Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2025 Jul:142:156696.
doi: 10.1016/j.phymed.2025.156696. Epub 2025 Mar 26.

Refined qingkailing attenuates reactive astrocytes and glial scar formation after ischemia stroke via the EGFR/PLCγ pathway

Zi-Lin Ren  1 , Chu-Xin Zhang  1 , Yu-Xiao Zheng  1 , Cong-Ai Chen  2 , Dan-Chen  3 , Xin Lan  1 , Xin Yan  4 , Ying Liu  1 , Yan-Hui He  1 , Jia-Lin Cheng  1 , Jin-Hua Han  1 , Qing-Guo Wang  1 , Xue-Qian Wang  5 , Fa-Feng Cheng  6 , Chang-Xiang Li  7
Affiliations

Refined qingkailing attenuates reactive astrocytes and glial scar formation after ischemia stroke via the EGFR/PLCγ pathway

Zi-Lin Ren et al. Phytomedicine. 2025 Jul.

Abstract

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.

Keywords: Astrocyte; EGFR/PLCγ signaling pathway; Glial scar; Ischemic stroke; Refined qingkailing.

PubMed Disclaimer

Conflict of interest statement

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper

LinkOut - more resources