C. schoenanthus essential oil (CSEO) on the immune system, antioxidant balance, and histological changes in the kidney and spleen of female BALB/C mice. The chemical composition of CSEO was analyzed using GC-MS. Twenty-nine compounds were identified, representing 99.04% of the total detected. The main components were Piperitone (47.93%), Elemol (11.91%), 2-Carene (10.69%), β-eudesmol (7.67%), α-eudesmol (5.12%), and γ-eudesmol (4.24%). For bioassay, the mice were divided into three groups: control, 0.5% CSEO (G1), and 1% CSEO (G2). The effects of CSEO on various markers, including malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), urea, creatinine, and cytokines (IL-4, TNF-α, and TGF-β1), were evaluated. Additionally, kidney and spleen histopathological examinations were conducted. The treatment groups showed a significant increase in IL-4, TNF-α, and TGF-β1 levels compared to the control group, except for G1, which showed a non-significant decrease in TGF-β1 levels. Group 2 exhibited a significant increase in MDA levels compared to the control group, while group 1 had a nonsignificant increase. Both treatments showed a significant increase in GSH levels, while SOD and CAT levels showed a non-significant increase in G2 and a non-significant decrease in G1. Urea levels showed a non-significant increase, while creatinine levels were significantly decreased in G2 and non-significantly decreased in G1 compared to the control group. The histopathological examinations revealed congested red pulp with activated hematopoiesis and focal fibrosis in spleen sections of both G1 and G2. The study suggests that medicinal herbs such as CSEO need to be used with caution, and their effects should be evaluated carefully, especially in terms of dose-dependent effects. The results indicate that high doses of CSEO may increase the levels of some cytokines and antioxidants and have harmful effects on kidney architecture, congested red pulp, and fibrosis with increased hematopoiesis. Therefore, the random use of medicinal herbs may have harmful effects and needs to be carefully controlled to ensure safe use.

PHARMACODYNAMIC EVALUATION OF DIETARY SUPPLEMENTATION OF AVERRHOA CARAMBOLA FRUIT EXTRACT AGAINST LEAD ACETATE-INDUCED HEPATOTOXICITY IN RATS

Lead is a toxicant that may induce a wide range of social, biochemical, and physiological changes in humans. This study is undertaken to evaluate the pharmacodynamic effects of dietary supplementation of Averrhoa carambola, fruit extract (ACF) against lead acetate-induced hepatotoxicity in rats. Six groups of rats were used in this study namely, control, lead acetate (20 mg kg-1, ip), lead acetate (20 mg kg-1, ip) + 200 mg kg-1 silymarin orally (reference drug), lead acetate + 100 mg kg-1 ACF orally, lead acetate + 150 mg kg-1 ACF orally and lead acetate + 200 mg kg-1 ACF extract orally. All experimental groups except the control received the lead acetate by intraperitoneal route for 5 days and normal saline or silymarin or ACF by oral route employing an orogastric cannula for seven days. Lead intoxication leads to a significant increase in ALT and AST activities, malondialdehyde (MDA), and a significant decline in liver homogenate, reduced glutathione (GSH) level, and superoxide dismutase (SOD) activity. Different doses of ACF supplement, as well as silymarin, led to improving biochemical parameters of serum and liver and prohibited the lead acetate-induced significant changes in plasma and antioxidant status of the liver. ACF or silymarin supplement exhibited more antioxidant activity. Conclusively, the present work results reveals that the treatment of lead-intoxicated rats with A. carambola fruit extract supplement revealed a significant increase in GSH level, CAT, SOD activity, and a decrease in TBARS levels as compared to lead-intoxicated rats, indicating its antioxidant activity

Royal jelly arranges apoptotic and oxidative stress pathways and reduces damage to liver tissues of rats by down-regulation of Bcl-2, GSK3 and NF-κB and up-regulation of caspase and Nrf-2 protein signalling pathways

