Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Refined qingkailing attenuates reactive astrocytes and glial scar formation after ischemia stroke via the EGFR/PLCγ pathway.
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Ren Zi-Lin, Zhang Chu-Xin, Zheng Yu-Xiao, Chen Cong-Ai, Dan-Chen, Lan Xin, Yan Xin, Liu Ying, He Yan-Hui, Cheng Jia-Lin, Han Jin-Hua, Wang Qing-Guo, Wang Xue-Qian, Cheng Fa-Feng, Li Chang-Xiang
Аннотация
BACKGROUND: Ischemic stroke (IS) is the main cause of disability worldwide, and glial scar can impair neurological recovery during the post-stroke period. Refined qingkailing (RQKL) has been demonstrated to be neuroprotective after IS.
PURPOSE: The purpose of our study was to investigate the effect of RQKL on glial scar after IS.
METHODS: In this work, rats were used as the model subjects for middle cerebral artery occlusion (MCAO), with 7 and 14 days serving as the critical observational intervals. The treatments of oxygen and glucose deprivation/reoxygenation (OGD/R) were applied to primary astrocytes and an astrocyte-neuron co-culture model.
RESULTS: RQKL was effective in improving neurological dysfunction, brain histopathologic manifestations, and reducing the degree of brain atrophy at different stages of glial scar. It also decreased the expression of glial fibrillary acidic protein (GFAP), neurocan, and brevican, and increased the expression of microtubule associated protein 2 (MAP2). In primary astrocyte culture, RQKL reduced the activation and proliferation of astrocytes. In an astrocyte and neuron co-culture model, RQKL decreased the expression of GFAP and brevican in astrocytes, and increased the expression of MAP2 and NF200 in neurons. Epidermal growth factor receptor (EGFR) and p-PLCγ expression was strongly increased following IS, according to both in vivo and in vitro tests, while RQKL decreased EGFR and p-PLCγ expression.
CONCLUSION: When considered collectively, these findings imply that the EGFR/PLCγ signaling pathway is crucial for the activation of astrocytes and the formation of glial scars following IS. Also, RQKL affects neurons by blocking the EGFR/PLCγ signaling pathway on astrocytes, which diminishes the activation of astrocytes and the development of glial scars.
PURPOSE: The purpose of our study was to investigate the effect of RQKL on glial scar after IS.
METHODS: In this work, rats were used as the model subjects for middle cerebral artery occlusion (MCAO), with 7 and 14 days serving as the critical observational intervals. The treatments of oxygen and glucose deprivation/reoxygenation (OGD/R) were applied to primary astrocytes and an astrocyte-neuron co-culture model.
RESULTS: RQKL was effective in improving neurological dysfunction, brain histopathologic manifestations, and reducing the degree of brain atrophy at different stages of glial scar. It also decreased the expression of glial fibrillary acidic protein (GFAP), neurocan, and brevican, and increased the expression of microtubule associated protein 2 (MAP2). In primary astrocyte culture, RQKL reduced the activation and proliferation of astrocytes. In an astrocyte and neuron co-culture model, RQKL decreased the expression of GFAP and brevican in astrocytes, and increased the expression of MAP2 and NF200 in neurons. Epidermal growth factor receptor (EGFR) and p-PLCγ expression was strongly increased following IS, according to both in vivo and in vitro tests, while RQKL decreased EGFR and p-PLCγ expression.
CONCLUSION: When considered collectively, these findings imply that the EGFR/PLCγ signaling pathway is crucial for the activation of astrocytes and the formation of glial scars following IS. Also, RQKL affects neurons by blocking the EGFR/PLCγ signaling pathway on astrocytes, which diminishes the activation of astrocytes and the development of glial scars.