ArticleFrontiers in pharmacology2025
Bletilla striata polysaccharide induces autophagy through PI3K/AKT signaling pathway to promote the survival of cross-boundary flap in rats.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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