Qilong capsule regulates microglial function and inhibits platelet activation after multiple cerebral infarctions by regulating the P2Y

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Tác giả: Xiaodi Fan, Jiaming Gao, Jianxun Liu, Shengnan Shi, Wenting Song, Linjuan Sun, Mingjiang Yao, Min Zhan, Yehao Zhang, Xiaoyu Zheng

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: Ireland : Journal of ethnopharmacology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 693290

ETHNOPHARMACOLOGICAL RELEVANCE: Multiple cerebral infarctions (MCIs) represent a common type of ischaemic stroke that affects or even endangers a patient's life. Qilong capsule (QLC), a Chinese patent medicine made from Buyang Huanwu Decoction (BYHWD) is suitable for treating the sequelae of ischaemic stroke, such as multi-infarct dementia (MID). However, its biological mechanism has not been fully explored. AMI OF THE STUDY: The aim of this study was to explore the mechanism of QLC in treating MCI and its sequelae. METHODS: Male SD rats aged 7-8 weeks and weighing 210-230 g were used as an MCI model, and QLC was used as interventions. The neurobehavioural effects of QLC on MCI model rats were evaluated by observing body weight, neurological function score, and forelimb grip and water maze test results. The effects of QLC on neurons and microglia were observed via haematoxylin‒eosin (HE) staining, silver staining, transmission electron microscopy and positron emission tomography/computed tomography (PET/CT). The effects of QLC on platelets were observed via the platelet aggregation rate and flow cytometry (FCM). Finally, the mechanism of QLC was verified via ELISA, immunofluorescence staining and Western blotting. RESULTS: These experiments showed that QLC improves neurobehavioural measures, forelimb grip strength, and spatial memory after MCI by ameliorating brain tissue and neuronal damage. QLC also effectively inhibited the inflammatory response after MCI. We also found that QLC can decrease microglia activation and reduce the expression of translocator protein 18 kDa (TSPO). QLC can improve platelet aggregation and reduce the expression of CD62p and CD61, indicating that QLC has a significant anti-platelet aggregation effect. At the molecular level, we found that QLC affects the content of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), reduces the expression of recombinant purinergic receptor P2Y, G protein coupled 12 (P2Y CONCLUSIONS: QLC can ameliorate neuronal necrosis and MID induced by MCI and has an antiplatelet aggregation effect in rats. QLC may treat MID by regulating P2Y
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