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SGLT2 抑制改善纳米塑料诱导的内皮过早衰老和功能障碍。

SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction.

机构信息

College of Pharmacy, Mokpo National University, 1666 Yeongsan-ro, Cheonggye-Myeonn, Muan-Gun, Jeonnam, 58554, Republic of Korea.

Division of Cardiology, College of Medicine, Heart Reasearch Institute and Biomedical Research Institute, Chung-Ang University Hospital, Chung-Ang University, Seoul, 06974, Republic of Korea.

出版信息

Sci Rep. 2023 Apr 17;13(1):6256. doi: 10.1038/s41598-023-33086-2.

DOI:10.1038/s41598-023-33086-2
PMID:37069192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10110533/
Abstract

Nano plastics (NPs) have been a significant threat to human health and are known to cause premature endothelial senescence. Endothelial senescence is considered one of the primary risk factors contributing to numerous cardiovascular disorders. Recent studies have suggested that inhibition of sodium glucose co-transporter (SGLT2) ameliorates endothelial senescence and dysfunction. Therefore, our study intends to explore the role of SGLT2 in NPs-induced endothelial senescence and dysfunction. Porcine coronary artery and its endothelial cells were treated with NPs in the presence or absence of Enavogliflozin (ENA), a SGLT2 inhibitor and then SGLTs expression, senescence markers and vascular function were evaluated. NPs significantly up-regulated SGLT2 and ENA significantly decreased NPs-induced senescence-associated-β-gal activity, cell-cycle arrest, and senescence markers p53 and p21 suggesting that inhibition of SGLT2 prevents NPs-induced endothelial senescence. In addition, ENA decreased the formation of reactive oxygen species with the downregulation of Nox2, and p22. Furthermore, SGLT2 inhibition also up regulated the endothelial nitric oxide synthase expression along with improving vascular function. In conclusion, premature endothelial senescence by NPs is, at least in part, associated with SGLT2 and it could be a potential therapeutic target for preventing and/or treating environmental pollutants-induced cardiovascular disorders mediated by endothelial senescence and dysfunction.

摘要

纳米塑料（NPs）对人类健康构成了重大威胁，已知会导致内皮过早衰老。内皮衰老被认为是导致许多心血管疾病的主要危险因素之一。最近的研究表明，抑制钠-葡萄糖协同转运蛋白（SGLT2）可改善内皮衰老和功能障碍。因此，我们的研究旨在探讨 SGLT2 在 NPs 诱导的内皮衰老和功能障碍中的作用。用 NPs 处理猪冠状动脉及其内皮细胞，同时存在或不存在 SGLT2 抑制剂依那格列净（ENA），然后评估 SGLTs 表达、衰老标志物和血管功能。NPs 显著上调 SGLT2，ENA 显著降低 NPs 诱导的衰老相关-β-半乳糖苷酶活性、细胞周期停滞和衰老标志物 p53 和 p21，表明抑制 SGLT2 可预防 NPs 诱导的内皮衰老。此外，ENA 通过下调 Nox2 和 p22 降低活性氧的形成。此外，SGLT2 抑制还可上调内皮型一氧化氮合酶的表达，同时改善血管功能。总之，NPs 引起的内皮过早衰老至少部分与 SGLT2 有关，它可能是预防和/或治疗由内皮衰老和功能障碍介导的环境污染物引起的心血管疾病的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/8299a131d108/41598_2023_33086_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/70f141d6d8b6/41598_2023_33086_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/93160a0a010a/41598_2023_33086_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/0546fb94f196/41598_2023_33086_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/894c383f9f97/41598_2023_33086_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/8299a131d108/41598_2023_33086_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/70f141d6d8b6/41598_2023_33086_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/93160a0a010a/41598_2023_33086_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/0546fb94f196/41598_2023_33086_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/894c383f9f97/41598_2023_33086_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec9e/10110533/8299a131d108/41598_2023_33086_Fig5_HTML.jpg

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