Kidney GSH Research Articles

Aqueous Leaf Extract of Azadirachta indica Protects Against Gentamicin-Induced Kidney Injury via Decreases in Renal Function, Inflammation, and Apoptosis Markers.

The effect of the aqueous extract of Azadirachta indica (AAI) on gentamicin (GEN)-induced kidney injury was investigated. The study involves 20 adult male Wistar rats (housed in four separate plastic cages) such that graded dosages of AAI were administered to the experimental group for 14 days per oral (PO) before exposure to GEN toxicity (100 mg/kg) for 1 week. At the end of the study, comparisons of some markers of renal functions, antioxidant status, and inflammatory and apoptotic markers were made between the control, GEN, and AAI-pretreated groups at P < .05. The result showed that GEN treatment caused a significant increase (P < .05) in body weight, kidney weight, urea, bilirubin, kidney injury molecule 1 (KIM 1), cystatin C, malondialdehyde (MDA), reduced glutathione (GSH), tumor necrotic factor alpha (TNF-α), interleukin-1 (IL-2), caspase-3, and B-cell lymphoma-2 associated X (BAX) as well as a significant decrease (P < .05) in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (Gpx), and B-cell lymphoma (BCL)-2 level. Pre-treatment with graded doses of AAI caused a significant increase in urea, CAT, and GPx as well as a significant decrease (P < .05) in kidney weight, bilirubin, KIM 1, cystatin C, MDA, GSH, SOD, TNF-α, IL-2, caspase-3, BAX, and BCL-2. There was an appreciable difference in the kidney histology of the AAI pre-treated groups compared with the GEN. Hence, the extract has prophylactic potential in managing GEN-induced nephrotoxicity by decreasing the markers of renal function and inflammation and downregulating the markers of apoptosis.

Iristectorin A Ameliorates Cisplatin-Induced Hepatorenal Injury in Mice Through Modulation of the Nrf2/HO-1 Signaling Pathway.

Cisplatin (CIS) is a chemotherapeutic agent frequently used in cancer treatment. However, depending on the dosage and duration of use, CIS can lead to hepatotoxicity and nephrotoxicity. Iristectorin A (IRIS), a natural flavonoid, has been found to exhibit antioxidant and protective effects. In this paper, we scrutinized the effects and molecular mechanisms of the IRIS on CIS-induced liver and kidney damage in mice. IRIS administration alleviated CIS-induced elevations in AST, ALT, ALP, BUN, and creatinine levels by approximately 12%, 15%, 11%, 21%, and 15%, respectively. It also inhibited liver and kidney MDA levels by approximately 29% and 28%, while enhancing liver and kidney GSH, SOD, and CAT levels by 47%-60%, 85%-70%, and 90%-55%, respectively. IRIS enhanced liver and kidney mRNA expression levels of Nrf2 (by approximately 1.6- and 1.5-fold, respectively), HO-1 (by 1.5- and 1.5-fold, respectively), and Bcl-2 (by 1.5- and 1.4-fold, respectively). In addition, IRIS suppressed the mRNA expression levels of NF-κB (by 0.7- and 0.7-fold), TNF-α (by 0.7- and 0.7-fold), Bax (by 0.8- and 0.7-fold), and Cas-3 (by 0.9- and 0.7-fold). Protein expression analysis revealed that IRIS increased Nrf2 (by 1.5- to 1.2-fold) and Bcl-2 levels (by 1.3- to 1.7-fold), and reduced Bax (by 0.7- to 0.8-fold) and Cas-3 (by 0.8- and 0.8-fold) levels altered by CIS treatment. Moreover, IRIS administration prevented histopathological changes in the liver and kidney caused by CIS. Ultimately, IRIS was found to substantially mitigate CIS-induced hepatorenal injury by targeting oxidative stress, inflammation, and apoptosis through regulation of the Nrf2/HO-1 signaling pathway. Therefore, IRIS holds potential as a therapeutic adjuvant in the use of CIS.

Unraveling the Potential of Saccharum officinarum and Chlorella vulgaris towards 5-Fluorouracil-Induced Nephrotoxicity in Rats.

