Dataset Information

Ginsenoside Rg3 Attenuates Angiotensin II-Mediated Renal Injury in Rats and Mice by Upregulating Angiotensin-Converting Enzyme 2 in the Renal Tissue.

ABSTRACT: Angiotensin II- (Ang II-) mediated renal injury represents a major pathogenetic mechanism in most chronic kidney diseases. Our previous research demonstrated that ginsenoside Rg3 (Rg3) attenuates Ang II elevation in the myocardium in spontaneously hypertensive rats (SHR). It is possible that Rg3 has similar effects in the renal tissue. In this research, we first demonstrated that Rg3 could attenuate Ang II increase in the kidney of SHR and reduce hypertensive nephropathy progression. Then, we found that Rg3 attenuated Ang II increase by upregulating angiotensin-converting enzyme 2 (ACE2) in the renal tissue. We confirmed this finding in an exogenous Ang II-infused mice model of renal injury, and two models showed consistent results. In conclusion, Rg3 attenuates Ang II-mediated renal injury in rats and mice by upregulating ACE2 in the renal tissue. This research is the first to demonstrate that Rg3 increases tissue ACE2 levels in vivo.

SUBMITTER: Liu H

PROVIDER: S-EPMC6915024 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Publications

Ginsenoside Rg3 Attenuates Angiotensin II-Mediated Renal Injury in Rats and Mice by Upregulating Angiotensin-Converting Enzyme 2 in the Renal Tissue.

Liu Hui H Jiang Yichuan Y Li Min M Yu Xiaofeng X Sui Dayun D Fu Li L

Evidence-based complementary and alternative medicine : eCAM 20191129

Angiotensin II- (Ang II-) mediated renal injury represents a major pathogenetic mechanism in most chronic kidney diseases. Our previous research demonstrated that ginsenoside Rg3 (Rg3) attenuates Ang II elevation in the myocardium in spontaneously hypertensive rats (SHR). It is possible that Rg3 has similar effects in the renal tissue. In this research, we first demonstrated that Rg3 could attenuate Ang II increase in the kidney of SHR and reduce hypertensive nephropathy progression. Then, we fo ...[more]

PMID: 31885658

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Project description:Evolution of glomerulonephritis (GN) to tubulointerstitial disease is a universal antecedent to the development of chronic kidney disease (CKD). There is also evidence that angiotensin converting enzyme (ACE) inhibition may attenuate the development of CKD in some forms of glomerulonephritis. We tested the role of ACE inhibition in a model of GN in which complement-dependent tubulointerstitial disease develops. GN was induced in C57BL/6 mice with intraperitoneal injections of horse spleen apoferritin (HSA) using lipopolysaccharide (LPS) as an adjuvant. Four groups of six animals were studied: saline-injected control mice treated with captopril or water, and GN mice treated with captopril or water. GN developed in all HSA-treated animals. In those receiving captopril, however, proteinuria (albumin/creatinine ratio) was significantly reduced by captopril treatment. Array screening was used to examined the expression of collagen-related genes and determine if these effects could be mediated by regulation of collagen genes. Six genes were identified for further analysis by quantitative RT-PCR. This model demonstrates that tubulointerstitial disease can be attenuated by ACE inhibition, with clinical, histologic, and gene expression measures. All protocols were approved by the Institutional Animal Care and Use Committee at SUNY Upstate Medical University. We employed four groups of six mice each: saline-injected control mice with and without captopril, and GN with and without captopril. C57BL/6 mice were purchased from The Jackson Laboratories (Bar Harbor, ME). Glomerulonephritis (GN) was induced by intraperitoneal (i.p.) injection of 10 mg of apoferritin from horse spleen (HSA, Sigma, St. Louis, MO) five days per week, with i.p. injection of 100 micrograms lipopolysaccharide (LPS, from Salmonella minnesota; EMD Biosciences, La Jolla, CA), as adjuvant, three times per week. Control animals received equal volumes of 0.15 M NaCl by i.p. injection. Injections were begun when the mice were approximately eight weeks of age and were continued for six weeks. Captopril, at 100 mg/kg/day was given in the drinking water. After 9 weeks, the animals were euthanized and kidneys were removed for RNA purification and analysis.

Dataset Information

Ginsenoside Rg3 Attenuates Angiotensin II-Mediated Renal Injury in Rats and Mice by Upregulating Angiotensin-Converting Enzyme 2 in the Renal Tissue.

Publications

Ginsenoside Rg3 Attenuates Angiotensin II-Mediated Renal Injury in Rats and Mice by Upregulating Angiotensin-Converting Enzyme 2 in the Renal Tissue.

Similar Datasets

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