Poly(ADP-ribose) polymerase inhibition reveals a potential mechanism to promote neuroprotection and treat neuropathic pain
Prashanth Komirishetty
Aparna Areti
Ranadeep Gogoi
Ramakrishna Sistla
Ashutosh Kumar
摘要：Neuropathic pain is triggered by the lesions to peripheral nerves which alter their structure and function. Neuroprotective approaches that limit 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 atfer the nerve injury. hTey provoke oxidative DNA damage and consequent over-activation of the poly(ADP-ribose) polymerase (PARP) upregulates pro-inlfammatory 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 beneifts in treating experimental neuropathy. hTis article reviews the in-volvement of PARP over-activation in trauma induced neuropathy and therapeutic signiifcance of PARP inhibitors in the experimental neuropathy and neuropathic pain.
机标关键词：neuropathic painfree radicalsmitochondrial dysfunctionstructure and functionoxidative DNA damageperipheral nervesneuronal deathnerve injury
论文发表日期：2016-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：4( 1545-1548 )
英文信息