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姜黄素通过 NF-κB 通路保护施万细胞免受高糖诱导的炎症反应和细胞凋亡。

Curcumin protect Schwann cells from inflammation response and apoptosis induced by high glucose through the NF-κB pathway.

机构信息

Department of Anatomy, School of Basic Medical Sciences, Health Science Center, Hubei Minzu University, Enshi, Hubei 445000, China; Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic diseases, Hubei Minzu University, Enshi, Hubei 445000, China.

Department of Anatomy, School of Basic Medical Sciences, Health Science Center, Hubei Minzu University, Enshi, Hubei 445000, China.

出版信息

Tissue Cell. 2022 Aug;77:101873. doi: 10.1016/j.tice.2022.101873. Epub 2022 Jul 16.

DOI:10.1016/j.tice.2022.101873
PMID:35868051
Abstract

Demyelination disease as diabetes mellitus (DM) complication is characterized by apoptosis of Schwann cells (SCs) and several reports have demonstrated that high glucose content can induce an inflammation response and lead to the apoptosis of SCs. For NF-κB plays a pivotal role in the inflammatory response, hence we hypothesized that high glucose content can induce inflammation though the NF-κB pathway. First we verified that 150 mM high glucose can increase the expression of cleaved caspase 3, interleukin (IL)- 1β, Cyto-C and NF-κB with time through Western blot and increase the apoptosis of RSC96s through Flow Cytometry. Then we found that high glucose can increase the nuclear translocation NF-κB through confocal system which can promote the expression of inflammation genes such as IL-1β. Curcumin has been reported to possess anti-inflammation activities to protect cells. In this study, we found that application with 25 μM curcumin could alleviate the inflammation response and protect the cells from apoptosis. We revealed that the expression of NF-κB and p-NF-κB was decreased and the translocation was also inhibited after curcumin application. Accordingly, the secretion of IL-1β and the apoptosis of RSC96s induce by high glucose was suppressed. Our cumulative findings suggest that curcumin can protect SCs from apoptosis through the inhibition of the inflammatory response though the NF-κB pathway.

摘要

糖尿病(DM)并发症引起的脱髓鞘疾病的特征是施万细胞(SCs)的凋亡,有几项报道表明,高葡萄糖含量可诱导炎症反应并导致SCs 的凋亡。由于 NF-κB 在炎症反应中起着关键作用,因此我们假设高葡萄糖含量可以通过 NF-κB 途径诱导炎症。首先,我们通过 Western blot 验证了 150 mM 高葡萄糖可以随时间增加裂解的 caspase 3、白细胞介素(IL)-β、Cyto-C 和 NF-κB 的表达,并通过流式细胞术增加 RSC96s 的凋亡。然后,我们发现高葡萄糖可以通过共聚焦系统增加核转位 NF-κB,从而促进炎症基因如 IL-1β 的表达。姜黄素已被报道具有抗炎活性以保护细胞。在这项研究中,我们发现应用 25 μM 姜黄素可以减轻炎症反应并保护细胞免于凋亡。我们发现姜黄素应用后 NF-κB 和 p-NF-κB 的表达减少,转位也受到抑制。因此,高葡萄糖诱导的 IL-1β 分泌和 RSC96s 的凋亡受到抑制。我们的综合研究结果表明,姜黄素可以通过抑制 NF-κB 途径的炎症反应来保护 SCs 免于凋亡。

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