Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity.

Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity. Research Abstract Details 

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Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity. Abstract Text:

Julie Chao,Huey-Jiun Li,Yu-Yu Yao,Bo Shen,Lin Gao,Grant Bledsoe,Lee Chao,

The progression of renal disease displays several characteristics, including proteinuria, apoptosis, inflammation, and fibrosis. In this study, we investigated the effect of long-term infusion of kinin in protection against salt-induced renal damage in Dahl salt-sensitive rats. Dahl salt-sensitive rats were fed a high-salt diet for 2 weeks and were then infused with bradykinin (500 ng/h) via subcutaneously implanted minipumps for 3 weeks. Kinin infusion attenuated salt-induced impaired renal function as evidenced by reduced proteinuria, serum creatinine, and blood urea nitrogen levels without apparent effect on blood pressure. Morphological analysis indicated that kinin administration reduced salt-induced glomerular sclerosis, tubular dilatation, luminal protein cast formation, and interlobular arterial thickness. Kinin also significantly lowered collagen I, III, and IV deposition and their mRNA levels. Moreover, kinin reduced interstitial monocyte/macrophage accumulation, as well as tubular cell apoptosis and caspase-3 activity. Protection of renal injury by kinin was associated with increased renal NO levels and reduced nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate oxidase activities and superoxide generation. Suppression of oxidative stress by kinin was accompanied by reduced transforming growth factor-beta1 protein and mRNA levels, as well as decreased phosphorylation of mitogen-activated protein kinases. This is the first study to demonstrate that kinin infusion can directly protect against salt-induced renal injury without blood pressure reduction by inhibiting apoptosis, inflammation, and fibrosis via suppression of oxidative stress, transforming growth factor-beta1 expression, and mitogen-activated protein kinase activation.

Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity. Publishing Authors By Initials

J Chao,HJ Li,YY Yao,B Shen,L Gao,G Bledsoe,L Chao,

For similar chemical actions and uses: pharmacologic actions: therapeutic uses: cardiovascular agents: vasodilator agents research abstracts see: chemical actions and uses: pharmacologic actions: therapeutic uses: cardiovascular agents: vasodilator agents research

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Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Hypertension

VOLUME: 49

Page Numbers: 490-7

Journal Abbreviation: Hypertension

ISSN: 1524-4563

DAY: 15

MONTH: 01

YEAR: 2007

Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7906255

Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity. Keywords Mesh Terms:

KEYWORDS: Vasodilator Agents

MESH TERMS: administration & dosage

Chemical & Substance for Abstract: Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity. Information

Substance Name: Mitogen-Activated Protein Kinases

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Kinin infusion prevents renal inflammation, apoptosis, and fibrosis via inhibition of oxidative stress and mitogen-activated protein kinase activity.

AFFILIATION: Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA. chaol@musc.edu

Country: United States

AGENCY: United States PHS

GRANT: H-29397

ACRONYM: DK

MEDLINETA: Hypertension

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