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Schisantherin A protects renal tubular epithelial cells from hypoxia/reoxygenation injury through the activation of PI3K/Akt signaling pathway
Author(s) -
Gong Jiachuan,
Wang Xuezhen
Publication year - 2018
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22160
Subject(s) - pi3k/akt/mtor pathway , protein kinase b , chemistry , reactive oxygen species , apoptosis , tumor necrosis factor alpha , viability assay , hypoxia inducible factors , reperfusion injury , pharmacology , biochemistry , immunology , medicine , ischemia , gene
Schisantherin A (SchA), a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra sphenanthera , was reported to possess anti‐inflammatory and antioxidant activities. However, its protective effect against renal ischemia‐reperfusion (I/R) injury in human renal tubular epithelial cells subjected to hypoxia/reoxygenation (H/R) has never been studied. Thus, herein, we investigated the effect of SchA on renal I/R injury in vitro . Our results demonstrated that SchA pretreatment significantly improved HK‐2 cell viability exposed to H/R. Pretreatment with SchA markedly inhibited the levels of reactive oxygen species and malondialdehyde, as well as suppressed the production of tumor necrosis factor‐α (TNF‐α), interleukin‐1β, and interleukin‐6 in H/R‐stimulated HK‐2 cells. In addition, SchA also suppressed H/R‐induced HK‐2 cell apoptosis. Furthermore, this protective effect of SchA was mediated through the PI3K/Akt signaling pathway in HK‐2 cells. These findings showed that SchA may exert a protective effect on renal tubular epithelial cells against H/R injury through the activation of PI3K/Akt signaling pathway.