Salvianolic acid B protects against sepsis‑induced liver injury via activation of SIRT1/PGC‑1α signaling
- Hongling Su
- Zhisheng Ma
- Aixia Guo
- Hong Wu
- Xiangmin Yang
Affiliations: Department of Gastroenterology, Xidian Group Hospital, Xi'an, Shaanxi 710000, P.R. China, Department of General Surgery, Xidian Group Hospital, Xi'an, Shaanxi 710000, P.R. China
- Published online on: July 17, 2020 https://doi.org/10.3892/etm.2020.9020
Copyright: © Su
et al. This is an open access article distributed under the
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Liver injury occurs frequently during sepsis, which leads to high mortality and morbidity. A previous study has suggested that salvianolic acid B (SalB) is protective against sepsis‑induced lung injury. However, whether SalB is able to protect against sepsis‑induced liver injury remains unclear. The present study aimed to investigate the effects of SalB on sepsis‑induced liver injury and its potential underlying mechanisms. Sepsis was induced in mice using a cecal ligation and puncture (CLP) method. The mice were treated with SalB (30 mg/kg intraperitoneally) at 0.5, 2 and 8 h after CLP induction. Pathological alterations of the liver were assessed using hematoxylin and eosin staining. The serum levels of alanine transaminase (ALT), aspartate aminotransferase (AST), tumor necrosis factor (TNF)‑α and interleukin (IL)‑6 were measured. The hepatic mRNA levels of TNF‑α, IL‑6, Bax and Bcl‑2 were also detected. The results suggested that treatment with SalB ameliorated sepsis‑induced liver injury in the mice, as supported by the mitigated pathologic changes and lowered serum aminotransferase levels. SalB also decreased the levels of the inflammatory cytokines TNF‑α and IL‑6 in the serum and the liver of the CLP model mice. In addition, SalB significantly downregulated Bax expression and upregulated Bcl‑2 expression, and upregulated the expression levels of SIRT1 and PGC‑1α. However, when sirtuin 1 (SIRT1) small interfering RNA was co‑administered with SalB, the protective effects of SalB were attenuated and the expression levels of SIRT1 and PGC‑1α were reduced. In summary, these results indicate that SalB mitigates sepsis‑induced liver injury via reduction of the inflammatory response and hepatic apoptosis, and the underlying mechanism may be associated with the activation of SIRT1/PGC‑1α signaling.