Behl Tapan, Yadav Harlokesh N, Sharma Pyare L
Department of Chitkara College of Pharmacy, Chitkara University, Punjab, India.
Department of All India Institute of Medical Sciences, New Delhi, India.
Curr Mol Pharmacol. 2021;14(1):2-10. doi: 10.2174/1874467213666200512114943.
Alcoholic neuropathy is a chronic disorder caused by the excessive consumption of alcohol. Damage to the nerves results in unusual sensations in the limbs, decreased mobility and loss of some body functions.
Alcohol is considered a major cause for exclusively creating the debilitating condition of the neuropathic state. This review critically examines the key mediators involved in the pathogenesis of alcoholic neuropathy and the targets, which, upon selective inhibition, alleviate the progression of alcoholic neuropathy.
A thorough study of research and review articles available on the internet from PubMed, MEDLINE, and concerned sites was performed on alcoholic neuropathy.
Impairment in axonal transportation is quite common with the progression of alcoholic neuropathy. Nutritional deficiencies lead to axonal neuropathies that escalate a variety of complications that further worsen the state. PKC and PKA play a significant role in the pathogenesis of alcoholic neuropathy. PKC plays a marked role in modulating NMDA receptor currents, manifesting excitations in neurons. MMPs are involved in the number of pathologies that destroy the CNS and reduction in the level of endogenous antioxidants like α-tocopherol, vitamin E with ethanol, promotes oxidative stress by generating free radicals and lipid peroxidation.
Oxidative stress is implicated in the activation of MMPs, causing disruption in the blood-brain barrier, the latter are involved in the trafficking and passage of molecules in and out of the cell. Chronic alcohol consumption leads to the downregulation of CNS receptors, consequently precipitating the condition of alcoholic neuropathy.
酒精性神经病变是一种由过度饮酒引起的慢性疾病。神经损伤会导致肢体出现异常感觉、活动能力下降以及一些身体功能丧失。
酒精被认为是导致神经病变这种使人衰弱状况的主要原因。本综述批判性地研究了酒精性神经病变发病机制中涉及的关键介质以及那些经选择性抑制后可缓解酒精性神经病变进展的靶点。
对来自PubMed、MEDLINE及相关网站上可获取的关于酒精性神经病变的研究和综述文章进行了全面研究。
随着酒精性神经病变的进展，轴突运输受损相当常见。营养缺乏会导致轴索性神经病变，进而引发各种并发症，使病情进一步恶化。蛋白激酶C（PKC）和蛋白激酶A（PKA）在酒精性神经病变的发病机制中起重要作用。PKC在调节N-甲基-D-天冬氨酸（NMDA）受体电流方面发挥显著作用，表现为神经元兴奋。基质金属蛋白酶（MMPs）参与多种破坏中枢神经系统的病理过程，而乙醇会使内源性抗氧化剂如α-生育酚（维生素E）水平降低，通过产生自由基和脂质过氧化作用促进氧化应激。
氧化应激与MMPs的激活有关，导致血脑屏障破坏，后者参与分子进出细胞的运输和通道形成。长期饮酒会导致中枢神经系统受体下调，从而引发酒精性神经病变。
