Hua Guo, Qinglan Zhang, Haipo Yuan, Lin Zhou, Fang-Fang Li, Sheng-Ming Wang, Gang Shi, Maojuan Wang
{"title":"一氧化氮通过PPARγ/eNOS信号通路介导II型糖尿病炎症","authors":"Hua Guo, Qinglan Zhang, Haipo Yuan, Lin Zhou, Fang-Fang Li, Sheng-Ming Wang, Gang Shi, Maojuan Wang","doi":"10.1155/2020/8889612","DOIUrl":null,"url":null,"abstract":"<p><p>Inflammation accounts for the process of type II diabetes mellitus (T2DM), the specific mechanism of which is still to be elucidated yet. Nitric oxide (NO), a critical inflammation regulator, the role of which is the inflammation of T2DM, is rarely reported. Therefore, our study is aimed at exploring the effect of NO on the inflammation in T2DM and the corresponding mechanism. We analyzed the NO levels in plasma samples from T2DM patients and paired healthy adults by Nitric Oxide Analyzer then measured the expression of inflammatory cytokines (C-reactive protein, heptoglobin, IL-1<i>β</i>, TNF-<i>α</i>, IL-6) in insulin-induced HepG2 cells treated with NO donor or NO scavenger, and the PPAR<i>γ</i>, eNOS, C-reactive protein, heptoglobin, IL-1<i>β</i>, TNF-<i>α</i>, and IL-6 levels were detected by RT-PCR and western blot in insulin-induced HepG2 cells transfected with si-PPAR<i>γ</i>. The results showed that excess NO increased the inflammation marker levels in T2DM, which is activated by the PPAR<i>γ</i>/eNOS pathway. These findings will strengthen the understanding of NO in T2DM and provide a new target for the treatment of T2DM.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"8889612"},"PeriodicalIF":3.5000,"publicationDate":"2020-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/8889612","citationCount":"11","resultStr":"{\"title\":\"Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPAR<i>γ</i>/eNOS Signaling Pathway.\",\"authors\":\"Hua Guo, Qinglan Zhang, Haipo Yuan, Lin Zhou, Fang-Fang Li, Sheng-Ming Wang, Gang Shi, Maojuan Wang\",\"doi\":\"10.1155/2020/8889612\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Inflammation accounts for the process of type II diabetes mellitus (T2DM), the specific mechanism of which is still to be elucidated yet. Nitric oxide (NO), a critical inflammation regulator, the role of which is the inflammation of T2DM, is rarely reported. Therefore, our study is aimed at exploring the effect of NO on the inflammation in T2DM and the corresponding mechanism. We analyzed the NO levels in plasma samples from T2DM patients and paired healthy adults by Nitric Oxide Analyzer then measured the expression of inflammatory cytokines (C-reactive protein, heptoglobin, IL-1<i>β</i>, TNF-<i>α</i>, IL-6) in insulin-induced HepG2 cells treated with NO donor or NO scavenger, and the PPAR<i>γ</i>, eNOS, C-reactive protein, heptoglobin, IL-1<i>β</i>, TNF-<i>α</i>, and IL-6 levels were detected by RT-PCR and western blot in insulin-induced HepG2 cells transfected with si-PPAR<i>γ</i>. The results showed that excess NO increased the inflammation marker levels in T2DM, which is activated by the PPAR<i>γ</i>/eNOS pathway. These findings will strengthen the understanding of NO in T2DM and provide a new target for the treatment of T2DM.</p>\",\"PeriodicalId\":20439,\"journal\":{\"name\":\"PPAR Research\",\"volume\":\"2020 \",\"pages\":\"8889612\"},\"PeriodicalIF\":3.5000,\"publicationDate\":\"2020-11-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1155/2020/8889612\",\"citationCount\":\"11\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"PPAR Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1155/2020/8889612\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"PPAR Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/2020/8889612","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway.
Inflammation accounts for the process of type II diabetes mellitus (T2DM), the specific mechanism of which is still to be elucidated yet. Nitric oxide (NO), a critical inflammation regulator, the role of which is the inflammation of T2DM, is rarely reported. Therefore, our study is aimed at exploring the effect of NO on the inflammation in T2DM and the corresponding mechanism. We analyzed the NO levels in plasma samples from T2DM patients and paired healthy adults by Nitric Oxide Analyzer then measured the expression of inflammatory cytokines (C-reactive protein, heptoglobin, IL-1β, TNF-α, IL-6) in insulin-induced HepG2 cells treated with NO donor or NO scavenger, and the PPARγ, eNOS, C-reactive protein, heptoglobin, IL-1β, TNF-α, and IL-6 levels were detected by RT-PCR and western blot in insulin-induced HepG2 cells transfected with si-PPARγ. The results showed that excess NO increased the inflammation marker levels in T2DM, which is activated by the PPARγ/eNOS pathway. These findings will strengthen the understanding of NO in T2DM and provide a new target for the treatment of T2DM.
期刊介绍:
PPAR Research is a peer-reviewed, Open Access journal that publishes original research and review articles on advances in basic research focusing on mechanisms involved in the activation of peroxisome proliferator-activated receptors (PPARs), as well as their role in the regulation of cellular differentiation, development, energy homeostasis and metabolic function. The journal also welcomes preclinical and clinical trials of drugs that can modulate PPAR activity, with a view to treating chronic diseases and disorders such as dyslipidemia, diabetes, adipocyte differentiation, inflammation, cancer, lung diseases, neurodegenerative disorders, and obesity.