NECA alleviates inflammatory responses in diabetic retinopathy through dendritic cell toll-like receptor signaling pathway
作者全名：Li, Lanjiao; Chen, Jichun; Wang, Zhenyan; Xu, Yan; Yao, Hao; Lei, Wulong; Zhou, Xiyuan; Zheng, Minming
作者地址：[Li, Lanjiao; Chen, Jichun; Wang, Zhenyan; Xu, Yan; Yao, Hao; Lei, Wulong; Zhou, Xiyuan; Zheng, Minming] Chongqing Med Univ, Affiliated Hosp 2, Chongqing Key Lab Ophthalmol, Chongqing, Peoples R China
通信作者：Zhou, XY; Zheng, MM (通讯作者)，Chongqing Med Univ, Affiliated Hosp 2, Chongqing Key Lab Ophthalmol, Chongqing, Peoples R China.
来源：FRONTIERS IN IMMUNOLOGY
ESI学科分类：IMMUNOLOGY
WOS号：WOS:001248482300001
JCR分区：Q1
影响因子：5.7
年份：2024
卷号：15
期号：
开始页：
结束页：
文献类型：Article
关键词：NECA; diabetic retinopathy; dendritic cells; toll-like receptor; Treg cell; Th17 cell
摘要：Introduction This study examined the impact of 5'-(N- ethylcarboxamido)adenosine (NECA) in the peripheral blood of healthy individuals, those with diabetes mellitus, diabetic retinopathy (DR), and C57BL/6 mice, both in vivo and in vitro.Methods Enzyme-linked immunosorbent assay (ELISA) and flow cytometry (FCM) were used to evaluate the effects of NECA on dendritic cells (DCs) and mouse bone marrow-derived dendritic cells (BMDCs) and the effects of NECA-treated DCs on Treg and Th17 cells. The effect of NECA on the Toll-like receptor (TLR) pathway in DCs was evaluated using polymerase chain reaction (PCR) and western blotting (WB).Results FCM and ELISA showed that NECA inhibited the expression of surface markers of DCs and BMDCs, increased anti-inflammatory cytokines and decreased proinflammatory cytokines. PCR and WB showed that NCEA decreased mRNA transcription and protein expression in the TLR-4-MyD88-NF-k beta pathway in DCs and BMDCs. The DR severity in streptozocin (STZ) induced diabetic mice was alleviated. NECA-treated DCs and BMDCs were co-cultivated with CD4+T cells, resulting in modulation of Treg and Th17 differentiation, along with cytokine secretion alterations.Conclusion NECA could impair DCs' ability to present antigens and mitigate the inflammatory response, thereby alleviating the severity of DR.
基金机构：General projects of Chongqing Natural Science Foundation [CSTB2023NSCQ-MSX0115]; Kuanren Talents Program of the Second Affiliated Hospital of Chongqing Medical University [202228]; National Natural Science Foundation of China [82070976]; Future Medical Youth Innovation Team Development Support Program of Chongqing Medical University [(w0115)]; Chongqing Municipal Health Commission Medical Research Project [2024WSJK097]
基金资助正文：The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by General projects of Chongqing Natural Science Foundation (CSTB2023NSCQ-MSX0115), Kuanren Talents Program of the Second Affiliated Hospital of Chongqing Medical University (Grant No. 202228), National Natural Science Foundation of China (No. 82070976), Future Medical Youth Innovation Team Development Support Program of Chongqing Medical University (w0115), Chongqing Municipal Health Commission Medical Research Project (Grant No. 2024WSJK097).
