Tianjin Medical Journal ›› 2023, Vol. 51 ›› Issue (8): 820-824.doi: 10.11958/20221834

• Experimental Research • Previous Articles     Next Articles

Study of ginsenoside Rg1 antagonizes sodium arsenite-induced nephrotoxicity in C57BL/6 mice

YANG Yuan1,2(), SONG Shuang1, CHEN Rong2, LIU Yonglian1, LIU Chunyan1   

  1. 1 Department of Toxicology, School of Public Health, Guizhou Medical University, Guiyang 550025, China
    2 Ethnic Medicine Research Center, Hunan University of Medicine
  • Received:2022-11-07 Revised:2023-03-01 Published:2023-08-15 Online:2023-08-10

Abstract:

Objective To investigate the intervention effect of ginsenoside Rg1 (Rg1) against sodium arsenite (SA) induced nephrotoxicity in mice. Methods Twenty healthy male C57BL/6 mice were randomly divided into the control group (given deionized water by gavage), the SA exposure group (10.0 μg/g SA by gavage), the Rg1 intervention+SA exposure group (20.0 μg/g Rg1 was injected intraperitoneally 8 hours before SA exposure+10.0 μg/g SA gavage) and the Rg1 control group (20.0 μg/g Rg1 intraperitoneal injection). All of groups were given corresponding treatment once every other day for 14 days. HE staining was performed to observe pathological changes of renal tissue and renal tubular injury (TI) score. Serum creatinine (Scr) and renal glutathione (GSH), heme oxygenase-1 (HO-1) and malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay (ELISA). The expression levels of HO-1, phosphorylated mammalian target of rapamycin (p-mTOR), ubiquitin-binding protein P62 (SQSTM1/p62), unc-51-like kinase-1 (ULK1) and microtubule-associated protein light chain 3B (LC3-B) in renal tissue were detected by Western blot assay. LC3-B levels were detected by immunofluorescence staining. Results Compared with the control group, the TI score, Scr and expression levels of MDA, ULK1 and LC3-B in renal tissue were increased in the SA group, while expression levels of GSH and HO-1, p-mTOR and SQSTM1/p62 in renal tissue were decreased (P<0.05). The staining intensity of red spot LC3-B was enhanced and increased. Compared with the SA group, TI score, Scr and expression levels of MDA, ULK1 and LC3-B in renal tissue were decreased in the Rg1 +SA group, while expression levels of GSH, HO-1, p-mTOR and SQSTM1/p62 were increased (P<0.05). The immunofluorescence staining intensity of LC3-B was weakened and decreased. Conclusion Rg1 antagonizes SA-induced nephrotoxicity in mice, which may be associated with the activation of HO-1 signal and the inhibition of autophagy.

Key words: Ginsenoside Rg1, arsenic poisoning, heme oxygenase-1, autophagy, nephrotoxicity

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