European journal of pharmacology · 2026
Corilagin reduces ischemic stroke damage by neural stem cell-mediated neurorepair.
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Wang Qiang, Wei Mengzhen, Wu Rang, Ma Yu, Hu Jie, Ding Yanxin, Wang Shizhe, Jiang Hezhong, Wang Yawen, Gu Jian, Tan Rui
Аннотация
UNLABELLED: Ischemic stroke (IS) is a common and refractory cerebrovascular disease that imposes a heavy burden on patients' families and society due to its high incidence, complex pathological mechanisms, and high mortality rate. Corilagin, the primary active component of the traditional Tibetan medicines Terminalia chebula and Phyllanthus emblica, is widely used in Tibetan medicine for treating cerebrovascular diseases. This study aims to comprehensively elucidate the mechanism of Corilagin in treating cerebral ischemia in IS through RNA transcriptome sequencing, validate its neurorestorative effects in cerebral ischemic rats, and explore the therapeutic potential of Corilagin for IS.
METHODOLOGY: In vitro, a glucose-oxygen deprivation (OGD) model of neural stem cells (NSCs) was established. Cell viability was assessed using the CCK8 assay, followed by RNA extraction for transcriptome analysis.In vivo, the therapeutic efficacy of Corilagin was validated using a rat model of cerebral ischemia.
RESULTS: In the rat MCAO model, Corilagin was found to improve neurological deficits, promote the survival of damaged neurons in the cortex and hippocampal CA1 region, and exert neuroprotective effects. Transcriptome sequencing revealed that Corilagin acts on NSCs by regulating mitochondrial function, energy metabolism, and oxidative stress levels.Western blotting further validated its modulation of the HIF-α/ALDOA pathway. In the in vitro OGD model, Corilagin effectively mitigated NSC injury.
CONCLUSION: Corilagin exhibits therapeutic potential for ischemic stroke through neural stem cell-mediated neurorepair.
METHODOLOGY: In vitro, a glucose-oxygen deprivation (OGD) model of neural stem cells (NSCs) was established. Cell viability was assessed using the CCK8 assay, followed by RNA extraction for transcriptome analysis.In vivo, the therapeutic efficacy of Corilagin was validated using a rat model of cerebral ischemia.
RESULTS: In the rat MCAO model, Corilagin was found to improve neurological deficits, promote the survival of damaged neurons in the cortex and hippocampal CA1 region, and exert neuroprotective effects. Transcriptome sequencing revealed that Corilagin acts on NSCs by regulating mitochondrial function, energy metabolism, and oxidative stress levels.Western blotting further validated its modulation of the HIF-α/ALDOA pathway. In the in vitro OGD model, Corilagin effectively mitigated NSC injury.
CONCLUSION: Corilagin exhibits therapeutic potential for ischemic stroke through neural stem cell-mediated neurorepair.