Introduction Royal jelly (RJ) from the honey bee, Apis mellifera, is a traditional product that is widely used as a food supplement to support the medical treatment of various diseases. Material and methods Our study continued for 8 weeks. 42 Wistar albino (8 weeks old) male rats were used in the study. The study included 6 groups; Group 1: Control group (fed with standard diet), Group 2: RJ (100 mg/kg, bw), Group 3: F-50 (50 mg/kg, bw), group 4: F-100 (100 mg/kg, bw) group 5: F-50 (50 mg/kg, bw) + RJ (100 mg/kg, bw) Group 6: F-100 (100 mg/kg, bw) + RJ (100 mg/kg, bw). Malondialdehyde (MDA), catalase (CAT) and glutathione (GSH) activities in liver tissue were determined by spectrophotometer. Liver tissue samples were examined histopathologically and various protein levels were determined by Western blotting technique. Results RJ caused a significant decrease in MDA level, Bcl-2, GSK3 and NF-κB protein expression levels, whereas induced a significant increase in GSH level, CAT activities and Bax, BDNF, caspase-6, caspase-3, Nrf-2 protein expression levels. Conclusion Our findings suggest RJ to be used as a hepatoprotective agent in the clinic to modulate the toxic effects of fluoride and other chemicals in the future.

The Investigation of Ameliorating Effect of Methylene Blue on Cisplatin-Induced Neurotoxicity in Female Rats

Objective: Cisplatin is indispensable in many solid tumors, and peripheral neurotoxicity is an essential dose-limiting side effect. The study aims to investigate the ameliorating effect of methylene blue, which has anti-oxidant properties, in rats with neurotoxicity due to cisplatin treatment. Materials and methods: Twenty-four adult female rats were included in the study and divided into 3 groups. The first group (n=8), the control group, did not receive any treatment. The second (n=8) and the third (n=8) group received 2.5 mg/kg/day of cisplatin and 1 ml/kg/day of 0.9% NaCl (saline) twice a week for 4 weeks. Also, the third group received 20 mg/kg/day of methylene blue every day for 4 weeks. Blood samples were collected from rats for malondialdehyde (MDA), glutathione (GSH), tumor necrosis factor- α (TNF-α), and interleukin-6 (IL-6) levels, and electromyography (EMG) and motor function were evaluated. Results: In non-treated cisplatin injected rats, a significant increase in the lipid peroxidation product MDA and pro-inflammatory cytokines compared to the control group (p<0.001). Electromyography measurements also resulted in a significant decrease in cisplatin injected rats’ compound muscle action potential (CMAP) amplitude and prolongation in CMAP latency compared to the control group (p<0.05). A statistically significant decrease in MDA, TNF-α, and IL-6 levels and a statistically significant increase in GSH levels and CMAP amplitude was observed in the methylene blue-treated group compared to the group injected with cisplatin alone. Conclusions: We concluded that methylene blue has ameliorating effects against cisplatin-induced neurotoxicity (CIN) by enhancing anti-oxidative capacity, energy metabolism and suppressing inflammatory parameters and oxidative stress.

Ethanol Extract of Myrtle (Myrtus communis L.) Berries as a Remedy for Streptozotocin-Induced Oxidative Stress in Rats.

Streptozotocin (STZ) is an antitumor antibiotic indicating in the treatment of metastatic islet cell carcinoma of the pancreas. It is also used as a tool to create experimental diabetes models. The STZ exposure at a high dose causes severe damage to cells of humans and other mammals. The goal of the present study was to assess the protective effects of the ethanol extract of the Myrtle (Myrtus communis L.) berries, which is a well-known medicinal plant due to its rich phenolic content and beneficial effects on health, against STZ-induced oxidative stress in the diabetic rats.Diabetes was induced by STZ (40mg/kg, i.p.) in the rats. After diabetes induction, a significant increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), and blood glucose levels as well asa significant decrease in superoxide dismutase (SOD) activities and glutathione (GSH) levels was observed. The rats were treated to three different ethanol extracts of Myrtle berries (0.25, 0.5, and 1g/kg) by oral gavage for 14days. At the end of the experiment, ALT, AST, MDA, and blood glucose levels of the rats significantly decreased while significant increases in GSH levels and SOD activities were observed.We believe that our findings may contribute to the development of new drugs in the treatment of many global disorders due to the antioxidant activity of the ethanol extract of Myrtus communis L. berries.

