EGCG Promotes Neurite Outgrowth through the Integrin β 1/FAK/p38 Signaling Pathway after Subarachnoid Hemorrhage

Yuyuan Zhang; Mengguo Han; Xiaoxue Sun; Guojun Gao; Guoying Yu; Liong Huang; Ying Chen

doi:10.1155/2021/8810414

EGCG Promotes Neurite Outgrowth through the Integrin β 1/FAK/p38 Signaling Pathway after Subarachnoid Hemorrhage

Evid Based Complement Alternat Med. 2021 Jan 25:2021:8810414. doi: 10.1155/2021/8810414. eCollection 2021.

Authors

Yuyuan Zhang¹, Mengguo Han¹, Xiaoxue Sun¹, Guojun Gao², Guoying Yu^{1

3}, Liong Huang², Ying Chen^{1

3}

Affiliations

¹ College of Life Sciences, Henan Normal University, Xinxiang, China.
² Department of Neurosurgery, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, China.
³ Institute of Biomedicine, Henan Normal University, Xinxiang, China.

Abstract

The abnormal neurites have long been regarded as the main player contributing to the poor outcome of patients with subarachnoid hemorrhage (SAH). (-)-Eigallocatechin-3-gallate (EGCG), the major biological component of tea catechin, exhibited strong neuroprotective effects against central nervous system diseases; however, the role of EGCG-mediated neurite outgrowth after SAH has not been delineated. Here, the effect of reactive oxygen species (ROS)/integrin β1/FAK/p38 pathway on neurite outgrowth was investigated. As expected, oxyhemoglobin- (OxyHb-) induced excessive ROS level was significantly reduced by EGCG as well as antioxidant N-acetyl-l-cysteine (NAC). Consequently, the expression of integrin β1 was significantly inhibited by EGCG and NAC. Meanwhile, EGCG significantly inhibited the overexpression of phosphorylated FAK and p38 to basal level after SAH. As a result, the abnormal neurites and cell injury were rescued by EGCG, which eventually increased energy generation and neurological score after SAH. These results suggested that EGCG promoted neurite outgrowth after SAH by inhibition of ROS/integrin β1/FAK/p38 signaling pathway. Therefore, EGCG might be a new pharmacological agent that targets neurite outgrowth in SAH therapy.