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西他列汀可保护肾小球内皮细胞免受高糖诱导的功能障碍和损伤。

Sitagliptin protects renal glomerular endothelial cells against high glucose-induced dysfunction and injury.

机构信息

Department of Nephrology, Henan Provincial People's Hospital, Zhengzhou, Henan, China.

出版信息

Bioengineered. 2022 Jan;13(1):655-666. doi: 10.1080/21655979.2021.2012550.

DOI:10.1080/21655979.2021.2012550
PMID:34967261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8805972/
Abstract

Sitagliptin is a well-established anti-diabetic drug that also exerts protective effects on diabetic complications. Previous work reveals that sitagliptin has a protective effect on diabetic nephropathy (DN). Vascular impairment frequently occurs in diabetic renal complications. Here, we evaluated the protective function of sitagliptin in human renal glomerular endothelial cells (HrGECs) under high glucose (HG) conditions. Expressions of the pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-8 (IL-8) were assessed using real-time PCR and ELISA. Endothelial cells permeability was assayed using the fluorescein isothiocyanate dextran (FITC-dextran) and trans-endothelial electrical resistance (TEER) assay. The results show that sitagliptin mitigated HG-induced oxidative stress in HrGECs with decreased levels of mitochondrial reactive oxygen species (ROS), Malondialdehyde (MDA), and 8-hydroxydeoxyguanosine (8-OHdG). Sitagliptin inhibited HG-induced production of pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-8 (IL-8) in HrGECs. It also ameliorated HG-induced aggravation of HrGECs permeability and reduction of the tight junction component claudin-5. Moreover, kruppel Like Factor 6 (KLF6) mediated the protective effects of sitagliptin on endothelial monolayer permeability against HG. Collectively, sitagliptin reversed the HG-induced oxidative stress, inflammation, and increased permeability in HrGECs via regulating KLF6. This study suggests that sitagliptin might be implicated as an effective strategy for preventing diabetic renal injuries in the future.

摘要

西他列汀是一种成熟的抗糖尿病药物，对糖尿病并发症也有保护作用。先前的工作表明，西他列汀对糖尿病肾病（DN）有保护作用。糖尿病肾并发症常伴有血管损伤。在这里，我们评估了高糖（HG）条件下西他列汀对人肾小球内皮细胞（HrGEC）的保护作用。采用实时 PCR 和 ELISA 检测促炎细胞因子白细胞介素-1β（IL-1β）和白细胞介素-8（IL-8）的表达。用荧光素异硫氰酸酯葡聚糖（FITC-dextran）和跨内皮电阻（TEER）测定内皮细胞通透性。结果表明，西他列汀减轻了 HG 诱导的 HrGEC 氧化应激，降低了线粒体活性氧（ROS）、丙二醛（MDA）和 8-羟基脱氧鸟苷（8-OHdG）的水平。西他列汀抑制了 HG 诱导的 HrGEC 中促炎细胞因子白细胞介素-1β（IL-1β）和白细胞介素-8（IL-8）的产生。它还改善了 HG 诱导的 HrGEC 通透性增加和紧密连接蛋白 claudin-5 减少。此外，Krüppel 样因子 6（KLF6）介导了西他列汀对内皮单层通透性的保护作用，防止 HG 损伤。综上所述，西他列汀通过调节 KLF6 逆转了 HG 诱导的 HrGEC 氧化应激、炎症和通透性增加。这项研究表明，西他列汀可能成为未来预防糖尿病肾损伤的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/9d33ac04f362/KBIE_A_2012550_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/26baf7c6ba09/KBIE_A_2012550_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/793a1daee9f8/KBIE_A_2012550_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/9dc257cf98d2/KBIE_A_2012550_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/a9822078f7b5/KBIE_A_2012550_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/781337d02c81/KBIE_A_2012550_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/b9f9219d1686/KBIE_A_2012550_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/286604c59340/KBIE_A_2012550_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/9d33ac04f362/KBIE_A_2012550_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/26baf7c6ba09/KBIE_A_2012550_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/793a1daee9f8/KBIE_A_2012550_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/9dc257cf98d2/KBIE_A_2012550_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/a9822078f7b5/KBIE_A_2012550_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/781337d02c81/KBIE_A_2012550_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/b9f9219d1686/KBIE_A_2012550_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/286604c59340/KBIE_A_2012550_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4720/8805972/9d33ac04f362/KBIE_A_2012550_F0008_OC.jpg

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