Brain Levels of Reduced Glutathione and Malondialdehyde in Honey-Fed Wistar Rats

This research sought to verify the effect of natural honey on brain levels of malondialdehyde (MDA) and reduced glutathione (GSH) in rats. Forty nine male and female Wistar rats were used for the experiment. The rats were allotted into seven groups of seven rats in each group. For one month, rats in groups 1-4 were fed with 100% feed, 20%, 30% and 40% honey respectively. The remaining 3 groups were fed with amounts of refined fructose and glucose equivalent to those in 20%, 30% and 40% honey. The brains were then excised, homogenized and used for biochemical analysis. Results showed that honey in all concentrations caused a significant increase in GSH levels but only 20% honey caused a significant decrease in MDA level when compared with control. Also, fructose feeding at 20%, 30% and 40% increased both brain GSH and MDA levels. Consequently, the influence of GSH as an antioxidant against brain lipid peroxidation needs further studies for better understanding since an increase in GSH for fructose- and honey-fed rats did not cause a simultaneous decrease in MDA content.

Activation of NRF2 and ATF4 Signaling by the Pro-Glutathione Molecule I-152, a Co-Drug of N-Acetyl-Cysteine and Cysteamine.

I-152 combines two pro-glutathione (GSH) molecules, namely N-acetyl-cysteine (NAC) and cysteamine (MEA), to improve their potency. The co-drug efficiently increases/replenishes GSH levels in vitro and in vivo; little is known about its mechanism of action. Here we demonstrate that I-152 not only supplies GSH precursors, but also activates the antioxidant kelch-like ECH-associated protein 1/nuclear factor E2-related factor 2 (KEAP1/NRF2) pathway. The mechanism involves disulfide bond formation between KEAP1 cysteine residues, NRF2 stabilization and enhanced expression of the γ-glutamil cysteine ligase regulatory subunit. Accordingly, a significant increase in GSH levels, not reproduced by treatment with NAC or MEA alone, was found. Compared to its parent compounds, I-152 delivered NAC more efficiently within cells and displayed increased reactivity to KEAP1 compared to MEA. While at all the concentrations tested, I-152 activated the NRF2 pathway; high doses caused co-activation of activating transcription factor 4 (ATF4) and ATF4-dependent gene expression through a mechanism involving Atf4 transcriptional activation rather than preferential mRNA translation. In this case, GSH levels tended to decrease over time, and a reduction in cell proliferation/survival was observed, highlighting that there is a concentration threshold which determines the transition from advantageous to adverse effects. This body of evidence provides a molecular framework for the pro-GSH activity and dose-dependent effects of I-152 and shows how synergism and cross reactivity between different thiol species could be exploited to develop more potent drugs.

The Effect of N-Acetylcysteine on Oxidant/Antioxidant Status in Irradiated Rats

N-Acetylcysteine (NAC) is both a strong antioxidant and a glutathione precursor. The effect of NAC on the oxidant/antioxidant status of some tissues of the irradiated rats was investigated. Twenty one rats were assigned to 3 groups; the control group, the irradiation group, for which physiological saline solution was administered as i.p. for three days and then, 9 Gy gamma irradiation was applied, and 3rd irradiation + NAC group for which NAC was adminis-tered as i.p. for three days as 300 mg/kg body weight and then the same dose of irradiation was applied. Upon irradia-tion, the increase determined in malondialdehyde (MDA) was significant in the liver, kidney, and brain tissues of the rats (P˂0.05). While glutathione peroxidase (GSH-Px) activity decreased in all of the tissues and superoxide dismutase (SOD) activity only in the liver (P˂0.01), glutathione (GSH) levels significantly increased in the kidney and ovarium tissues (P˂0.001). While NAC administration returned the increased MDA levels in the kidney and brain as a result of irradiation to normal levels (P˂0.05), it was determined that it did not return the increased MDA levels in the liver tissue to the normal level (P˂0.001). While NAC addition led to a significant increase in GSH levels of the liver, heart, spleen, brain and ovarium tissues compared to both control and irradiation groups, it caused a significant decrease in the kid-ney tissue compared to irradiation group (P˂0.001). As a result of NAC addition, a significant decrease was determined in spleen GSH-Px activity, heart and ovarium SOD activity compared to control and irradiation groups (P˂0.05). It can be asserted that GSH increasing by the addition of NAC is the main antioxidant that has a role in decreasing oxidative stress occurring as a result of irradiation. In the examination of MDA values, it was found that the addition of NAC pro-tected the kidney and brain against the oxidative damage induced by irradiation but NAC addition could remain insuffi-cient for the liver.

