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

Jianjun Wang,Chengwu Guo,Bin Huang,Conghui Li,Xiangjuan Zhou,Yang Luo,Zhao Peng,Junhong Wu,Xi Fu,Xiaolin Rao,Weijun Tang,Yinjuan Tang,Xuejun Kuang

doi:10.1515/tnsci-2020-0143

Jianjun Wang, Chengwu Guo + Show 11 more

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https://doi.org/10.1515/tnsci-2020-0143

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Journal: Translational neuroscience	Publication Date: Oct 8, 2020
Citations: 7	License type: CC BY 4.0

Affiliation: Xiangnan University

Abstract

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.

Highlights

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
Compared with the sham group, modified neurological severity score (mNSS) was upregulated in response to ICH after 7 days, whereas EGCG decreased mNSS in mice after ICH; EGCG did not decrease mNSS in mice after ICH when miR-137-3p and Ad-poly (ADP-ribose) polymerase 1 (PARP-1) were used (Figure 2a)
We revealed that EGCG can exert neuroprotective roles in brachial plexus root avulsion (BPRA) and spinal cord injury (SCI) [8,38]

Summary

Introduction

Abstract: 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. 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. 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

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Conclusion