5-Fluorouracil (5-FU) is often used as a chemotherapeutic agent in treating tumors and is said to have adverse effects, including nephrotoxicity. Therefore, the present study aimed to evaluate the protective effects of Chlorella vulgaris (VL) and Saccharum officinarum L. (SOL) against 5-FU-induced nephrotoxicity in rats through the measurement of renal histology, kidney damage indicators, and antioxidant measures. A total of forty-eight male rats were allotted into six groups: group 1 acted as a control negative group (control), group 2 received 5-FU and worked as a control positive group (FU), group 3 received SOL 15 mL/kg (SOL), group 4 received VL 400 mg/kg (VL), group 5 received 5-FU+SOL (5-FU+SOL), and group 6 received 5-FU+VL (5-FU+VL). After fifteen days, blood and renal tissue specimens were collected for hematological, biochemical, molecular, and histopathological examinations. Findings of the current investigation showed that 5-FU leads to hematological alterations and kidney injury evinced by elevated serum concentrations of uric acid, creatinine, and urea (p < 0.01), and a marked increase in kidney MDA and NO levels with a reduction in kidney CAT, SOD and GSH activities (p < 0.05). Alterations of the histopathological structure of kidney tissue in the FU group were noticed compared to the other groups. 5-FU administration elevated expression levels of TNF-α, lipocalin 2, and KIM1 (p < 0.01) compared to the control ones. 5-FU-induced nephrotoxicity was ameliorated after treatment with SOL and VL via their free radical scavenging, potent antioxidant, and anti-inflammatory effects. In conclusion, our findings demonstrate that the treatment with SOL and VL significantly improved nephrotoxicity induced by 5-FU in rats.

The Effects of Thymus Caramanicus Jalas Extract and Its Main Constituent Carvacrol Against Cisplatin-Induced Nephrotoxicity in Mice.

Cisplatin, an anti-cancer chemotherapy drug, has nephrotoxic effects. Thymus caramanicus Jalas (TCJ) has antioxidant effects due to its main components. In the current research, we assessed the impact of TCJ extract and its main compound on cisplatin-induced nephrotoxicity in mice. Forty-two male mice were used in the study. Depending on their group, the animals received saline, carvacrol (10 mg/kg), or TCJ extract (50, 100, and 150 mg/kg) for 10 days. On the fifth day, mice received cisplatin (7.5 mg/kg, i.p.). After 10 days, serum creatinine (Cr) and blood urea nitrogen (BUN) levels were measured. Additionally, malondialdehyde (MDA) and glutathione (GSH) contents, as well as the activity levels of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx), and total antioxidant capacity (TAC) were measured in the kidney tissues. The western blotting method was used to determine the kidney's expression of cleaved caspase-3, Bax, Bcl-2, nuclear factor kappa-B (NF-κB), and tumor necrosis factor-alpha (TNF-α). Kidney tissue damage score (KTDS) was assessed using the hematoxylin-eosin (H&E) staining method. Cisplatin significantly increased serum Cr, KTDS, MDA, BUN levels, NF-κB, TNF-α, cleaved caspase-3, and Bax protein expression in the cisplatin group compared to the control group (P < 0.01). Additionally, cisplatin significantly decreased the kidney tissue's TAC and GSH content, activity levels of SOD, catalase, and GPx indicators, and expression of Bcl-2 protein (P < 0.05). TCJ and carvacrol significantly ameliorated these indicators in the cisplatin + TCJ (150 mg/kg) and cisplatin + carvacrol (10 mg/kg) groups compared to the cisplatin group (P < 0.05). TCJ (150 mg/kg) and its main component, carvacrol, could somewhat reduce cisplatin-induced nephrotoxicity through their anti-inflammatory, antioxidant, and anti-apoptotic effects.

Therapeutic and antioxidant effects of lactoperoxidase on aflatoxin B1-induced nephrotoxicity in adult male rats

Background and objective Aflatoxin B1 (AFB1), a type of mycotoxin, is present in food and feed and is toxic to both people and animals. Histological effects of AFB1 on the rat kidney have not been well understood. The objective of this study was to evaluate the therapeutic effect of lactoperoxidase (LPO) against aflatoxin B1-induced nephrotoxicity in a trial to improve its clinical use. Materials and methods Adult male Wistar rats (150–200 g b.w) were randomly divided into four groups (10 rats each): (1) healthy control group, (2) healthy rats treated IP with LPO (50mg/kg/day) for 6 weeks, (3) rats intoxicated orally with AFB1 (80 µg/ kg/day) for 6 weeks, and (4) Animals treated with LPO for 6 weeks after intoxication with AFB1. Results and conclusion The results showed that LPO was successful in reducing aflatoxin B1-induced nephrotoxicity after 6 weeks of treatment. This was demonstrated by the significant decrease in blood urea, urea nitrogen, creatinine, uric acid, potassium, magnesium, phosphorus, TNF-α, IL-1β, as well as kidney NO, MDA, and DNA damages matched with a significant increase in CD4 and albumin levels as well as kidney GSH and SOD. Furthermore, the LPO was successful in aflatoxin B1-induced tissue degenerations, reflecting its therapeutic potential. In conclusion, due to their antioxidant and radical scavenging properties, LPO may be as effective in improving nephrons from aflatoxin B1-induced nephrotoxicity.