Upregulation of Antioxidant Gene Expressions and Enzyme Activity Against Acrylamide-Induced Neurotoxicity in Mice after Grape Seed Extract Treatment

Background: The risk of occupational exposure to acrylamide is high and long-term acrylamide exposure can cause neurotoxicity. Thus, therapeutic agents that can protect against acrylamide-induced neurotoxicity are needed. Objective: To investigate whether Grape Seed Extract (GSE) protects against acrylamide-induced neurotoxicity in mice. Methods: Mice were divided into saline, GSE, acrylamide, GSE followed by acrylamide, acrylamide followed by GSE, and simultaneous acrylamide and GSE treatment groups. Gene expression and antioxidant enzyme levels were then determined using RT-PCR and biochemical assays. Results: Gpx1 (P &lt; 0.05), Prdx3 (P &lt; 0.01), SOD1 (P &lt; 0.05), and CAT (P &lt; 0.05) significantly upregulated in GSE-treated mice, compared to those in untreated controls. In contrast, Gpx1 (P &lt; 0.05), Prdx3 (P &lt; 0.05), SOD1 (P &lt; 0.05), and CAT (P &lt; 0.05) significantly downregulated in acrylamide-treated mice compared to those in untreated controls. Results of the treatment with GSE before exposure to acrylamide or simultaneously with acrylamide indicated that GSE restored Gpx1, Prdx3, SOD1, and CAT expression to similar levels as those in the control group. GSE treatment after exposure to acrylamide did not exert any neuroprotective effects against acrylamide, as revealed by significant downregulation of Gpx1 (P &lt; 0.05), Prdx3 (P &lt; 0.01), SOD1 (P &lt; 0.05), and CAT (P &lt; 0.05) compared to that in untreated controls. Animals treated with grape seed before acrylamide treatment showed no significant change in LPO activities and a significant increase in GSH levels, compared to those in untreated controls. Conclusion: GSE exerted neuroprotective effects against acrylamide-induced neurotoxicity. Acrylamide caused oxidative stress 20 days post-exposure. However, grape seed treatment before exposure to acrylamide restored all test parameters to levels similar to control values.

Possiple Protective Role of Ascorbic Acid on Ethanol Induced Testicular Toxicity in Male Albino Rats

Background: Exposure to ethanol results in many pathophysiologic changes in the function of the reproductive system caused by the alcohol itself and the effects of its metabolism in recurrent use. Ascorbic acid is a powerful antioxidant that can neutralize harmful compounds and potentiate the antioxidant capacity. Aim: this study was aimed to evaluate the protective effects of ascorbic acid against testicular changes caused by ethanol in adult male albino rats. Materials and Methods: Forty adult male rats were randomly distributed into four groups treated for 63 consecutive days, control group: was treated with distilled water only orally by gastric tube. Ascorbic acid group: was treated with ascorbic acid (100 mg/day/rat) dissolved in distilled water (dilution 50%), once daily orally by gastric tube. Ethanol group: was treated with ethanol (0.7g/kg) dissolved in distilled water (dilution 50% ), once daily orally by gastric tube. Ethanol and ascorbic acid group: was treated with ethanol and ascorbic acid in the same previous doses orally by gastric tube. At the end of the study, rats were weighed then blood samples were obtained from each group to estimate the level of testosterone. Then the rats were sacrificed. The testes were dissected and weighed then used for evaluation of oxidative parameters (GSH and MDA), histopathological examination of testes by light and electron microscope. Results: Concomitant administration of ascorbic acid with ethanol resulted in a highly significant rise in body weight, with increase in mean testosterone level but this rise was insignificant, there was a highly significant decrease in MDA level and there was a highly significant increase in GSH level. Regarding histopathological results in the group of ascorbic acid with ethanol showed improvement in all histopathological changes induced by ethanol. As regard ultrastructure changes, microscopic examination in ethanol group revealed thickening of basement membrane, mitochondrial changes, degenerated spermatid, with decrease in the sperm count results which were improved in the group of ascorbic acid with ethanol. Conclusion: oral administration of ethanol daily for 63 consecutive days in adult albino rats caused various testicular lesions which were significantly reduced with combined administration of ascorbic acid as antioxidant

Uroprotective effect of pantoprazole against cyclophosphamide-induced cystitis in mice.

