Objective: The main objective of this study is to investigate the antioxidant and nephroprotective efficacy of moringa oleifera seed extract (MOSE) against cisplatin which induced acute renal injury. Methods: Forty male Wister rats were equally segregated into 4 groups (10 rats per group): group I (0.5 ml of sterile saline orally), group II (200 mg MOSE/kg b. wt orally for 10 consecutive days), group III (7.5 mg cisplatin/kg b. wt/intraperitonially as a single dose on the 5th day of the experiment) and group IV (200 mg moringa oleifera seed extract (MOSE)/kg orally for 10 d followed by 7.5 mg cisplatin/kg body weight/intraperitonially once as a single dose on the 5th day of the experiment. Serum biochemical analysis of renal biomarkers (urea, uric acid, and creatinine), oxidative stress markers (malondialdehyde [MDA]), a crucial antioxidant enzyme (catalase) and the expression of renal activity interleukin (IL)-6, (IL)-10 and Tumer necrotic factor (TNF-α) mRNA were determined. Histopathological examination of renal tissue was done. Results: Cisplatin induced renal damage, increased renal biomarkers (urea, creatinine and uric acid)(375.87±1.65, 5.238±0.25, 4.47±0.25). Tissue concentrations of malondialdehyde, IL-6 and TNF-α.(387.56±0.97, 2.188±0.20, 3.06±0.27)compared to control group(140.58±1.25,0.938±0.017, 1.24±0.17), (163.99±1.34, 1.008±0.05, 0.982±0.026) Moreover, cisplatin induced significantly down-regulation of anti-inflammatory (IL-10) and catalase (0.780±0.47, 1.62±0.06) compared to control one (1.010±0.02, 3.12±0.11),. The histopathological examination showed renal tissue damage and degeneration of tubules in the cortical portion in cisplatin group. However, interestingly concurrent adminsteration of the MOSE with cisplatin can alleviated the renal damage, oxidative stress and renal toxicity caused by cisplatin. Conclusion: These results suggest that the antioxidant and the anti-inflammatory effects of MOSE alleviate the cisplatin-induced nephrotoxicity.
Drug-induced hepatotoxicity is a frequent cause of liver injury worldwide. The present study was designed to evaluate the possible hepato-protective potential Agaricus bisporus extract (ABE; a type of mushrooms) in albino rats using Carbon tetrachloride (CCl4)-model of liver injury. Forty-two albino rats were utilized in this experiment arranged randomly in seven groups, six rats each, of different treatments. He-patic injury model was induced by administration of CCl4 (25% in corn oil) at a dose of 2.5 ml/kg, interperitoneally, twice weekly for 8 weeks (+ve control); test group rats received ABE at escalating doses of 200 or 400 mg/kg, orally, daily for 8 weeks with exposure to CCl4; standard group rats received Silymarin at dose of 100 mg/kg, orally, daily for 8 weeks along with CCl4; further 2 groups of rats received only ABE at the same dose levels; while rats of -ve control group received only the vehicles of the used drugs. Blood and liver tissue sam-ples were picked out at the end of the experimental course for different assays. Biochemical analysis revealed that ABE exhibited dose-dependent hepatoprotection indicated by almost normalized biomarkers, including, enzymatic liver function parameters, namely, AST, ALT, GGT & ALP with potential % of 93.1, 58.2, 65.2, 68.9, respectively, after ABE large dose when standardized by Silymarin; non-enzymatic parameters, namely, total protein, albumin, globulins, total bilirubin, conjugated bilirubin, unconjugated bilirubin, TAGs, Cholesterol, HDL, LDL & VLDL with potential % of 59.3, 54.5, 57.3, 81.8, 81.0, 80.0, 75.5, 90.4, 80.8, 84.5 & 78.7, respectively, after ABE large dose when standardized by Silymarin. The mechanism of the obtained hepatoprotection of ABE may be based on impeding the oxidative stress mediated by the used hepatotoxin, indicated by reduced MDA (37.9 % of Silymarin), and restored SOD, Catalase & GPx in liver homogenate with potentials of 94.9, 63.0 & 88.4 % of Silymarin, respectively. Pathological findings, both macroscopic and microscopic, were supportive to the biochemical findings, where the pathological lesions caused by CCl4 as fatty degeneration of hepatocytes with vacuolated cytoplasm, proliferated fibrous connective tissue with eosinophilic edematous fluid cells plus focal and diffuse necrotic areas and hyperplastic biliary epithelium, were ameliorated dose-dependently when ABE was administered together with CCl4. Data of the present study may suggest ABE as a good natural source for promising hepatoprotective and antioxidative remedies.
