EGCG treats ICH via up-regulating miR-137-3p and inhibiting Parthanatos

• Main Authors: 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
• Format: Article
• Language: English
• Published: De Gruyter 2020-10-01
• Series: Translational Neuroscience
• Subjects: intracranial hemorrhage; (−)-epigallocatechin-3-gallate; mir-137-3p; parthanatos
• Online Access: https://doi.org/10.1515/tnsci-2020-0143

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.