Persicarin isolated from Oenanthe javanica protects against diabetes-induced oxidative stress and inflammation in the liver of streptozotocin-induced type 1 diabetic mice

Aim. To investigate the combination effects and mechanisms of valsartan (angiotensin II type 1 receptor blocker) and LAF237 (DPP-IV inhibitor) on prevention against oxidative stress and inflammation injury in db/db mice aorta.Methods. Db/db mice (n=40) were randomized to receive valsartan, LAF237, valsartan plus LAF237, or saline. Oxidative stress and inflammatory reaction in diabetic mice aorta were examined.Results. Valsartan or LAF237 pretreatment significantly increased plasma GLP-1 expression, reduced apoptosis of endothelial cells isolated from diabetic mice aorta. The expression of NAD(P)H oxidase subunits also significantly decreased resulting in decreased superoxide production and ICAM-1 (fold change: valsartan : 7.5 ± 0.7,P<0.05; LAF237: 10.2 ± 1.7,P<0.05), VCAM-1 (fold change: valsartan : 5.2 ± 1.2,P<0.05; LAF237: 4.8 ± 0.6,P<0.05), and MCP-1 (fold change: valsartan: 3.2 ± 0.6, LAF237: 4.7 ± 0.8;P<0.05) expression. Moreover, the combination treatment with valsartan and LAF237 resulted in a more significant increase of GLP-1 expression. The decrease of the vascular oxidative stress and inflammation reaction was also higher than monotherapy with valsartan or LAF237.Conclusion. These data indicated that combination treatment with LAF237 and valsartan acts in a synergistic manner on vascular oxidative stress and inflammation in type 2 diabetic mice.

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In vivo imaging of oxidative stress in the kidney of diabetic mice and its normalization by angiotensin II type 1 receptor blocker

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2005.02.174 ◽

2005 ◽

Vol 330 (2) ◽

pp. 415-422 ◽

Cited By ~ 44

Author(s):

Toshiyo Sonta ◽

Toyoshi Inoguchi ◽

Shingo Matsumoto ◽

Keiji Yasukawa ◽

Mieko Inuo ◽

...

Keyword(s):

Oxidative Stress ◽

Angiotensin Ii ◽

In Vivo Imaging ◽

Receptor Blocker ◽

Diabetic Mice

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Oxidative stress contributes to the impaired sonic hedgehog pathway in type 1 diabetic mice with myocardial infarction

Experimental and Therapeutic Medicine ◽

10.3892/etm.2015.2766 ◽

2015 ◽

Vol 10 (5) ◽

pp. 1750-1758 ◽

Cited By ~ 6

Author(s):

QING XIAO ◽

YA YANG ◽

XIAO-YA ZHAO ◽

LI-SHAN HE ◽

YUAN QIN ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Sonic Hedgehog ◽

Hedgehog Pathway ◽

Diabetic Mice ◽

Sonic Hedgehog Pathway

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Impairment of type H vessels by NOX2-mediated endothelial oxidative stress: critical mechanisms and therapeutic targets for bone fragility in streptozotocin-induced type 1 diabetic mice

Theranostics ◽

10.7150/thno.50907 ◽

2021 ◽

Vol 11 (8) ◽

pp. 3796-3812

Author(s):

Xiao-Fan Hu ◽

Geng Xiang ◽

Tian-Ji Wang ◽

Yu-Bo Ma ◽

Yang Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Therapeutic Targets ◽

Bone Fragility ◽

Diabetic Mice

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Angiotensin II Type 1 Receptor Antagonism Mediates Uncoupling Protein 2-Driven Oxidative Stress and Ameliorates Pancreatic Islet β-Cell Function in Young Type 2 Diabetic Mice

Antioxidants and Redox Signaling ◽

10.1089/ars.2007.1590 ◽

2007 ◽

Vol 9 (7) ◽

pp. 869-878 ◽

Cited By ~ 61

Author(s):

Kwan Yi Chu ◽

Po Sing Leung

Keyword(s):

Oxidative Stress ◽

Cell Function ◽

Uncoupling Protein ◽

Uncoupling Protein 2 ◽

Diabetic Mice ◽

Β Cell ◽

Β Cell Function ◽

Type 2 Diabetic

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Angiotensin II Type 1 Receptor-Dependent Oxidative Stress Mediates Endothelial Dysfunction in Type 2 Diabetic Mice

Antioxidants and Redox Signaling ◽

10.1089/ars.2009.2831 ◽

2010 ◽

Vol 13 (6) ◽

pp. 757-768 ◽

Cited By ~ 41

Author(s):

Wing Tak Wong ◽

Xiao Yu Tian ◽

Aimin Xu ◽

Chi Fai Ng ◽

Hung Kay Lee ◽

...