Evaluation of Himalayan nettle (Urtica ardens) extract meal in common carp (Cyprinus carpio) feed: Impact on growth performance, digestive enzyme activity and antioxidant capacity

This research aims to evaluate the impact of an extract derived from the leaves of Himalayan nettle (Urtica ardens) leaf extract on common carp, Cyprinus carpio, growth, digestive enzymes, fish body carcass composition, antioxidant system, and water quality parameters. For a duration of 90 days, experimental diets containing nettle extract were given to 150 fish (12.38 ± 0.53 g) in 15 tanks (10 fish per tank). The five groups in triplicate were: control or T0 (untreated), T1 (fed 0.3% extract), T2 (0.6% extract), T3 (0.9% extract), and T4 (1.2% extract). Results revealed that nettle extract in the diet increases common carp growth up to 0.9% concentration of extract. Its feed conversion ratio decreases, while weight gain and specific growth rate rise significantly compared to the control diet. No mortality was observed during the 90-day experiment. Dietary nettle extract did not affect whole-body fibre and crude ash percentages (p > 0.05). Nettle-fed and control groups showed significant differences in crude protein, body fat, and total body moisture (p < 0.05). After a 90-day feeding trial, 0.9% nettle extract-fed fish had higher protease, amylase, lipase, and cellulase levels than the control group (p < 0.05). When nettle content reached 1.2%, enzyme activity decreased. Orthophosphate production peaked at 4 and 8 hours after feeding, while ammonia excretion peaked at 2 and 6 hours. The control group excreted the most ammonia and orthophosphate, while the 0.9% group excreted the least. Liver and kidney SOD levels were higher in common carp fed a 0.6% nettle extract diet. Feeding with a 0.9% nettle extract diet improved hepatic lipid peroxidation, gut and liver glutathione. Gut and kidney SOD, catalase, LPO, and GSH increased dramatically on the 1.2% diet. Statistically, the 0.9% nettle extract (T3) group showed the overall best results compared to the control diet. These findings demonstrate the potential of nettle extract as a dietary supplement in aquaculture.

Evaluation of Effect of Montelukast in the Model of Streptozotocin Induced Diabetic Nephropathy in Rats.

Diabetic nephropathy is a progressive condition and a leading cause of end-stage renal disease. Oxidative stress and inflammation play an important role in its pathogenesis. In pre-clinical studies, Montelukast had shown renoprotective and anti-oxidant properties, hence the study was planned to evaluate the effect of Montelukast in a Streptozotocin (STZ) induced model of diabetic nephropathy. 40 Wistar rats of either sex were randomly divided into four groups viz. 1. Vehicle control group, 2. Enalapril (5 mg/kg), 3. Montelukast low-dose (10 mg/kg) and 4. High-dose (20 mg/kg) group. On day 1, diabetes was induced using a single dose of STZ (60 mg/kg) intraperitoneally. Diabetes induction was verified based on fasting blood glucose (FBG) levels on day 7 and from day 8 to day 42, rats were given study drugs. FBG, serum creatinine, blood urea nitrogen (BUN) and urine microalbumin levels were assessed pre-study and post-study. Assessments of kidney malondialdehyde (MDA), reduced glutathione (GSH) and renal histopathology were carried out at the end of the study. Montelukast 10 mg/kg group showed significantly lower urine microalbumin levels compared to the vehicle control group (p < 0.05). Montelukast 20 mg/kg group showed significantly lower levels of FBG, serum creatinine, BUN and urine microalbumin compared to the vehicle control group (p < 0.05). In addition, Montelukast 20 mg/kg group also showed better effects on kidney MDA and GSH levels (p < 0.05) and histopathological scores compared to the vehicle control group. Montelukast showed a protective effect in the model of diabetic nephropathy because of its antioxidant effect.

