Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-kappa B Suppression
Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-kappa B Suppression
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Interleukin-10 通过抑制 NF-kappa B 保护雪旺细胞免受晚期糖基化终产物诱导的细胞凋亡
DOI：
10.1055/a-0826-4374
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发表时间：
2020
影响因子：
1.8
通讯作者：
Peng Liang
中科院分区：
文献类型：
--
作者：
Xu Shiqing;Bao Weijie;Men Xiuli;Liu Ying;Sun Jie;Li Jing;Liu Honglin;Cai Hanqing;Zhang Wenjian;Lou Jinning;Peng Liang
Demyelination resulting from Schwann cell injury is a main pathological feature of diabetic neuropathy, and a key contributor to this process may be inflammation due to advanced glycation end products (AGEs). Therefore, protection by anti-inflammation agents is anticipated. In this study, we showed that interleukin-10 (IL-10), an anti-inflammatory cytokine, inhibits apoptosis of Schwann cells induced by AGEsin vitro. We isolated and cultured Schwann cells from rat sciatic nerves. As detected by flow cytometry, apoptosis of Schwann cells markedly increased following incubation with AGEs for 48 h. However, pretreatment with IL-10 inhibited AGE-induced apoptosis. The effect of IL-10 on NF-κB, which is a very important regulator of inflammation, was also evaluated, and results showed high levels of phospho-NF-κB and nuclear localization of NF-κB in cells incubated with AGEs but low levels of phospho-NF-κB and cytoplasmic localization in the cells incubated with IL-10, indicating the activation of NF-κB by AGEs and inhibition of NF-κB by IL-10. Moreover, incubating Schwann cells with an NF-κB inhibitor (caffeic acid phenethyl ester) for 30 min before adding AGEs mimicked IL-10, lowering the amount of reactive oxygen species and activity of caspase-3 and also decreasing apoptosis in Schwann cells. These results indicate that IL-10 may protect Schwann cells against AGE-induced apoptosis by attenuating oxidative stress via the inhibition of activation of NF-κB.
