Department of Clinical Medicine, Zhejiang University City College School of Medicine, Hangzhou, Zhejiang 310015, P.R. China.
Clinical Laboratory, The Second People's Hospital of Hangzhou, Hangzhou, Zhejiang 310015, P.R. China.
Mol Med Rep. 2017 Aug;16(2):1685-1690. doi: 10.3892/mmr.2017.6832. Epub 2017 Jun 21.
It has previously been demonstrated that glucose is important in the process of stem cell aging. However, the mechanisms of cell senescence induced by high glucose (HG) remain to be elucidated. The preliminary study indicated that D‑galactose induced mesenchymal stem cell (MSCs) aging. The present study demonstrated, following treatment with 11.0 or 22.0 mM HG for 14 days, that HG significantly promoted MSCs aging and the expression levels of phosphorylated (p-)phosphatidylinositol 3-kinase/protein kinase B (Akt) and p‑mammalian target of rapamycin signaling (mTOR) in the HG groups were increased compared with the control group. However, following Akt inhibition with 1.0 or 10.0 nM MK‑2206, which is an Akt‑specific small molecule inhibitor, the senescence‑cell value in the HG group was significantly decreased compared with the control group. These results indicated that HG induced MSCs senescence and this effect was primarily mediated via the Akt/mTOR signaling pathway.
先前已经证明葡萄糖在干细胞衰老过程中很重要。然而，高葡萄糖（HG）诱导细胞衰老的机制仍有待阐明。初步研究表明，半乳糖诱导间充质干细胞（MSCs）衰老。本研究表明，用 11.0 或 22.0 mM HG 处理 14 天后，HG 显著促进 MSCs 衰老，HG 组磷酸化（p-）磷脂酰肌醇 3-激酶/蛋白激酶 B（Akt）和 p-雷帕霉素靶蛋白（mTOR）的表达水平较对照组升高。然而，用 Akt 特异性小分子抑制剂 1.0 或 10.0 nM MK-2206 抑制 Akt 后，HG 组的衰老细胞值较对照组显著降低。这些结果表明，HG 诱导 MSCs 衰老，这种作用主要通过 Akt/mTOR 信号通路介导。