Expected adverse health influences due to exposure to glyphosate-based herbicide (GBH) and its environmental outcomes using Wistar rats as experimental animals

A sum of 32 Wistar rats were divided into four equal groups, each containing 8 rats. Study animals were freely subject to normal rodent diet and tap water. One group was put as control. The applied agents were exposed to glyphosate-based herbicide (GBH-400 mg kg–1) GSH (nmol g–1 tissue), (GBH-600 mg kg–1) GSH (nmol g–1 tissue) and (GBH-850 mg kg–1) GSH (nmol g–1 tissue) once per day as oral gavage for 6 weeks. Study results clearly revealed that (GBH) significantly (p≤0.05) decreased the levels of GSH in liver, kidney, and brain tissues, due to many reasons including poor diet, chronic disease, infection and constant stress, besides aging. Biological negative influences of glyphosate herbicide through the scientific community, including government and non-government organizations have increased their interest in detecting and controlling the environmental agents responsible for damages to the human health and sustainability of the ecosystems.

Bee Venom Causes Oxidative Stress, Biochemical and Histopathological Changes in the Kidney of Mice.

Accidents with venomous bees are a serious worldwide health concern. Since the kidney has been reported as the main venom-target organ, the present study was undertaken to investigate the in vivo nephrotoxic effect of Algerian bee venom (ABV) (Apis mellifera intermissa) collected in the middle east of Algeria. A preliminary study was performed on ABV to identify the ABV using SDS-PAGE analysis and to determine the in vivo intraperitoneal median lethal dose (LD50) using the Probit analysis test. In vivo nephrotoxic effect was assessed through the determination of physiological and kidney biochemical markers in mice intraperitoneally injected with ABV at doses of 0.76 (D1); 1.14 (D2) and 2.29 mg/kg body weight (bwt) (D3), corresponding respectively to LD50/15, LD50/10, and LD50/5 (i.p. LD50=11.48 mg/kg bwt) for seven consecutive days. Results revealed a marked decrease in body weight gain and food intake, and an increase in absolute and relative kidney weights in ABV D2 and D3 treated mice compared with controls. Furthermore, ABV D2 and D3 resulted in a significant increase in serum creatinine, urea, and uric acid. ABV-induced oxidative stress was evidenced by a significant increase in kidney MDA level, and a significant depletion in kidney GSH level, and catalase activity. Meanwhile, no marked changes in the above-mentioned parameters were noticed in ABV D1. Accordingly, the adverse nephrotoxic effect of ABV was proved by the dose-dependent kidney histological changes. In summary, the results of the present study evidence that ABV at doses of 1.14 (D2) and 2.28 mg/kg body weight (bwt) can cause marked changes in kidney biochemical and major antioxidant markers, and histological architecture.

Ameliorative Effects of Zn and Se Supplementation on Heavy Metal Mixture Burden via Increased Renal Metal Excretion and Restoration of Redoxo-Inflammatory Alterations.

Heavy metals (HM)in the environment have provoked global attention because of its deleterious effects. This study evaluated the protection offered by Zn or Se or both against HMM-induced alterations in the kidney. Male Sprague Dawley rats were distributed into 5 groups of 7 rats each. Group I served as normal control with unrestricted access to food and water. Group II received Cd, Pb, and As (HMM) per oral daily for 60 days while groups III and IV received HMM in addition to Zn and Se respectively for 60 days. Group V received both Zn and Se in addition to HMM for 60 days. Metal accumulation in feces was assayed at days 0, 30, and 60 while accumulation in the kidney and kidney weight were measured at day 60. Kidney function tests, NO, MDA, SOD, catalase, GSH, GPx, NO, IL-6, NF-Κb, TNFα, caspase 3, and histology were assessed. There is a significant increase in urea, creatinine, and bicarbonate ions while potassium ions decreased. There was significant increase in renal function biomarkers, MDA, NO, NF-Κb, TNFα, caspase 3, and IL-6 while SOD, catalase, GSH, and GPx decrease. Administration of HMM distorted the integrity of the rat kidney, and co-treatment with Zn or Se or both offered reasonable protection suggesting that Zn or Se could be used as an antidot against the deleterious effects of these metals.

