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.

Highlights

  • Ginsenoside Rg3 (Rg3), an uncommon ginsenoside transformed from other ginsenosides during heating [1], shows strong antitumor activity [2,3,4,5,6]

  • Our study indicated that Rg3 exerts cardioprotective effects not depending on blood pressure reduction in spontaneously hypertensive rats (SHR), possibly in association with attenuated angiotensin II (Ang II) increase in the myocardium [10]

  • It is known that Ang II increase mediates inflammation, oxidative stress, and fibrosis in the myocardium [11], which could be attenuated by Rg3

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Summary

Introduction

Ginsenoside Rg3 (Rg3), an uncommon ginsenoside transformed from other ginsenosides during heating [1], shows strong antitumor activity [2,3,4,5,6]. Rg3 has been reported to have cardiovascular protective effects through multiple mechanisms [6, 9, 10], including antiinflammation, antioxidative stress, and antifibrosis. Our study indicated that Rg3 exerts cardioprotective effects not depending on blood pressure reduction in spontaneously hypertensive rats (SHR), possibly in association with attenuated angiotensin II (Ang II) increase in the myocardium [10]. It is known that Ang II increase mediates inflammation, oxidative stress, and fibrosis in the myocardium [11], which could be attenuated by Rg3

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