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MTCC1325在阿尔茨海默病诱导的大鼠脑细胞膜结合转运ATP酶系统中的作用。

Role of MTCC1325 in membrane-bound transport ATPases system in Alzheimer's disease-induced rat brain.

作者信息

Mallikarjuna Nimgampalle, Praveen Kukkarasapalli, Yellamma Kuna

机构信息

Division of Neurobiology, Department of Zoology, Sri Venkateswara University, Tirupati, Andhra Pradesh, India.

出版信息

Bioimpacts. 2016;6(4):203-209. doi: 10.15171/bi.2016.27. Epub 2016 Dec 29.

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder, clinically characterized by memory dysfunction and progressive loss of cognition. No curative therapeutic or drug is available for the complete cure of this disease. The present study was aimed to evaluate the efficacy of MTCC1325 in ATPases activity in the selected brain regions of rats induced with Alzheimer's. For the study, 48 healthy Wistar rats were divided into four groups: group I as control group, group II as AD model (AD induced by intraperitoneal injection of D-Galactose, 120 mg/kg body weight for 6 weeks), group III as normal control rats which were orally administered only with MTCC1325 for 60 days, and group IV where the AD-induced rats simultaneously received oral treatment of MTCC1325 (10ml/kg body weight, 12×10 CFU/mL) for 60 days. The well known membrane bound transport enzymes including Na, K-ATPases, Ca-ATPases, and Mg-ATPases were assayed in the selected brain regions of hippocampus and cerebral cortex in all four groups of rats at selected time intervals. Chronic injection of D-Galactose caused lipid peroxidation, oxidative stress, and mitochondrial dysfunction leading to the damage of neurons in the brain, finally bringing a significant decrease (-20%) in the brain total membrane bound ATPases over the controls. Contrary to this, treatment of AD-induced rats with MTCC1325 reverted all the constituents of ATPase enzymes to near normal levels within 30 days. MTCC1325 exerted a beneficial action on the entire ATPases system in AD-induced rat brain by delaying neurodegeneration.

摘要

阿尔茨海默病(AD)是一种神经退行性疾病,临床特征为记忆功能障碍和认知能力逐渐丧失。目前尚无治愈该疾病的治疗方法或药物。本研究旨在评估MTCC1325对阿尔茨海默病诱导大鼠选定脑区ATP酶活性的影响。在本研究中,48只健康的Wistar大鼠被分为四组:第一组为对照组,第二组为AD模型组(通过腹腔注射D-半乳糖诱导AD,剂量为120 mg/kg体重,持续6周),第三组为正常对照大鼠,仅口服MTCC1325 60天,第四组为AD诱导大鼠同时接受MTCC1325口服治疗(10ml/kg体重,12×10 CFU/mL)60天。在选定的时间间隔,对所有四组大鼠海马体和大脑皮层的选定脑区中包括钠钾ATP酶、钙ATP酶和镁ATP酶在内的著名膜结合转运酶进行了测定。长期注射D-半乳糖会导致脂质过氧化、氧化应激和线粒体功能障碍,从而导致大脑神经元受损,最终使大脑总膜结合ATP酶比对照组显著降低(-20%)。与此相反,用MTCC1325治疗AD诱导的大鼠可在30天内使ATP酶的所有成分恢复到接近正常水平。MTCC1325通过延缓神经退行性变对AD诱导的大鼠脑内整个ATP酶系统发挥有益作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acd/5326668/f222d20ebe76/bi-6-203-g001.jpg

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