Carnosic acid alleviates chlorpyrifos-induced oxidative stress and inflammation in mice cerebral and ocular tissues

International audienc

Piperine Enhances the Antioxidant and Anti-Inflammatory Activities of Thymoquinone against Microcystin-LR-Induced Hepatotoxicity and Neurotoxicity in Mice

Microcystin- (MC-) LR is the most frequent cyanotoxin produced by Microcystis aeruginosa cyanobacteria in the contaminated freshwater environment. MC represents a health hazard to humans and animals. Therefore, the present study was designed to evaluate the potential ameliorative effect of thymoquinone (TQ) and/or piperine (PP) against MC toxicity in mice. Fifty-six mice were randomly divided into seven experimental groups. Group I is the normal control that received distilled water for 21 days; Group II (TQ) was treated with TQ (10 mg/kg, i.p) for 21 days; Group III (PP) was treated with PP (25 mg/kg, i.p) for 21 days; Group IV (MC) was treated with MC (10 μg/kg, i.p) for 14 days and served as the toxic control; and Groups V, VI, and VII received TQ and/or PP 7 days prior to MC and continued for 14 days with MC. The results revealed that MC elicited hepatotoxicity and neurotoxicity which was evident due to the significant elevation of serum AST, ALT, γGT, ALP, LDH, IL-1β, IL-6, and TNF-α levels. Furthermore, MC markedly increased MDA and NO contents along with reduction of GSH, SOD, CAT, and GSH-Px in liver and brain tissues. The electron transport chain may be a possible target for MC. TQ and/or PP ameliorated the MC-mediated oxidative damage in the liver and brain which might be attributed to their antioxidant properties. However, the concurrent treatment of TQ and PP showed the best regimen as a result of the PP-enhanced bioavailability of TQ

Fucoidan alleviates microcystin-LR-induced hepatic, renal, and cardiac oxidative stress and inflammatory injuries in mice

International audienceFucoidans (FUCs) are sulfated polysaccharides that have a wide range of bioactivities. The current study was designed toevaluate the antioxidant potential of FUC against microcystin-LR (MC-LR)-induced toxicity. Five mice groups (n = 8) wereused. Group 1 received saline, Group 2 received oral FUC 100 mg/kg/day for 21 days, Group 3 received i.p. MC-LR 10 μg/kg/day for 14 days, Group 4 received MC-LR plus FUC 50 mg/kg/day, and Group 5 received MC-LR plus FUC 100 mg/kg/day. Thepresent study showed that MC-LR administration was associated with significant increases (p < 0.01) in serum concentrations ofhepatic (aspartate transferase, alanine transferase, and alkaline phosphatase), renal (urea and creatinine), and cardiac (creatinekinase and CK-MB) injury biomarkers, as well as serum lactate dehydrogenase, cholesterol, and pro-inflammatory cytokines(interleukins-1β and 6, and tumor necrosis factor-α), compared with the control group. Further, MC-LR-intoxicated miceexhibited significantly higher (p < 0.01) hepatic, renal, and cardiac tissue levels of malondialdehyde and nitric oxide, as wellas lower tissue levels of reduced glutathione and activities of glutathione peroxidase, superoxide dismutase, and catalase enzymesin comparison with control mice. Treatment by FUC significantly ameliorated all the above-mentioned alterations in a dosedependent manner with frequent restoration of the normal ranges in the FUC 100 mg/kg/day dose group. Moreover, treatment byFUC alone at 100 mg/kg/day was not associated with significant negative alterations in the assessed biochemical parameters,highlighting its safety at this dose. In conclusion, treatment by FUC significantly ameliorated organ injury, induced by MC-LR inmouse hepatic, renal, and cardiac tissues

The ameliorative effects of ceftriaxone and vitamin E against cisplatin-induced nephrotoxicity

International audienceNephrotoxicity is a common adverse effect of treatment with cisplatin (CDDP). This study was performed to evaluate the antioxidant and nephroprotective efficacy of ceftriaxone (CTX) and vitamin E (Vit.E), alone and in combination against CDDP-induced acute renal injury. Fifty-six male albino rats were equally divided into seven groups, receiving (I) normal saline, (II) CTX (100 mg/kg, intraperitoneal [i.p] injection), (III) Vit.E (100 mg/kg orally), (IV) CDDP (5 mg/kg i.p injection), (V) CDDP plus CTX, (VI) CDDP plus Vit.E, and (VII) CDDP plus CTX in combination with Vit.E. All treatments were administered daily for 10 days except CDDP, which was given as a single dose at the sixth day of the study. Compared to normal control rats, CDDP-injected rats showed significantly (p < 0.05) higher serum levels of renal injury biomarkers (uric acid, urea, and creatinine) and tumor necrosis factor-α (TNF-α), as well as increased renal tissue concentrations of malondialdehyde, nitric oxide, and TNF-α. Moreover, CDDP administration was associated with significantly lower (p < 0.05) renal tissue levels of reduced glutathione and activities of endogenous antioxidant enzymes (glutathione peroxidase, superoxide dismutase, and catalase) and total antioxidant capacity. All these alterations were significantly ameliorated in CDDP-injected rats, receiving CTX and/or Vit.E, compared to rats receiving CDDP alone. Interestingly, the antioxidant and anti-inflammatory effects were more marked in the CTX-Vit.E combination group, compared to groups receivingeither drug alone. In conclusion, CTX and Vit.E (especially in combination) could counteract the nephrotoxic effect of CDDP, probably through their antioxidant activities