Exp Clin Endocrinol Diabetes 2020; 128(02): 89-96
DOI: 10.1055/a-0826-4374
Article
© Georg Thieme Verlag KG Stuttgart · New York

Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-κB Suppression

Shiqing Xu
1   Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China
,
Weijie Bao
2   The People’s Hospital of He Bi, Hebi, China
,
Xiuli Men
3   Department of Pathophysiology, North China University of Science and Technology, Tangshan, China
,
Ying Liu
4   Department of Gynecology & Obstetrics, China-Japan Friendship Hospital, Beijing, China
,
Jie Sun
4   Department of Gynecology & Obstetrics, China-Japan Friendship Hospital, Beijing, China
,
Jing Li
5   Department of Stomatology, China-Japan Friendship Hospital, Beijing, China
,
Honglin Liu
1   Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China
,
Hanqing Cai
6   Department of Endocrinology, The Second Hospital of Jilin University, Changchun, China
,
Wenjian Zhang
7   Suzhou Rely Bio-Tech Co., Ltd. Suzhou, China
,
Jinning Lou
7   Suzhou Rely Bio-Tech Co., Ltd. Suzhou, China
,
Liang Peng
1   Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China
› Author Affiliations
Funding: This work was supported by grants from National Nature Science Foundation of China (81670758 to L.P. and 81370918 to X.M.), Beijing Municipal Natural Science Foundation of China (7182147 to L.P.), Capital’s Funds for Health Improvement and Research (2018–2–4062 to L.P.), Young medical talents award program of Chinese academy of medicine (2018RC310023) and Nature Science Foundation of Jilin Province (20180101113JC to H.C.).
Further Information

Publication History

received 31 October 2018
revised 05 December 2018

accepted 20 December 2018

Publication Date:
14 January 2019 (online)

Abstract

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 AGEs in 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.

 
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