氧化应激和线粒体功能障碍是帕金森病（PD）进展中起关键作用的机制。心叶青藤（Tinospora cordifolia）具有广泛的生物活性，包括免疫调节、抗菌、抗氧化和抗炎特性。本研究探究了心叶青藤乙醇提取物（TCE）对罗滕酮（Rotenone，ROT）中毒帕金森小鼠的神经保护活性。分为四组实验小鼠：对照组、ROT组（皮下注射2 mg/kg体重的ROT）、TCE + ROT组（口服200 mg/kg体重的TCE + ROT）和仅TCE组。小鼠经过一周的TCE预处理后，同时注射ROT处理35天。ROT中毒后，分析了动作活动、抗氧化潜能和线粒体功能障碍。在ROT中毒小鼠组中观察到线粒体电子传递链（mETC）复合物活性下降、线粒体膜电位（Ψm）丧失、Bax/Bcl-2比值增加及半胱氨酸蛋白酶-3（caspase-3）表达增加。我们的结果还显示ROT诱导的活性氧（ROS）介导的α-突触核蛋白（α-syn）聚集和线粒体功能障碍。然而，TCE的预处理和联用治疗在ROT中毒情况下显著减少了α-syn聚集，并通过改变线粒体电位和增加mETC活性改善了细胞的线粒体功能。TCE还降低了Bax/Bcl-2比值和半胱氨酸蛋白酶-3的表达，从而减少了细胞的凋亡。总而言之，通过调节氧化应激，最终减少线粒体功能障碍和细胞死亡，TCE在帕金森小鼠模型中对罗滕酮诱发的毒性保护神经元具有显著疗效。

Oxidative stress and mitochondrial dysfunction are leading mechanisms that play a crucial role in the progression of Parkinson's disease (PD). Tinospora cordifolia shows a wide range of biological activities including immunomodulatory, antimicrobial, antioxidant, and anti-inflammatory properties. This study explored the neuroprotective activities of T. cordifolia ethanolic extract (TCE) against Rotenone (ROT)-intoxicated Parkinsonian mice. Four experimental groups of mice were formed: control, ROT (2 mg/kg body wt, subcutaneously), TCE (200 mg/kg body wt, oral) + ROT, and TCE only. Mice were pretreated with TCE for a week and then simultaneously injected with ROT for 35 days. Following ROT-intoxication, motor activities, antioxidative potential, and mitochondrial dysfunction were analyzed. Decrease in the activity of the mitochondrial electron transport chain (mETC) complex, loss of mitochondrial membrane potential (Ψm), increase in Bax/Bcl-2 (B-cell lymphoma 2) ratio, and caspase-3 expression are observed in the ROT-intoxicated mice group. Our results further showed ROT-induced reactive oxygen species (ROS)-mediated alpha-synuclein (α-syn) accumulation and mitochondrial dysfunction. However, pre- and cotreatment with TCE along with ROT-intoxication significantly reduced α-syn aggregation and improved mitochondrial functioning in cells by altering mitochondrial potential and increasing mETC activity. TCE also decreases the Bax/Bcl-2 ratio and also the expression of caspase-3, thus reducing apoptosis of the cell. Altogether, TCE is effective in protecting neurons from rotenone-induced cytotoxicity in the Parkinsonian mouse model by modulating oxidative stress, ultimately reducing mitochondrial dysfunction and cell death.