Wang Jianjun, Kuang Xuejun, Peng Zhao, Li Conghui, Guo Chengwu, Fu Xi, Wu Junhong, Luo Yang, Rao Xiaolin, Zhou Xiangjuan, Huang Bin, Tang Weijun, Tang Yinjuan
Affiliated hospital, Xiangnan University, Chenzhou, 423000, Hunan Province, China.
Department of Clinical, Xiangnan University, Chenzhou, 423000, Hunan Province, China.
Transl Neurosci. 2020 Oct 8;11(1):371-379. doi: 10.1515/tnsci-2020-0143. eCollection 2020.
Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (-)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos.
在临床环境中，颅内出血（ICH）若没有有效的治疗方法，会导致高死亡率和残疾率。（-）-表没食子儿茶素-3-没食子酸酯（EGCG）在中枢神经系统中发挥着重要作用，为治疗氧化损伤相关疾病提供了一种有前景的治疗药物。MiR-137可以抑制氧化应激和细胞凋亡，以减轻神经元损伤。然而，EGCG在调节miR-137-3p和神经元Parthanatos中的作用仍不清楚。在本研究中，我们构建了ICH小鼠模型，以研究EGCG通过上调miR-137-3p和抑制神经元Parthanatos的抗氧化作用。我们发现，EGCG上调了miR-137-3p并抑制了神经元Parthanatos，促进了功能恢复，减轻了ICH诱导的脑损伤，并降低了ICH后小鼠的氧化应激。然而，在抑制miR-137-3p并激活Parthanatos后，EGCG无法发挥神经保护作用。这些综合结果表明，EGCG可能上调miR-137-3p并抑制神经元Parthanatos，以加速ICH后小鼠的功能恢复，为EGCG成为治疗与Parthanatos相关的神经元损伤的新策略奠定了基础。
