PI3K/AKT/mTOR信号通路蛋白表达水平分析

2025-05-13 MedSci xAi 发表于广东省
本文通过Western blot分析PI3K/AKT/mTOR信号通路蛋白表达水平,揭示重组贻贝粘附蛋白对伤口愈合的促进作用,并详细解析蛋白磷酸化在细胞增殖与分化中的关键作用。
Western blot (WB) analysis of protein expression levels in the PI3K/AKT/mTOR signaling pathway showed that the protein expression levels of PI3K, p-AKT, p-mTOR, and the p-AKT/AKT ratio in the model group were significantly lower than those in the normal group (P < 0.05). The expression level of PI3K decreased from 1.042 ± 0.395 to 0.283 ± 0.146, the expression level of p-AKT decreased from 0.994 ± 0.051 to 0.283 ± 0.068, and the expression level of p-mTOR decreased from 1.023 ± 0.207 to 0.144 ± 0.114. Compared with the model control group, the expression level of PI3K in the recombinant mussel adhesive protein (rMAP) wound tissue was significantly increased (P < 0.05), and the expression levels of p-AKT and p-mTOR in each drug group were significantly increased (P < 0.05). The p-AKT content in the rMAP group increased from 0.283 ± 0.068 to 0.632 ± 0.095, and the p-mTOR content increased from 0.144 ± 0.114 to 0.533 ± 0.086. There was no significant difference in the expression levels of AKT and mTOR among the experimental groups (P > 0.05). The p-AKT/AKT ratio in the rMAP group was significantly higher than that in the model group (P < 0.05), increasing from 0.367 ± 0.044 to 0.596 ± 0.093, and the p-mTOR/mTOR ratio increased from 0.961 ± 1.188 to 1.373 ± 1.140, although this difference was not statistically significant. These results indicate that the establishment of a rat model of superficial second-degree non-chronic skin injury leads to reduced expression levels of PI3K/AKT/mTOR-related proteins, signal pathway dysregulation, and delayed wound healing. rMAP promotes wound tissue healing by activating the PI3K/AKT/mTOR signaling pathway through the phosphorylation of AKT and mTOR, participating in cell proliferation and differentiation, and regulating protein expression.
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