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异甘草素通过 SIRT1 依赖的机制抑制炎症和氧化应激来预防高血糖引起的肾脏损伤。

Isoliquiritigenin prevents hyperglycemia-induced renal injuries by inhibiting inflammation and oxidative stress via SIRT1-dependent mechanism.

机构信息

Department of Pediatric Surgery, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, China.

Department of Endocrinology, Jiangshan People's Hospital, Jiangshan, Zhejiang, China.

出版信息

Cell Death Dis. 2020 Dec 7;11(12):1040. doi: 10.1038/s41419-020-03260-9.

DOI:10.1038/s41419-020-03260-9
PMID:33288747
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7721869/
Abstract

Diabetic nephropathy (DN) as a global health concern is closely related to inflammation and oxidation. Isoliquiritigenin (ISL), a natural flavonoid compound, has been demonstrated to inhibit inflammation in macrophages. Herein, we investigated the effect of ISL in protecting against the injury in STZ-induced type 1 DN and in high glucose-induced NRK-52E cells. In this study, it was revealed that the administration of ISL not only ameliorated renal fibrosis and apoptosis, but also induced the deterioration of renal function in diabetic mice. Mediated by MAPKs and Nrf-2 signaling pathways, respectively, upstream inflammatory response and oxidative stress were neutralized by ISL in vitro and in vivo. Moreover, as further revealed by the results of molecular docking, sirtuin 1 (SIRT1) binds to ISL directly, and the involvement of SIRT1 in ISL-mediated renoprotective effects was confirmed by studies using in vitro models of SIRT1 overexpression and knockdown. In summary, by reducing inflammation and oxidative stress, ISL has a significant pharmacological effect on the deterioration of DN. The benefits of ISL are associated with the direct binding to SIRT1, the inhibition of MAPK activation, and the induction of Nrf-2 signaling, suggesting the potential of ISL for DN treatment.

摘要

糖尿病肾病 (DN) 作为一个全球性的健康问题，与炎症和氧化密切相关。甘草素 (ISL) 作为一种天然黄酮类化合物，已被证明可以抑制巨噬细胞中的炎症反应。本研究旨在探讨 ISL 对 STZ 诱导的 1 型糖尿病肾病和高糖诱导的 NRK-52E 细胞损伤的保护作用。研究结果表明，ISL 的给药不仅改善了糖尿病小鼠的肾脏纤维化和细胞凋亡，还加重了其肾功能的恶化。在体内和体外，ISL 通过 MAPKs 和 Nrf-2 信号通路分别中和了上游的炎症反应和氧化应激。此外，分子对接的结果进一步表明，SIRT1 直接与 ISL 结合，通过 SIRT1 过表达和敲低的体外模型研究证实了 SIRT1 在 ISL 介导的肾脏保护作用中的参与。综上所述，ISL 通过减轻炎症和氧化应激，对 DN 的恶化具有显著的药理作用。ISL 的益处与 SIRT1 的直接结合、MAPK 激活的抑制以及 Nrf-2 信号的诱导有关，提示 ISL 具有治疗 DN 的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/daceead9afa3/41419_2020_3260_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/5fb802664568/41419_2020_3260_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/bc3364c3416a/41419_2020_3260_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/3a1bc9c0717e/41419_2020_3260_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/c6708cab33f5/41419_2020_3260_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/04afd481915b/41419_2020_3260_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/daceead9afa3/41419_2020_3260_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/5fb802664568/41419_2020_3260_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/bc3364c3416a/41419_2020_3260_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/3a1bc9c0717e/41419_2020_3260_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/c6708cab33f5/41419_2020_3260_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/04afd481915b/41419_2020_3260_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bd/7721869/daceead9afa3/41419_2020_3260_Fig6_HTML.jpg

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