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 explorin...

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Main Authors: Hua Guo, Qinglan Zhang, Haipo Yuan, Lin Zhou, Fang-fang Li, Sheng-Ming Wang, Gang Shi, Maojuan Wang
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2020/8889612
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author Hua Guo
Qinglan Zhang
Haipo Yuan
Lin Zhou
Fang-fang Li
Sheng-Ming Wang
Gang Shi
Maojuan Wang
author_facet Hua Guo
Qinglan Zhang
Haipo Yuan
Lin Zhou
Fang-fang Li
Sheng-Ming Wang
Gang Shi
Maojuan Wang
author_sort Hua Guo
collection DOAJ
description 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.
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institution Kabale University
issn 1687-4757
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language English
publishDate 2020-01-01
publisher Wiley
record_format Article
series PPAR Research
spelling doaj-art-0e67c136b4f54aea90e1e05a44079a402025-02-03T00:58:52ZengWileyPPAR Research1687-47571687-47652020-01-01202010.1155/2020/88896128889612Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling PathwayHua Guo0Qinglan Zhang1Haipo Yuan2Lin Zhou3Fang-fang Li4Sheng-Ming Wang5Gang Shi6Maojuan Wang7Department of Clinical Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaDepartment of Endocrinology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, ChinaDepartment of Endocrinology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaDepartment of Ophthalmology, Huai’an Second People's Hospital, The Affiliated Huai’an Hospital of Xuzhou Medical University, Huai’an, Jiangsu Province, ChinaDepartment of Ophthalmology, Huai’an Second People's Hospital, The Affiliated Huai’an Hospital of Xuzhou Medical University, Huai’an, Jiangsu Province, ChinaDepartment of Stomatology, Huai’an Second People’s Hospital, The Affiliated Huai’an Hospital of Xuzhou Medical University, Huai’an, Jiangsu Province, ChinaDepartment of Pharmacy Services, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaDepartment of Outpatient, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaInflammation 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.http://dx.doi.org/10.1155/2020/8889612
spellingShingle Hua Guo
Qinglan Zhang
Haipo Yuan
Lin Zhou
Fang-fang Li
Sheng-Ming Wang
Gang Shi
Maojuan Wang
Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway
PPAR Research
title Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway
title_full Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway
title_fullStr Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway
title_full_unstemmed Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway
title_short Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway
title_sort nitric oxide mediates inflammation in type ii diabetes mellitus through the pparγ enos signaling pathway
url http://dx.doi.org/10.1155/2020/8889612
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