Erythrocytic, Enzymatic, and Histological Markers of Oxidative Stress in Subacute and Chronic Stage Infections in Wistar Rats (Rattus norvegicus) Infected with Trypanosoma brucei brucei

Trypanosomiasis is a complex of diseases caused by a haemoprotozoan parasite of medical and veterinary importance. One of the leading factors that cause morbidity and death in trypanosomiasis is oxidative stress. The oxidative stress biomarkers in trypanosomiasis at the subacute and chronic stages of infection were investigated in this study. A total of twenty-four Wistar rats were used; the animals were placed in two groups: group A (subacute and chronic) and group B (control). The weight and body temperature of the experimental animals were determined using a digital weighing balance and thermometer. A hematology analyzer was used to determine the erythrocyte indices. Spectrophotometry was used to estimate enzyme (superoxide dismutase, catalase, and glutathione) activities in the serum, kidney, and liver of experimental animals. Liver, kidney, and spleen were harvested and analyzed for histological changes. The mean body weight of the infected decreased compared to the control (P < 0.05). The mean body temperature of infected individuals increased (35-37°C) compared to the control (P < 0.05). The erythrocyte indices of the infected and control groups indicate a significant decrease (P < 0.05). In erythrocyte indices, only MCHC indicated a nonsignificant decrease (P > 0.05). The SOD of serum shows a significant increase (P < 0.05), and no significant increase SOD (P > 0.05) in kidney and the liver SOD indicates a significant decrease (P < 0.05). The serum, kidney, and liver show a significant increase (P < 0.05) in CAT. The serum GSH from the findings indicates a nonsignificant increase (P > 0.05), and the kidney and liver GSH shows a significant increase (P < 0.05). The correlation analysis for SOD shows nonsignificant negative correlation for serum/kidney, and the serum/liver and kidney/liver show significant positive correlation. The result of CAT shows significant correlations for serum and kidney, serum and liver, and kidney/liver with a positive correlation. The GSH result shows no significant negative correlation for serum/kidney and no significant positive correlation for serum/liver and kidney/liver. The histological damage in the kidney, liver, and spleen was much higher in the chronic stage than in the subacute stage and no tissue damage in the control group. In conclusion, subacute and chronic stage trypanosome infection is associated with changes in hematological indices, antioxidants of the liver, spleen and kidney, and histological architecture.

Role of cineole in alleviation of acute kidney injury and renal function recovery following gentamicin administration in rats.

Gentamicin leads to kidney failure by producing free radicals and inflammation in renal tissue. Cineole as a terpenoid has antioxidant properties. Antioxidants can play an effective role in preserving the oxidant-antioxidant balance. Hence, this study investigated the effects of cineole on acute kidney injury (AKI) and renal function recovery following gentamicin administration in rats. 36 male Wistar rats were randomly divided into 6 equal groups; healthy control, gentamicin, DMSO carriers, cineole 50, cineole 100, and vitamin E. After 12 days of treatment, the animals were anesthetized with ketamine and xylazine. Serum and kidney samples were taken for biochemical and gene expression experiments. Cineole 50 and 100 groups increased the levels of serum glutathione (GSH) (<0.05), kidney and serum glutathione peroxidase (GPX) (<0.001), kidney catalase (CAT) (<0.001), serum nitric oxide (NO) (<0.001), and the GPX gene (<0.05) compared with the gentamicin group. These treatment groups had decreased levels of kidney malondialdehyde (MDA) (<0.001), serum creatinine (<0.001), urine protein, and the Interleukin 6 (IL-6) gene (<0.05) compared with the gentamicin group. Cineole 50 increased the serum MDA (<0.001), urea, and CAT gene (>0.05) and decreased the kidney GSH (<0.05) and the tumor necrosis factor-alpha (TNF-α) gene (<0.05). Cineole 100 increased the kidney GSH (<0.05) and decreased the serum MDA (<0.001), urea, CAT gene (>0.05), and TNF-α gene (>0.05) compared with the gentamicin group. Improvement in histological alterations was displayed in cineole groups compared with the gentamicin group. Cineole can reduce kidney damage caused by nephrotoxicity following gentamicin consumption through its antioxidant and anti-inflammatory properties.

Intervention effects of drugs on GSH and SOD enzyme activity of rats kidney acutely poisoned by nickel carbonyl