The aim of the present study was to evaluate the potential uroprotective effect of pantoprazole (PPZ) in a mouse model of cyclophosphamide (CP)-induced hemorrhagic cystitis (HC) due to its antioxidant and anti-inflammatory properties. Balb/c mice received a single intraperitoneal (i.p.) injection of CP (300mg/kg) to induce HC. PPZ (20, 50, and 100mg/kg/day;i.p.) was administered for 3 consecutive days before the induction of HC. Mesna (30mg/kg;i.p.) was administered 20min before, 4 and 8h after CP injection to compare the protective effects of PPZ. After 24h of HC induction, the bladders were removed for functional studies, biochemical analyses, and histopathological examination. In vitro contractility studies demonstrated that CP-induced HC decreased the responsiveness of detrusor muscle strips to acetylcholine (ACh), which was reversed by PPZ pretreatment at all doses tested. However, mesna treatment was not able to improve responsiveness to ACh. Biochemical analyses showed that CP caused significant elevation of malondialdehyde (MDA), reduction of total glutathione (GSH), and increment of proinflammatory cytokine tumor necrosis factor-alpha (TNF-α) level, which were measured in bladder homogenates. PPZ pretreatment at three doses found to be effective in reducing the CP-induced elevation of MDA and TNF-α levels. The highest dose of PPZ (100mg/kg) caused a significant increase in GSH level. CP induced severe HC with marked bladder edema and histological disturbances which were partially abolished by PPZ pretreatment. Our results indicate that PPZ pretreatment could attenuate CP-induced HC by interfering with oxidative stress and modulating proinflammatory cytokines.

Effect of exercise on type 2 diabetes-associated cognitive impairment in rats

OBJECTIVES: Type 2 diabetes (T2D)-associated cognitive impairment is highly prevalent especially among the geriatric population. Here, we investigate the role of exercise in T2D-associated cognitive decline in rats.METHODS: T2D was induced using high-fat diet (15 days) followed by low-dose STZ (25mg/kg). The T2D animals were subjected to aerobic exercise on running wheel for 6 weeks. Effect of aerobic exercise on cognitive performance of T2D animals was measured using step-down and transfer latency tests. This was followed by the measurement of reduced glutathione levels in hippocampal homogenates. We also measured hippocampal AchE activity and levels of neuroinflammatory markers such as IL-1 β, TNF-α and MCP-1. Morphology and density of hippocampal neurons were also determined by histopathological studies.RESULTS: Exercise led to the following changes in T2D animals. It led to decrease in fasting blood glucose level (<250 mg/kg) and HbA1c (8.5 ± 0.23) compared to diabetic (11.73 ± 0.14) animals and improved insulin resistance. There was an increase in step-down latency (p < 0.001) and a decrease in transfer latency (p < 0.01) suggesting improved cognitive function. A significant increase in GSH levels (1.828 ± 0.024) compared to diabetic group (1.52 ± 0.03; p < 0.001) and decrease in AchE activity (1.4 ± 0.05) compared to diabetic group (1.65 ± 0.03; p < 0.05) were also observed. It reduced the levels of neuroinflammatory markers such as IL-1β, TNF-α and MCP-1 (p < 0.01). Hippocampal sections showed higher CA1 and CA3 neuronal density (p < 0.001) than T2D group.CONCLUSION: We may conclude that aerobic exercise could partially reverse diabetes-associated cognitive decline by reducing oxidative stress and inflammatory milieu in T2D animal brain.

