The aim of the work was to study the influence of vaspin on oxidative stress-induced apoptosis of mouse mesenchymal stem cells (MSCs). MSCs originated from bone marrow of C57BL/6 mouse were treated with vaspin and/or H2O2 in a dose-dependent manner. Cellular viability detected by CCK-8 and cell apoptosis studied by flow cytometry and TUNEL assay were observed in these cells. The protein expressions of PI3K, p-PI3K, Akt, p-Akt, T-ERK1/2, p-ERK1/2, p38, p-p38, JNK, and p-JNK were tested by Western blot. Vaspin had no significant effect on cellular viability, but significantly reduced H2O2-induced apoptosis. Western blot assay showed that pretreatment with vaspin promoted the activation of p-p38. Inhibition of p38 by SB203580 suppressed the protective effect of vaspin on oxidative stress-induced apoptosis. Vaspin inhibits oxidative stress-induced apoptosis of MSCs via the activation of MAPK/p38 signaling pathway. These findings indicate that vaspin is prone to osteoporosis protection.

中文翻译：

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Vaspin 通过 MAPK/p38 通路保护小鼠间充质干细胞免受氧化应激诱导的细胞凋亡。

这项工作的目的是研究 vaspin 对氧化应激诱导的小鼠间充质干细胞 (MSCs) 凋亡的影响。用 vaspin 和/或 H2O2 以剂量依赖性方式处理源自 C57BL/6 小鼠骨髓的 MSC。在这些细胞中观察到通过CCK-8检测的细胞活力和通过流式细胞术和TUNEL测定研究的细胞凋亡。Western blot检测PI3K、p-PI3K、Akt、p-Akt、T-ERK1/2、p-ERK1/2、p38、p-p38、JNK和p-JNK的蛋白表达。Vaspin 对细胞活力没有显着影响，但显着降低了 H2O2 诱导的细胞凋亡。蛋白质印迹分析表明，用 vaspin 预处理促进了 p-p38 的活化。SB203580 对 p38 的抑制抑制了 vaspin 对氧化应激诱导的细胞凋亡的保护作用。Vaspin 通过激活 MAPK/p38 信号通路抑制氧化应激诱导的 MSCs 凋亡。这些发现表明 vaspin 易于保护骨质疏松症。