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降糖通脉方通过 SnoN 和 TGF-β1/Smads 信号通路减轻糖尿病肺损伤。

Jiangtang Tongmai Prescription Reduced Diabetic Lung Injury Through SnoN and TGF-β1/Smads Signaling Pathway.

机构信息

Clinical College of Traditional Chinese Medicine, Hubei University of Chinese Medicine, Wuhan, China.

Medical Ward, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, China.

出版信息

Front Endocrinol (Lausanne). 2022 Jun 17;13:846583. doi: 10.3389/fendo.2022.846583. eCollection 2022.

DOI:10.3389/fendo.2022.846583
PMID:35784541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9248361/
Abstract

By establishing a rat diabetes model in rats with intervening treatment by Jiangtang Tongmai Prescription (JTTMP), this study explored the restorative pairing effect of JTTMP on diabetic lung injury. The model of type II diabetes model was used to establish the rat diabetes model, using a high-fat diet and streptozotocin (STZ) induction. Different doses of JTTMP and metformin were administered as a therapeutic to intervene, and blood was collected to assess the blood glucose level of each group of rats. HE (Hematoxylin and eosin (H&E) staining was performed to detect the morphological changes in rat lung tissue and enzyme-linked immunoassay ELISA was used to detect and quantify the expression of interleukin (IL)-6, TNF tumor necrosis factor-ɑa, and IL-1β in serum and the lung tissue of each group of rats. The level expression of TGF-β1 [transforming growth factor (TGF)-β1), SnoN (transcriptional co-repressor Ski-N terminal (SnoN)], Smad2, Smad3, Smad7, and other signaling pathway proteins were assessed by Western blot. In comparison with the normal control (NC) group, rats in the diabetes model (DM) group lost weight and showed significantly increased blood sugar levels. The levels of TGF-β1 and Smad2/3 were increased in the DM group but Smad7 decreased. After 8 weeks of JTTMP intervention, the level of TGF-β1 and Smad2/3 decreased but Smad7 increased, blood sugar decreased significantly and the expression of inflammatory factors in lung tissue decreased. Therefore, JTTMP may activate SnoN and the downstream TGF-β1/Smads signaling pathway to repair diabetic lung injury, which suggests its application has potential for future clinical treatment of diabetes with lung injury.

摘要

通过在大鼠糖尿病模型中进行干预治疗姜唐通脉方(JTTMP),本研究探讨了 JTTMP 对糖尿病肺损伤的修复作用。采用高脂饮食和链脲佐菌素(STZ)诱导建立 2 型糖尿病模型,建立大鼠糖尿病模型。用不同剂量的 JTTMP 和二甲双胍作为治疗进行干预,并采集血液评估各组大鼠的血糖水平。进行 HE(苏木精和伊红(H&E)染色)染色以检测大鼠肺组织的形态变化,并使用酶联免疫吸附测定(ELISA)检测和定量血清和各组大鼠肺组织中白细胞介素(IL)-6、肿瘤坏死因子-ɑa(TNF-α)和 IL-1β的表达。通过 Western blot 评估 TGF-β1[转化生长因子(TGF)-β1]、SnoN(Ski-N 端转录共抑制因子(SnoN))、Smad2、Smad3、Smad7 等信号通路蛋白的水平表达。与正常对照组(NC)相比,糖尿病模型(DM)组大鼠体重减轻,血糖水平明显升高。DM 组 TGF-β1 和 Smad2/3 水平升高,但 Smad7 降低。JTTMP 干预 8 周后,TGF-β1 和 Smad2/3 水平降低,Smad7 升高,血糖明显降低,肺组织中炎症因子表达降低。因此,JTTMP 可能通过激活 SnoN 和下游 TGF-β1/Smads 信号通路来修复糖尿病肺损伤,这表明其应用具有未来治疗糖尿病合并肺损伤的临床潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb9/9248361/d01f4b6aec1a/fendo-13-846583-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb9/9248361/3d7942478483/fendo-13-846583-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb9/9248361/11ef01b627e4/fendo-13-846583-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb9/9248361/d01f4b6aec1a/fendo-13-846583-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb9/9248361/3d7942478483/fendo-13-846583-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb9/9248361/11ef01b627e4/fendo-13-846583-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb9/9248361/d01f4b6aec1a/fendo-13-846583-g003.jpg

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