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ARTICLE

20(R)-ginsenoside Rg3, a product of high-efficiency thermal deglycosylation of ginsenoside Rd, exerts protective effects against scrotal heat-induced spermatogenic damage in mice

by WEI LIU, ZI WANG, JING LENG, HENG WEI, SHEN REN, XIAOJIE GONG, CHEN CHEN, YINGPING WANG, RUI ZHANG, WEI LI

1 College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, 130118, China
2 National & Local Joint Engineering Research Center for Ginseng Breeding and Development, Changchun, 130118, China
3 Key Laboratory of Biotechnology and Bioresources Utilization, College of Life Science, Dalian Minzu University, Dalian, 116600, China
4 School of Biomedical Sciences, University of Queensland, Brisbane, 4072, Australia

* Address correspondence to: Rui Zhang, ; Wei Li,
# These authors contributed equally to this work

(This article belongs to the Special Issue: Cellular Biomechanics in Health and Diseases)

BIOCELL 2020, 44(4), 655-669. https://doi.org/10.32604/biocell.2020.013202

Received 29 July 2020; Accepted 03 September 2020; Issue published 24 December 2020

Abstract

Heat stress (HS) reaction can lead to serious physiological dysfunction associated with cardiovascular and various organ diseases. Ginsenoside Rg3 (G-Rg3) is a representative component of ginseng rare saponin and can protect against multiple organs, also used as functional food to adjust the balance of the human body, but the therapeutic effect and molecular mechanism of G-Rg3 on male diseases under HS are underexplored. The aim of the present study, G-Rg3 was prepared through the efficient conversion of ginsenoside Rd and investigate the contribution of G-Rg3 to testicular injury induced exposure to HS. All mice were divided into four groups as follows: normal group, HS group, and HS+G-Rg3 (5 and 10 mg/kg) groups. G-Rg3 was administered orally for 14 days, then exposed to a single scrotal heat treatment (43°C, 18min) on the 7th day. After HS treatment, the morphology of testis and epididymis changes, and caused a significant loss of multinucleated giant cells, desquamation of germ cells in destructive seminiferous tubules, and degenerative Leydig cells, further destroying the production of sperm. After administration G-Rg3 (5 and 10 mg/kg/day) for 2 weeks, the spermatogenic-related indexes of testosterone levels and superoxide dismutase (SOD) activity, glutathione (GSH) content significantly (p < 0.01) increase compared with the HS group. Moreover, G-Rg3 treatment effectively ameliorated the production of malondialdehyde (MDA) (p < 0.05 or p < 0.01). Importantly, G-Rg3 exhibited the protective potential against HS-induced injury not only suppressing the protein levels of heme oxygenase-1 (HO-1), hypoxia-inducible factor-1α (HIF-1α), and heat shock protein 70 (HSP70) but also modulating the Bcl-2 family (p < 0.01 or p < 0.001) and activation of mitogen-activated protein kinase (MAPK) signaling pathways (p < 0.01). For most of the parameters tested, the HS+G-Rg3 (10 mg/kg) group exhibited potent effects compared with those exhibited by the low dose (5 mg/kg) group. In conclusion, the present study demonstrated that G-Rg3 exerted protective effects against HS-induced testicular dysfunction via inhibiting the MAPK-mediated oxidative stress and apoptosis in mice.

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