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白及多糖通过PI3K/AKT信号通路诱导自噬以促进大鼠跨区皮瓣存活。

Bletilla striata polysaccharide induces autophagy through PI3K/AKT signaling pathway to promote the survival of cross-boundary flap in rats.

作者信息

Yue Qin, Zeng Xinyi, Yang Minlan, Chen Jinhao, Liu Lin, Liu Hui

机构信息

Yangtze University Health Science Center, Jingzhou, China.

出版信息

Front Pharmacol. 2025 Mar 10;16:1544932. doi: 10.3389/fphar.2025.1544932. eCollection 2025.

DOI:10.3389/fphar.2025.1544932
PMID:40129948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11931138/
Abstract

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.

摘要

引言

皮瓣坏死是皮瓣移植中的常见问题。白及多糖（BSP）是中药白及的主要药用成分。本研究旨在探讨BSP促进皮瓣存活的机制。

方法

设计对照组、BSP低、中、高剂量组、BSP+自噬抑制剂3-甲基腺嘌呤（3-MA）组，建立大鼠背部跨区皮瓣模型。术后给药7天，取样本。

结果

根据皮瓣存活率、微血管密度、动脉内径、血管相关蛋白表达及药理毒性，确定BSP的最佳剂量为250mg/kg/d。通过检测自噬相关蛋白表达水平，发现BSP可激活自噬。自噬被阻断后，BSP的治疗效果被逆转。此外，BSP激活了PI3K/AKT信号通路。

讨论

研究表明，BSP通过激活PI3K/AKT信号通路诱导自噬，从而促进血管生成并提高皮瓣存活率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c392/11931138/ce8c878c8260/fphar-16-1544932-g014.jpg
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