Objective: To evaluate the intervention effect of various drugs on glutathione (GSH) and superoxide dismutase (SOD) enzyme activity of rats kidney with acute nickel carbonyl poisoning. Methods: In January 2019, The 250 SPF male SD rats were randomly divided into normal control group (n=10) , poisoned group (n=40) and treatment groups (n=200) according to the random number table method. And the treatment groups were divided into methylprednisolone group (20 mg/kg) , DDC group (100 mg/kg) , sodium selenite group (10 μmol/kg) , Shenfu huiyang decoction group (0.25 ml) and methylprednisolone combined with DDC group (100 mg/kg) , with 40 mice in each group. Except for the normal control group, rats in the other groups were exposed to nickel carbonyl for 30 min, at 4 h and 30 h after exposure, the rats in each treatment group were intraperitoneally injected with corresponding drugs, and kidney tissues were collected 3 d and 7 d after administration, with 10 mice in each group. The activities of GSH and SOD in kidney were measured by enzyme-linked immunosorbent assay, and using electron microscopy observe ultrastructure changes. Results: Compared to the control group, the activities of GSH and SOD enzyme of poisoned group were significantly decreased at 3 d or 7 d after 4 h or 30 h exposure, and the difference was statistically significant (P=0.000, 0.031, 0.001, 0.033) , the epithelial nuclei of proximal convoluted tubules were pyknosis and lysosome hyperplasia in the cytoplasm. And compared to poisoned group, the activities of GSH and SOD enzyme of methylprednisolone+DDC group were significantly increased at treatment with 7 d after 4 h exposure, the difference was statistically significant (P=0.022, 0.000) , and the activities of GSH and SOD enzyme of methylprednisolone and enzyme of methylprednisolone+DDC group were significantly higher at 7 days than at 3 days, the difference was statistically significant (P=0.020, 0.017, 0.018, 0.033) . The results of electron microscopy showed that the cell nuclei and cytoplasmic organelles of proximal convolute tubule were almost restored to normal tissue level of both methylprednisolone group and methylprednisolone+DDC group. Conclusion: The methylprednisolone and methylprednisolone+DDC have obvious repair effect on renal enzyme activity level of rats with acute nickel carbonyl poisoning, and the treatment effect is better for a long time of medication.

Effects of folic acid on oxidative damage of kidney in lead-exposed rats.

Lead (Pb) has many applications in daily life, but in recent years, various problems caused by lead exposure have aroused people's concern. Folic acid is widely found in fruits and has received more attention for its antioxidant function. However, the role of folic acid in lead-induced kidney injury in rats is unclear. This study was designed to investigate the effects of folic acid on oxidative stress and endoplasmic reticulum stress in the kidney of rats caused by lead exposure. Forty specific pathogen-free male Rattus norvegicus rats were randomly divided into control, lead, intervention, and folic acid groups. The levels of SOD, GSH-Px, GSH, and MDA were measured by biochemical kits. The protein levels of Nrf2, HO-1, CHOP, and GRP78 were measured by immunofluorescence. This study showed that lead exposure increased the blood levels of lead in mice. However, the intervention of folic acid decreased the levels of lead, but the difference was not statistically significant. Lead exposure causes oxidative stress by decreasing kidney SOD, GSH-Px, and GSH levels and increasing MDA levels. However, folic acid alleviated the oxidative damage caused by lead exposure by increasing the levels of GSH-Px and GSH and decreasing the levels of MDA. Immunofluorescence results showed that folic acid intervention downregulated the upregulation of kidney Nrf2, HO-1, GRP78, and CHOP expression caused by lead exposure. Overall, folic acid alleviates kidney oxidative stress induced by lead exposure by regulating Nrf2 and HO-1, while regulating CHOP and GRP78 to mitigate apoptosis caused by excessive endoplasmic reticulum stress.

Mitigative Effect of Vitex Negundo against Fluoride induced Oxidative Stress Mediated Cardio and Nephrotoxicity

The present study investigated the mitigative effect of Vitex negundo against sodium fluoride (NaF) induced cardio and nephrotoxicity. The hydroalcoholic extract of Vitex negundo leaves (HAEVNL) was prepared by the maceration method. Group I, Group II, and Group III served as normal, toxic, and plant control groups in the treatment schedule. Group IV and V (200 and 400 mg/kg b.wt, p.o) served as treatment groups. Group II, IV, and V treated with NaF (100ppm) through drinking water for 4 weeks. Cardiac and kidney parameters such as LDH, CK-MB, Lipid profile, Creatinine, Urea, and Uric acid were estimated. The heart and kidney tissues LPO, GSH, SOD, and CAT levels and histopathological studies were performed. Phytochemical investigation showed the alkaloids, saponins, phytosterols, flavonoids, phenols, and tannins. Rats administered with NaF have demonstrated a significant rise in the LDH, CK-MB, TC, TG, LDL-C, VLDL-C, Creatinine, Urea, and Uric acid. Tissue LPO levels increased while there was a significant decrease in serum HDL-C and tissue SOD, GSH, and CAT levels. Treatment with HAEVNL showed effective recovery against NaF-induced cardio and nephrotoxicity. The histopathological evaluation also added to the benefits of the Vitex negundo leaves. The study concluded that Vitex negundo leaf extract showed a significant antioxidant and mitigative effect against fluoride- induced cardio and nephrotoxicity in rats.