Background: Liquorice (Glycyrrhiza glabra) is a high valued plant and used in a lot of countries around the world. The liquorice (LQ) has a remarkable medicinal, nutritional and socio-economic value. Therefore this study was designed to clarify the protective effect of liquorice hydroethanolic extract against Thioacetamide (TAA) induced hepatotoxicity and hematotoxicity in rats.Materials and Methods: Seventy white Albino male rats were used in this study and after acclimatization rats were subjected to different treatments blood and tissue samples were collected after day 30 post administration, biochemical, antioxidant, hematological and histopathological examinations were utilized to investigate hepatoprotective activity of liquorice hydroethanolic extract.Results: TAA significant (P<0.05) increase the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and hepatic malondialdehyde (MDA) compared to control group and silymarin(SL)treated group as stander, admin-istration of LQ extract restore the toxic effect of TAA , while TAA significant (P<0.05) decrease the levels of catalase(CAT) ,hepatic glutathione(GSH) hepatic superoxide dismutase (SOD) , total protein and albumin level compared to control group and silymarin(SL)treated group as stander, LQ extract ameliorate toxic effect of TAA. TAA induce hematotoxicity in rats by significant (P<0.05) decrease Hb content and RBCs, whereas WBCs count significantly (P<0.05) increased throughout the period of administration when compared to the rats in control group and silymarin(SL)treated group as stander,LQ administration protect against the hematotoxicity effect of TAA, TAA induce histopathological alteration in liver tissue by comparison with control group and silymarin(SL)treated group as stander, while LQ extract showing improvement in the histopathological lesion compared with toxic effect induced by TAA.Conclusions: The hepatotoxicity and hematotoxicity induced by TAA were ameliorated by hydroethanolic extract of LQ especially in double dose (200 mg/kg b.wt). This effect was attributed to free radical scavenging activity and potent antioxidant activity of its components (flavonoid, tannin and saponin).
Background: Hyperlipidaemia is a common disease in middle-aged and elderly people. It has received attention, as it indirectly affects the normal metabolism, blood viscosity and vital organ functions. It is a risk factor for cardiovascular and cerebrovascular diseases. Therefore, the aim of the present study was to evaluate the possible antihyperlipidemic effect of Coriander sativum seed extract (CSSE) in rats fed on high-fat diet.Methods: A parallel study design was adopted on 42 albino rats, divided randomly into 7 groups with different treatments. After a 6 week-experimental course, blood samples were collected and analysed for lipid and organ function parameters. Phytochemical analysis was conducted on the used seed extract to detect the active principles underlying its effects.Results: CSSE (150 and 300 mg/kg, orally, once daily) along with a high-fat (1.5% cholesterol+1.5% coconut oil, in diet) diet resulted in a significant (p≤0.05) improvement in plasma lipid parameters, including, total cholesterol, triacyglycerols and lipoproteins, compared to the high-fat group. group. The extract significantly (p≤0.05) improved hepatic (total proteins, albumin, globulins, total conjugated and unconjugated bilirubins, AST, ALT, GGT), cardiac (CK-MB and troponin-I) and renal (urea, creatinine & uric acid) biomarkers. Phytoanalysis of CSSE revealed presence of phlobatannin and flavonoids. The protection % produced by small and large doses of CSSE were dose-dependent and parallel to those of the standard antihyperlipidemic rosuvastatin (2 mg/dl orally, daily).Conclusions: These data indicate that CSSE has a marked antihyperlipidemic effect and could be a source for a promising nutraceutical antihyperlipidemic drug depending on its high phenolic and flavonoid content.
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