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18β-Glycyrrhetinic acid inhibits the apoptosis of cells infected with rotavirus SA11.


Pharm Biol. 2021 Dec ;59(1):1098-1105. PMID: 34411493

Abstract Title: 

18β-Glycyrrhetinic acid inhibits the apoptosis of cells infected with rotavirus SA11 via the Fas/FasL pathway.


CONTEXT: 18β-Glycyrrhetinic acid (18β-GA), a pentacyclic triterpenoid saponin metabolite of glycyrrhizin, exhibits several biological activities.OBJECTIVE: We investigated the effects of 18β-GA on MA104 cells infected with rotavirus (RV) and its potential mechanism of action.MATERIALS AND METHODS: Cell Counting Kit-8 was used to assess tissue culture infective dose 50 (TCID) and 50% cellular cytotoxicity (CC) concentration. MA104 cells infected with RV SA11 were treated with 18β-GA (1, 2, 4, and 8 μg/mL, respectively). Cytopathic effects were observed. The virus inhibition rate, concentration for 50% of maximal effect (EC), and selection index (SI) were calculated. Cell cycle, cell apoptosis, and mRNA and protein expression related to the Fas/FasL pathway were detected.RESULTS: TCIDof RV SA11 was 10/100 µL; the CCof 18β-GA on MA104 cells was 86.92 µg/mL. 18β-GA showed significant antiviral activity; ECwas 3.14 μg/mL, and SI was 27.68. The ratio of MA104 cells infected with RV SA11 in the G0/G1 phase and the G2/M phase decreased and increased, respectively, after 18β-GA treatment. 18β-GA significantly induced apoptosis in the infected cells. Furthermore, after 18β-GA treatment, the mRNA and proteinexpression levels of Fas, FasL, caspase 3, and Bcl-2 decreased, whereas the expression levels of Bax increased.DISCUSSION AND CONCLUSIONS: The study demonstrates that 18β-GA may be a promising candidate for the treatment of RV SA11 infection and provides theoretical support for the clinical development of glycyrrhizic acid compounds for the treatment of RV infection.

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