Effects of melatonin and N-acetylcysteine on aluminum phosphide poisoning in rats.

Aluminum phosphide (ALP) poisoning is one of the deadliest types of poisoning in the world. The antioxidant properties of melatonin and N-acetylcysteine and their effects on reducing cell death have been identified. The aim of this study was to evaluate the effects of N-acetylcysteine and melatonin in the treatment of aluminum phosphide poisoning in rats. Fifty male Wistar rats weighing 200-250 g were tested in five groups of ten. The first group was the control group; the second group received (10 mg/kg) of ALP, the third group received (10 mg/kg) of ALP and (10 mg/kg) of melatonin, the fourth group received (10 mg/kg) of ALP and (10 mg/kg) of N-acetylcysteine, and the last group received (10 mg/kg) of ALP and (10 mg/kg) of melatonin and N-acetylcysteine. The plasma of samples was isolated, and the activity of antioxidant enzymes (glutathione S-transferase (GST), Superoxide dismutase (SOD), and catalase (CAT)) was analyzed. The concentrations of CAT, GST, Glutathione, GSH were decreased in plasma, liver, and kidneys of mice treated with aluminum phosphide; also, the concentrations of aspartate aminotransferase (AST), ALT, and AlK were increased (P < 0.05), while the activity of SOD did not change significantly (P > 0.05). Treatment with N-acetylcysteine and melatonin led to an increase in the activity of CAT, GST, and GSH in plasma, liver, and kidney. After the administration of N-acetylcysteine and melatonin to mice, the levels of all enzymes were close to normal, and the mice survived for 12-15 hours after administration. The administration of N-acetylcysteine (NAC) and melatonin at a dose of 10 mg/kg improves hepatic manifestations and prevents liver necrosis; also, they are considered potential therapeutic agents in the treatment of this poisoning.

Repression of inflammatory pathways with Boswellia for alleviation of liver injury after renal ischemia reperfusion

AimAcute kidney injury (AKI) is a sudden incident that is linked with a high lethality rate commonly due to distant organ injury. This study aims to explore the role of standardized Boswellia serrata (containing 35 % boswellic acid) in attenuating kidney and liver damage in a model of rats with renal insult. Main methodsSprague-Dawley rats, exposed to renal injury via ischemia-reperfusion model, were administered a daily regimen of 1000 or 2000 mg/kg Boswellia for seven days then rats were sacrificed on day eight. Alanine aminotransferase, aspartate aminotransferase, serum creatinine and blood urea nitrogen, were assayed. TLR9, oxidative stress markers; namely MDA and GSH, inflammatory cytokines; namely, IL-6, IL-1β, and TNF-α, as well as NF-κB were also measured. Key findingsRenal ischemia-reperfusion injury (IRI) impaired renal and liver function significantly, but Boswellia attenuated this impairment in a dose-dependent fashion. Histopathological assessment of kidney and liver confirmed that Boswellia decreased damage severity. A marked increase in TLR9, NF-κB, IL-6, IL-1β, TNF-α, and MDA besides decreased GSH levels were observed in the kidney and liver after renal IRI. Boswellia attenuated increases in TLR9, NF-κB, IL-1β, TNF-α, and IL-6 and boosted antioxidant defences via decreasing MDA and increasing GSH in kidney and liver. Anti-inflammatory and antioxidant effects of Boswellia were mostly comparable to those of silymarin. SignificanceWe conclude that the anti-inflammatory and antioxidant effects of Boswellia could be beneficial in ameliorating kidney and liver damage after AKI and that TLR9 might be the connection that signals liver injury in response to renal damage.

