EGCG Promotes Neurite Outgrowth through the Integrin β1/FAK/p38 Signaling Pathway after Subarachnoid Hemorrhage.

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

doi:10.1155/2021/8810414

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.

Highlights

A growing body of epidemiological and animal evidence demonstrated that green tea dramatically lowered the incidence of strokes and Alzheimer’s disease risk
Contrary to the reversible axonotmesis in myelinated and unmyelinated white matter, neurite degeneration might be less likely to be rescued in gray matter, which is mainly made up of neuronal cell bodies and dendrites. erefore, abnormal neurite morphology and length have been regarded as a common factor contributing to aging, neurodegenerative diseases, and central nervous system (CNS) injury [12,13,14]
Compared with the control group (2.2 ± 0.2), strong signals were captured in subarachnoid hemorrhage (SAH) group showing an increase in red fluorescence intensity (2.9 ± 0.1, p < 0.01 vs. control), whereas less signals were detected in the EGCG and NAC treatment group (p < 0.01 vs. SAH) (Figure 1)

Summary

Introduction

A growing body of epidemiological and animal evidence demonstrated that green tea dramatically lowered the incidence of strokes and Alzheimer’s disease risk. People who drank more than two cups of green tea per day exhibited less cognitive impairment after neuronal injury [1, 2]. It has been estimated that 36–55% survivors suffered impairment, disability, handicap, and poor quality of life during the first year after SAH, which might predict functional outcome of neuronal injury [10]. Contrary to the reversible axonotmesis in myelinated and unmyelinated white matter, neurite degeneration might be less likely to be rescued in gray matter, which is mainly made up of neuronal cell bodies and dendrites.

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