Objective: To evaluate the synergistic protective effect of Momordica charantia and Phyllanthus amarus combination (MC+PA) of doses 200 and 400 mg/kg on the liver in different experimental models of hepatotoxicity. Methods: The hepatoprotective activity was evaluated in ethanol and anti-tubercular drugs (isoniazid-INH, rifampicin-RIF) induced hepatotoxicity models. Hepatotoxicity in both models was induced to all groups except the normal control. Intoxicated rats were treated with silymarin and various doses of MC+PA for 8 d in ethanol-induced and 21 d in INH+RIF induced hepatotoxicity models. At the completion of study, the biochemical markers and the anti-oxidant status (SOD and MDA) were measured and also the histopathological evaluation of the liver tissue was carried out. Results: Combination therapy remarkably reduced the elevated profile of the biochemical markers and thereby improved the anti-oxidant status, thus exhibiting the synergistic hepatoprotective effect when compared with the positive control group (p<0.001). Histopathological evaluation demonstrated that MC+PA decreased the liver damage significantly in comparison with the positive group. Conclusion: The current work suggests that the combined extract showed synergistic effects on ethanol and anti-tubercular drugs induced hepatotoxicity models by significantly decreasing the liver damage.

Aims: In the present study we aimed to investigate Neuroprotective Effects of Nardostachys jatamansi Against BSO Induced Anxiety in Mice. Background: Oxidative stress is implicated in nervous system impairment and development of anxiety-like disorders. There is an immediate surge for identification of herbal supplements to treat oxidative stress mediated anxiety and neurodegeneration. Objective: In present study, we analyzed the metabolites present in 70 % ethanolic extract of Nardostachys jatamansi (NJE) by LC-ESI-MS/MS and RP-HPLC. Oxidative stress was induced using BSO (300 mg/kg) for 7 days after pretreatment with Nardostachys jatamansi extract (250 mg/kg) followed by assessing anxiety levels in mice using behavioural indices and biochemical parameters as well as western blot of two important biomarkers linking oxidative stress with anxiety viz glyoxalase 1 and glutathione reductase. Method: LC–ESI-MS/MS analysis aided in identification of the major metabolites present in NJE. RP-HPLC analysis for neurotransmitter content, behavioural tests for anxiety analysis, oxidative stress markers by biochemical analysis, and western blot analysis for oxidative stress markers were evaluated. Result: LC–ESI-MS/MS analysis aided in identification of the major metabolites present in NJE. A total of 15 metabolites were identified. RP-HPLC analysis for serotonin and melatonin content revealed an enriched melatonin content 72.19 ± 1.6 µg/g, however, serotonin could not be detected. The anxiolytic tests employed showed that BSO-induced oxidative stress for 7 days caused a significant decrement in time spent in open arm of EPM, in exploratory behavior in OFT and light compartment of LDB and also in a number of licks and shocks accepted in VCT. NJE further decreased oxidative stress mediated markers in serum viz cortisol, lipid peroxides and protein carbonyls in brain and improved the antioxidant status of brain (GPx, GR, GST, SOD, CAT, and ABTS). NJE also mitigated levels of choline and glutamate in brain. Moreover, NJE in-creased brain GABA and monoamine levels thereby effectively overcoming the anxiety-like effects of BSO. Conclusion: These results clearly suggest that OS mediates anxiety and NJE could be an effective remedy in treating oxidative stress mediated anxiety and neuropsychiatric disorders.