Abstract
Baicalein (BAI), one of the main components of Scutellaria baicalensis Georgi, possesses numerous pharmacological properties, including anti-cancer, anti-oxidative, anti-virus and anti-bacterial activities. The purpose of this study was to evaluate the hepatoprotective effect of baicalein against acetaminophen (APAP)-exposed liver injury in mice, and elucidate the underlying hepatoprotective mechanism. Baicalein pretreatment significantly alleviated the elevation of IL-6, IL-1β and TNF-α in serum and hepatic in a dose-dependent manner. It also dose-dependently reduced the hepatic malondialdehyde (MDA) concentration, as well as the depletion of hepatic superoxide dismutase (SOD), hepatic glutathione (GSH) and hepatic catalase (CAT). Moreover, pretreatment with baicalein significantly ameliorated APAP-exposed liver damage and histological hepatocyte changes. Baicalein also relieved APAP-induced autophagy by regulating AKT/mTOR pathway, LC3B and P62 expression. Furthermore, the hepatoprotective effect of baicalein to APAP-induced liver injury involved in Jak2/Stat3 and MAPK signaling pathway. Taken together, our findings suggested that baicalein exhibits the ability to prevent liver from APAP-induced liver injury and provided an underlying molecular basis for potential applications of baicalein to cure liver injuries.
Highlights
Adverse drug reactions (ADRs) are a significant cause of illness and death in the world [1].Drug-induced liver injury (DILI) is one of the serious ADRs which is an important clinical problem in the practice of hepatology [2]
We investigated the roles of BAI in the expression of phospho-Janus kinase signal transducers 2 (p-JAK2) and phospho-Signal transducer and activator of transcription 3 (p-STAT3) proteins in APAP-induced liver injury
We found that BAI altered the status of AKT/mammalian target target of of rapamycin rapamycin (mTOR) and induced down-regulation of phosphorylation of AKT mTOR in the liver at least partially mediated by the AKT/mTOR pathway
Summary
Drug-induced liver injury (DILI) is one of the serious ADRs which is an important clinical problem in the practice of hepatology [2]. DILI is caused by the biological activation of chemically active metabolites mediated by enzymes, which can lead to cell death and possible liver failure [1]. The particularity and poor prognosis of DILI make it a major safety issue in the process of drug development and result in a serious clinical and financial problem [3]. It has been recognized that oxidative stress, sterile inflammation and compensatory liver repair and regeneration were key signaling pathways during the development of DILI [4]. The inhibitions of inflammation, autophagy and oxidative stress might be considered as the potential strategies for the prevention and treatment of DILI
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