Bacopa monniera extract mitigates isoproterenol-induced cardiac stress via Nrf2/Keap1/NQO1 mediated pathway.

The present study was aimed to investigate the effect of standardised hydroalcoholic extract of Bacopa monniera (BME) against isoproterenol (ISO) induced cardiac stress. Isoproterenol (85 mg/kg body weight) was administered intraperitoneally to induce cardiac stress in rats. Bacopa monniera extract (BME75 and 150 mg/kg) was orally administered for 21 days followed by ISO on 22nd and 23rd experimental days. ISO caused significant cardiac damage, which was concomitant with increased apoptosis and attenuated expressions of Nrf2, HO-1, and regulating apoptotic protein expressions of Bax, Bcl2 and NOS2. Treatment with BME in rats significantly improved cardiac dysfunction by maintaining cardiac rhythm, myocardial integrity. Decreased oxidative stress by restored expressions of Nrf2, NQO1 and HO-1 followed by elevating antioxidant enzymes and total glutathione levels. Our present results suggest that the BME treatment strengthening the endogenous defence system through Nrf2 modulation and played a key role against cardiac oxidative stress induced by ISO in rats.

Restorative effect of l-Dopa treatment against Ochratoxin A induced neurotoxicity.

The toxic effects of Ochratoxin A (OTA), a fungal secondary metabolite of the genera Aspergillus and Penicillium with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) a Parkinson inducing drug were investigated to evaluate the neurotoxic effects exerted by OTA. OTA is known to contaminate food and feedstuff leading to a wide range of toxicity like nephrotoxicity, hepatotoxicity, and immunotoxicity. However, due to the dearth of available information on the possible mechanisms of OTA neurotoxicity and neurodegeneration the current study was undertaken. Hence, in this study, we examined the neurotoxic effects and the possible mechanism of action of neurodegeneration by OTA toxicity on mice brain by conducting a battery of behavioural studies and reviewing neurotransmitter levels and neuronal apoptotic pathways. Further, they were treated with l-Dopa, a precursor of dopamine (DA) to explore its ameliorative effects against OTA. The results of behavioural studies like gait analysis, spontaneous activity, cylinder test and pole test showed that OTA exhibits Parkinsonian physiognomies which were stabilized with l-Dopa treatment. Also, OTA toxicity showed insults on neurotransmitter levels and general brain function parameters that were normalized with l-Dopa treatment. The results of the present study suggest that OTA promotes neurodegeneration by targeting neuronal pathway leading to the development of Parkinson's diseases.