Keyword(s):

Oxidative Stress ◽

Angiotensin Ii ◽

Endothelial Dysfunction ◽

Diabetic Mice ◽

Type 2 Diabetic

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Fibroblast growth factor 21 Ameliorates diabetes-induced endothelial dysfunction in mouse aorta via activation of the CaMKK2/AMPKα signaling pathway

Cell Death and Disease ◽

10.1038/s41419-019-1893-6 ◽

2019 ◽

Vol 10 (9) ◽

Cited By ~ 7

Author(s):

Lei Ying ◽

Na Li ◽

Zhengyue He ◽

Xueqin Zeng ◽

Yan Nan ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Dysfunction ◽

Endothelial Function ◽

Signaling Pathway ◽

Oxidative Capacity ◽

Fibroblast Growth Factor 21 ◽

Diabetic Mice

Abstract Endothelial dysfunction initiates and exacerbates hypertension, atherosclerosis and other cardiovascular complications in diabetic mellitus. FGF21 is a hormone that mediates a number of beneficial effects relevant to metabolic disorders and their associated complications. Nevertheless, it remains unclear as to whether FGF21 ameliorates endothelial dysfunction. Therefore, we investigated the effect of FGF21 on endothelial function in both type 1 and type 2 diabetes. We found that FGF21 reduced hyperglycemia and ameliorated insulin resistance in type 2 diabetic mice, an effect that was totally lost in type 1 diabetic mice. However, FGF21 activated AMPKα, suppressing oxidative stress and enhancing endothelium-dependent vasorelaxation of aorta in both types, suggesting a mechanism that is independent of its glucose-lowering and insulin-sensitizing effects. In vitro, we identified a direct action of FGF21 on endothelial cells of the aorta, in which it bounds to FGF receptors to alleviate impaired endothelial function challenged with high glucose. Furthermore, the CaMKK2-AMPKα signaling pathway was activated to suppress oxidative stress. Apart from its anti-oxidative capacity, FGF21 activated eNOS to dilate the aorta via CaMKK2/AMPKα activation. Our data suggest expanded potential uses of FGF21 for the treatment of vascular diseases in diabetes.

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Blocking Type I Interferon Signaling Rescues Lymphocytes from Oxidative Stress, Exhaustion, and Apoptosis in a Streptozotocin-Induced Mouse Model of Type I Diabetes

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/148725 ◽

2013 ◽

Vol 2013 ◽

pp. 1-12 ◽

Cited By ~ 9

Author(s):

Hany M. Ibrahim ◽

Ibrahim A. El-Elaimy ◽

Heba M. Saad Eldien ◽

Badr Mohamed Badr ◽

Danny M. Rabah ◽

...

Keyword(s):

Oxidative Stress ◽

Immune Response ◽

Proinflammatory Cytokines ◽

Type I Interferon ◽

Type I ◽

Diabetic Mice ◽

Type I Ifn ◽

Proliferative Capacity ◽

Blocking Type

Elevated levels of type I interferon (IFN) during type 1 diabetes mellitus (T1D) are associated with a defective immune response. In the present study, we investigated whether blocking type I IFN signaling during streptozotocin- (STZ-) induced T1D in mice improves lymphocyte proliferation and escape from continuous apoptosis. Three groups of mice were examined: diabetic mice, type I IFN signaling-incompetent diabetic mice, and control nondiabetic mice. We first found that diabetes induction was accompanied by an elevation in the plasma levels of reactive oxygen species (ROS), hydroperoxide, malondialdehyde (MDN), and the proinflammatory cytokines IL-1α, IL-1β, IL-6, and CXCL10. Blocking type 1 IFN signaling in diabetic mice significantly decreased the levels of oxidative stress and proinflammatory cytokines. In addition, lymphocytes from diabetic mice exhibited a marked reduction in their proliferative capacity, increased apoptosis, upregulation of the exhaustion marker PD-1, and aberrant phosphorylation of STAT1, STAT2, AKT and IκB-α. Interestingly, following the blocking of type I IFN signaling in diabetic mice, the lymphocytes exhibited restored proliferative capacity, decreased apoptosis, normal expression of PD-1, and normal phosphorylation of STAT1, STAT2, AKT and IκB-α. Our data suggest that elevated levels of type I IFN during T1D trigger lymphocyte exhaustion and a defective lymphocyte-medicated immune response.

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