The effects of copper, zinc and bicarbonate in blood, kidney and liver in rats under intermittent hypobaric hypoxia

Intermittent hypobaric hypoxia is defined as to be below the normal values of partial oxygen pressure at tissue due to hypoxia periods. It can lead to increased reactive oxygen species which causes oxidative damage to DNA, lipids and proteins. The effect of antioxidant defense mechanism varies from tissue to tissue under hypoxic conditions. The aim of our study was to investigate the effects of bicarbonate, copper and zinc on antioxidant statue in blood, liver and kidney tissues under hypoxia.Forty adult male Sprague Dawley rats randomly divided into five groups (Control, Hypoxia, H+Zn, H+Cu and H+HCO3). Rats were exposed hypoxia a daily 8 h for 5 days/week until completing 3 weeks in hypoxia cabin at a simulated pressure of 400–500 mmHg. The animals of H+Zn, H+Cu and H+HCO3 experimental groups received through drinking water 30 mg/kg Zn, 7 mg/kg Cu and 3 mmol/kg NaHCO3, respectively. At the samples of blood, liver and kidney taken from rats at the end of experiment were measured the concentrations of Zn and Cu by ICP-OES device. The values of malondialdehyde (MDA) and glutathione (GSH) and the bicarbonate concentration were also obtained spectrophotometer and ABL800 devices, respectively.According to statistical evaluated, the kidney GSH values showed a significant increase in all experimental groups (p < 0.01). Increase in the plasma GSH values is also due to kidney cells. As a result of our investigation it is seen that the antioxidant response of kidney cells to hypoxia are more effective than applied dose levels of zinc, copper and bicarbonate ions at the study.

Boric acid supplementation affects antioxidant activity in ovariectomized female rats

This study aimed to investigate the protective effect of boric acid (BA) supplementation against oxidative stress (OS) in ovariectomized rats. A total of 48 nonpregnant female Wistar albino rats (180-250 g) were used in the experiment. The rats were divided into six equal groups (n = 8): Control, OVX, OVX + 5 mg/kg BA (OVX + BA5), OVX + 10 mg/kg BA (OVX + BA10), 5 mg/kg BA (BA5), and 10 mg/kg BA (BA10). The rats were intraperitoneally anesthetized with a combination of ketamine hydrochloride (85 mg/kg) and xylazine (10 mg/kg) and underwent a bilateral ovariectomy. Supplementation with 5 mg/kg and 10 mg/kg BA via oral gavage was started 2 weeks after ovariectomy and continued for 20 days. Catalase (CAT), glutathione S-transferase (GST), glutathione peroxidase (GPx), glutathione (GSH), and malondialdehyde (MDA) levels in the liver, kidney, and brain tissues of rats were analyzed by the spectrophotometric method. MDA concentrations in the liver tissue was increased in the OVX rats compared to the control group (p &lt;0.05). Liver GST activity was significantly decreased in the OVX rats, but it was increased with 5 mg/kg and 10 mg/kg BA supplementation (p &lt;0.05). Mean kidney GSH, GPx, and CAT activities in the OVX rats were increased with 5 mg/kg and 10 mg/kg BA supplementation (p &lt;0.05). In the brain tissue, GST activity was increased in the OVX rats treated with 10 mg/kg BA (p &lt;0.05). These results indicate that BA supplementation can enhance antioxidant defense mechanisms against OS after ovariectomy in female rats.

Effects of caffeic acid phenethyl ester use and inhibition of p42/44 MAP kinase signal pathway on caveolin 1 gene expression and antioxidant system in chronic renal failure model of rats

Effects of Caffeic acid phenethyl ester (CAPE) and/or PD98059 (PD) on the gene expression of Caveolin-1 (CAV1) and reduced glutathione (GSH), malondialdehyde (MDA), copper–zinc superoxide dismutase (CuZn-SOD), and catalase (CAT) enzyme activities were investigated in an experimental chronic renal failure model in rats. Eighty Wistar rats were divided into eight groups for a 28-day study: Control, CsA (Cyclosporine A), CsA-V (CsA solvent), CsA + PD (CsA + PD98059), CsA + PD + CAPE, CsA + CAPE, CAPE-V (CAPE solvent), and PD-V (PD98059 solvent). Serum blood urea nitrogen and creatinine levels, as well as histopathological findings indicated the development of renal failure in the CsA group. Kidney GSH levels decreased while MDA levels, CuZn-SOD, and CAT activities increased significantly in the CsA group compared to control indicating oxidative stress. CAV1 gene expression significantly decreased in the CsA group compared to the control. PD98059 and CAPE applications made positive improvements in the levels of the parameters investigated. PD98059 and CAPE applications in CsA given animals increased GSH and CAV1 gene expressions and decreased CuZn-SOD and CAT levels compared to the CsA group. In conclusion, it was shown that PD98059 and CAPE could attenuate the effects of chronic renal failure, and CAV1 is suggested as a therapeutic target and the inhibition of the p44/42 MAPK pathway may be a new approach for the treatment of renal degenerations.