Dopamine Pretreatment Protects Offspring Rats from LPS-Induced Hypertension and Kidney Damage by Inhibiting NLRP3 Activation in Kidney

Dopamine Pretreatment Protects Offspring Rats from LPS-Induced Hypertension and Kidney Damage by... This study was designed to explore the role of dopamine (DA) and NLRP3 in the mechanism of hypertension and renal impairment induced by prenatal exposure to lipopolysaccharide (LPS). Thirty pregnant rats were randomly divided into three groups, including control, LPS, and DA + LPS groups. Renal morphology changes were observed under microscope. The serum IL-1β and IL-18 concentration, mRNA, and protein expressions of NLRP3, ASC, and CASP1 in kidney of three-month old offspring rats were measured. Hematoxylin–eosin staining showed that the glomerular diameter decreased and cysts increased partly, glomerular balloons were adhered partly, there were moderate-to-severe hyperplasia dispersedly distributed in glomerular mesangial matrix in rats of LPS group. Serum IL-1β and IL-18 concentration in LPS group increased compared with control group and DA + LPS group. The average arterial pressure of offspring rats in LPS group increased significantly compared with control group and DA + LPS group. NLRP3 mRNA level in the LPS group increased significantly compared with the control group and the DA + LPS group in both male and female rats; NLRP3, ASC, and CASP1 protein expression in both renal cortex and renal medulla of LPS group increased significantly compared with control group and DA + LPS group in female rats. NLRP3 protein expression in LPS group increased significantly compared with control group and DA + LPS group in male rats. DA pretreatment exerts a protective effect on LPS-induced renal injury and hypertension in offspring rats, and the mechanism might be through inhibiting NLRP3 activation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Bioorganic Chemistry Springer Journals

Dopamine Pretreatment Protects Offspring Rats from LPS-Induced Hypertension and Kidney Damage by Inhibiting NLRP3 Activation in Kidney

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Publisher
Pleiades Publishing
Copyright
Copyright © 2018 by Pleiades Publishing, Ltd.
Subject
Life Sciences; Biochemistry, general; Bioorganic Chemistry; Organic Chemistry; Biomedicine, general
ISSN
1068-1620
eISSN
1608-330X
D.O.I.
10.1134/S1068162018010077
Publisher site
See Article on Publisher Site

Abstract

This study was designed to explore the role of dopamine (DA) and NLRP3 in the mechanism of hypertension and renal impairment induced by prenatal exposure to lipopolysaccharide (LPS). Thirty pregnant rats were randomly divided into three groups, including control, LPS, and DA + LPS groups. Renal morphology changes were observed under microscope. The serum IL-1β and IL-18 concentration, mRNA, and protein expressions of NLRP3, ASC, and CASP1 in kidney of three-month old offspring rats were measured. Hematoxylin–eosin staining showed that the glomerular diameter decreased and cysts increased partly, glomerular balloons were adhered partly, there were moderate-to-severe hyperplasia dispersedly distributed in glomerular mesangial matrix in rats of LPS group. Serum IL-1β and IL-18 concentration in LPS group increased compared with control group and DA + LPS group. The average arterial pressure of offspring rats in LPS group increased significantly compared with control group and DA + LPS group. NLRP3 mRNA level in the LPS group increased significantly compared with the control group and the DA + LPS group in both male and female rats; NLRP3, ASC, and CASP1 protein expression in both renal cortex and renal medulla of LPS group increased significantly compared with control group and DA + LPS group in female rats. NLRP3 protein expression in LPS group increased significantly compared with control group and DA + LPS group in male rats. DA pretreatment exerts a protective effect on LPS-induced renal injury and hypertension in offspring rats, and the mechanism might be through inhibiting NLRP3 activation.

Journal

Russian Journal of Bioorganic ChemistrySpringer Journals

Published: Mar 14, 2018

References

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