BackgroundMethotrexate (MTX) is an antimetabolite broadly used in treatment of cancer and autoimmune diseases. MTX-induced hepatotoxicity limits its application. We investigated hepatoprotective effects of turmeric in MTX-induced liver toxicity.MethodsAll experiments were performed on male Wistar albino rats that were randomly divided into six groups. Group one received saline orally for 30 days (control group), groups two and three received turmeric extract (100, 200 mg/kg respectively) orally for 30 days, group four received single dose, of MTX IP at day 30, groups five and six received turmeric extract 100 and 200 mg/kg orally respectively for 30 days and single dose of methoterxate IP (20 mg/kg) at day 30. Four days after MTX injection animals were sacrificed and evaluated. Blood ALT and AST (indicators of hepatocyte injury), ALP and bilirubin (markers of biliary function), albumin (reflect liver synthetic function) as well as the plasma TAS concentration (antioxidant defenses) were determined. The cellular antioxidant defense activities were examined in liver tissue samples using SOD, CAT, and GSH-Px for the oxidative stress, and MDA for lipid peroxidation. In addition, liver damage was evaluated histopathologically.ResultsMTX significantly induced liver damage (P < 0.05) and decreased its antioxidant capacity, while turmeric was hepatoprotective. Liver tissue microscopic evaluation showed that MTX treatment induced severe centrilobular and periportal degeneration, hyperemia of portal vein, increased artery inflammatory cells infiltration and necrosis, while all of histopathological changes were attenuated by turmeric (200 mg/kg).ConclusionTurmeric extract can successfully attenuate MTX-hepatotoxicity. The effect is partly mediated through extract’s antinflammatory activity.

Experiments carried out on mice demonstrated that administration of a platinum-based drug, cisplatin, extensively used in anticancer chemotherapy, exerts significant hyperalgesic effects; it intensifies both phases of pain behavioral reactions induced in the formalin test. When introduction of cisplatin was combined with i.p. injections of 100 mg/kg of an aqueous-alcoholic extract from the leaves of Salvia officinalis, the second phase of cisplatin-enhanced pain in the formalin test was effectively suppressed; the effect was comparable with that provided by injections of morphine or even more intense.

No abstract

Objective: Cisplatin (Cis) is a potent chemotherapeutic agent in clinical use which is associated with nephrotoxicity and neuropathic pain possibly through inflammatory response. Cerebrolysin (CBL), a mixture of neurotrophins, has analgesic and anti-inflammatory properties. The aim of the present study was to investigate the effects of cerebrolysin on cisplatin-induced neuropathic pain in mice.Materials and Methods: Mice were randomly divided into five groups: Control, Cis, Cis + CBL, Cis + Vitamin E (Vit E), and Cis + Morphine. CBL and Vit E were injected for four consecutive days following a single injection of Cis. On day 4, the mice were subjected to three behavioral tests: cold plate, hot plate, and formalin. Results:The results showed that mice treated with CBL had higher withdrawal thresholds for both the hot plate and cold plate tests and displayed lower hyperalgesia-related behaviors for the formalin test compared to the Cis group. Moreover, CBL induced higher anti-nociceptive effects than Vit E and lesser effects than morphine in both hot plate and cold plate tests. Furthermore, the analgesic effect of CBL was similar to the morphine effect in the late phase of the formalin test. Conclusion:These results indicate that CBL has an anti-nociceptive effect against cisplatin-induced neuropathic pain.