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Antioxidant and hepatoprotective effects of Boswellia ovalifoliolata bark extracts

Chinese Journal of Natural Medicines 2014年第9期12卷 663-671页

作者： Bandari Uma Mahesh Shweta Shrivastava Rajeswara Rao Pragada V.G.M.Naidu Ramakrishna Sistla Department of Pharmacology A.U.College of Pharmaceutical Sciences Andhra University Vishakhapatnam Andhra Pradesh India -530003 Department of Pharmacology & Toxicology National Institute of Pharmaceutical Education & Research (NIPER-Hyderabad) Balanagar Hyderabad Andhra Pradesh India-500037 Pharmacology Division Indian Institute of Chemical Technology Habsiguda Hyderabad Andhra Pradesh ndia-500007

Paracetamol(PCM) hepatotoxicity is related to reactive oxygen species(ROS) formation and excessive oxidative stress; natural antioxidant compounds have been tested as an alternative therapy. This study evaluated the hepatoprotective activity of an alcoholic extract of Boswellia ovalifoliolata(BO) bark against PCM-induced hepatotoxicity. BO extract also demonstrated antioxidant activity in vitro, as well as scavenger activity against 2, 2-diphenyl-1-picrylhydrazyl. Administration of PCM caused a significant increase in the release of transaminases, alkaline phosphatase, and lactate dehydrogenase in serum. Significant enhancement in hepatic lipid peroxidation and marked depletion in reduced glutathione were observed after parac intoxication with severe alterations in liver histology. BO treatment was able to mitigate hepatic damage induced by acute intoxication of PCM and showed a pronounced protective effect against lipid peroxidation, deviated serum enzymatic variables, and maintained glutathione status toward control. The results clearly demonstrate the hepatoprotective effect of BO against the toxicity induced by PCM.

关键词： extracts peroxidation glutathione dehydrogenase protective alcoholic antioxidant ABTS histology curcumin

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Poly(ADP-ribose) polymerase inhibition reveals a potential mechanism to promote neuroprotection and treat neuropathic pain

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Neural Regeneration Research 2016年第10期11卷 1545-1548页

作者： Prashanth Komirishetty Aparna Areti Ranadeep Gogoi Ramakrishna Sistla Ashutosh Kumar Department of Pharmacology and Toxicology National Institute of Pharmaceutical Education and Research (NIPER)-Hyderabad BalanagarIndia Department of Biotechnology National Institute of Pharmaceutical Education and Research (NIPER)-Guwahati Assam India Pharmacology Division Indian Institute of Chemical Technology (IICT) Hyderabad India

Neuropathic pain is triggered by the lesions to peripheral nerves which alter their structure and function. Neuroprotective approaches that jimit the pathological changes and improve the behavioral outcome have been well explained in different experimental models of neuropathy but translation of such strategies to clinics has been disappointing. Experimental evidences revealed the role of free radicals, especially per- oxynitrite after the nerve injury. They provoke oxidative DNA damage and consequent over-activation of the poly（ADP-ribose） polymerase （PARP） upregulates pro-inflammatory pathways, causing bioenergetic crisis and neuronal death. Along with these changes, it causes mitochondrial dysfunction leading to neu- ronal apoptosis. In related preclinical studies agents that neutralize the free radicals and pharmacological inhibitors of PARP have shown benefits in treating experimental neuropathy. This article reviews the in- volvement of PARP over-activation in trauma induced neuropathy and therapeutic significance of PARP inhibitors in the experimental neuropathy and neuropathic pain.

关键词： neuropathic pain poly(ADP-ribose) polymerase neuroinflammation oxidative stress bioenergeticcrisis

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