EFFECT OF FENUGREEK SEEDS (Trigonella foenum graecum), METHIONINE AND INDUCED OXIDATIVE STRESS ON SOME BIOCHEMICAL PARAMETERS AND ANTIOXIDANTS STATUS FOR SOME TISSUES IN QUAIL

This study was designed to detect an improvement ability of Fenugreek seeds and Methionine on some biochemical parameters and antioxidants status in quail females.The trial included six treatments: first (fenugreek seeds), second (fenugreek + H2O2), third (methionine), fourth (methionine + H2O2), fifth Oxidative stress (H2O2), sixth (control). The results showed that H2O2 treatment caused a significant increase (P ≤ 0.05) in glucose,T.G, T. cholesterol, LDL-C, VLDL-C and atherogenic risk index in blood serum, while HDL-C decreased significantly, as well as MDA level was increased significantly in tissues such as (heart, liver, kidney, pancreas and ovary) whereas GSH level was decreased compared with control group, Corticosterone hormone as well as elevated. Fenugreek seeds alone or with H2O2 treatment caused a significant decrease in glucose & T.G levels as well as in AST & ALT enzymes,while GSH level of heart tissue was increased. Methionine treatment caused a significant increase in GSH level of heart tissue while Corticosterone hormone decreased significantly indicating the antioxidant ability of antioxidants materials to exerted and improvement of some biochemical parameters and antioxidants status in quail females.

The Protective Effect of ettlingera coccinea (TUHAU) against Autoxidation-induced Ox Brain Homogenate

Oxidative stress involved in various pathological conditions. Plants have been proven to act as a natural exogenous antioxidant. The aim of this research is to investigate the protective effects of Etlingera coccinea leaves aqueous extract on autoxidation-induced ox brain homogenate. The brain homogenate was divided into 7 groups: control group with PBS solution, positive control group with 100 μg/ml ascorbic acid, test group with 25, 50, 100, 200 and 400 μg/ml of E. coccinea. The antioxidant potential of E. coccinea aqueous extract has been evaluated by antioxidant capacity assay such as Total phenolic content (TPC), radical scavenging assay (DPPH) and ferric reducing antioxidant power (FRAP). Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were also measured at 0 hr and 1 hr after 37°C water bath incubation to determine the antioxidant status and oxidative damage. TPC assay showed (4.85 ± 0.28) mg GAE/g of dry weight of E. coccinea leaves. Based on DPPH and FRAP assay, E. coccinea aqueous extract showed a dose-dependent antioxidant activity. MDA level in the 50 μg/ml E. coccinea was significantly lower compared to the other groups (p &lt; 0.05). The SOD activity was significantly increase in 400 μg/ml E. coccinea (p &lt; 0.05) compared to other groups. E. coccinea at the dose of 25 μg/ml and 50 μg/ml showed significant increase in GSH level compared to other groups (p &lt; 0.05). In conclusion, 25 μg/ml and 50 μg/ml of E. coccinea leave aqueous extracts exhibited a potential protective effect on autoxidation-induced ox brain homogenate. DOI : http://dx.doi.org./10.17576/JSKM-2018-06

The Protective Effect of ettlingera coccinea (TUHAU) against Autoxidation-induced Ox Brain Homogenate

Oxidative stress involved in various pathological conditions. Plants have been proven to act as a natural exogenous antioxidant. The aim of this research is to investigate the protective effects of Etlingera coccinea leaves aqueous extract on autoxidation-induced ox brain homogenate. The brain homogenate was divided into 7 groups: control group with PBS solution, positive control group with 100 μg/ml ascorbic acid, test group with 25, 50, 100, 200 and 400 μg/ml of E. coccinea. The antioxidant potential of E. coccinea aqueous extract has been evaluated by antioxidant capacity assay such as Total phenolic content (TPC), radical scavenging assay (DPPH) and ferric reducing antioxidant power (FRAP). Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were also measured at 0 hr and 1 hr after 37°C water bath incubation to determine the antioxidant status and oxidative damage. TPC assay showed (4.85 ± 0.28) mg GAE/g of dry weight of E. coccinea leaves. Based on DPPH and FRAP assay, E. coccinea aqueous extract showed a dose-dependent antioxidant activity. MDA level in the 50 μg/ml E. coccinea was significantly lower compared to the other groups (p < 0.05). The SOD activity was significantly increase in 400 μg/ml E. coccinea (p < 0.05) compared to other groups. E. coccinea at the dose of 25 μg/ml and 50 μg/ml showed significant increase in GSH level compared to other groups (p < 0.05). In conclusion, 25 μg/ml and 50 μg/ml of E. coccinea leave aqueous extracts exhibited a potential protective effect on autoxidation-induced ox brain homogenate. DOI : http://dx.doi.org./10.17576/JSKM-2018-06