自噬
PI3K/AKT/mTOR通路
蛋白激酶B
血管生成
化学
药理学
医学
信号转导
细胞生物学
癌症研究
细胞凋亡
生物
生物化学
作者
Yue Qin,Xinyi Zeng,Minlan Yang,Jinhao Chen,Lin Liu,Hui Liu
标识
DOI:10.3389/fphar.2025.1544932
摘要
Introduction Distal flap necrosis is a common problem in flap transplantation. Bletilla striata polysaccharide (BSP) is the main medicinal component of traditional Chinese medicine Bletilla striata. The purpose of this study was to investigate the mechanism of BSP promoting flap survival. Methods The control group, BSP low, medium and high dose groups, BSP + autophagy inhibitor 3-methyladenine (3-MA) group were designed to establish a model of cross-boundary flap in rat back. After 7 days of postoperative administration, the samples were taken. Results The optimal dose of BSP was determined to be 250 mg/kg/d according to the survival rate of flap, microvessel density, intra-arterial diameter, expression of vascular-related protein and pharmacological toxicity. By detecting the expression level of autophagy-related proteins, it was found that BSP could activate autophagy. After autophagy was blocked, the therapeutic effect of BSP was reversed. In addition, BSP activated the PI3K/AKT signaling pathway. Discussion Studies have shown that BSP induces autophagy by activating PI3K/AKT signaling pathway, thereby promoting angiogenesis and improving survival rate of flap.
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