Abstract
The cytoprotective properties of baicalin (1), a flavonoid glycoside isolated from Scutellaria baicalensis, have been investigated against injury to the liver caused by ischemia/reperfusion (I/R). Rats were subjected to 60 min of ischemia followed by 5 h of reperfusion, and 1 was administered intraperitoneally 24 and 1 h before ischemia. Following I/R, the levels of serum alanine aminotransferase and hepatic lipid peroxidation were elevated, whereas the hepatic glutathione content was decreased, with these changes attenuated by 1. Serum levels of tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 were markedly increased by I/R, but suppressed by 1. Baicalin attenuated increases in inducible nitric oxide synthase, cyclooxygenase (COX)-2, and TNF receptor 1-associated protein expression and augmented an increase in heme oxygenase-1 (HO-1). The increase in TNF-α, IL-6, and, COX-2 mRNA expression was attenuated by 1, while the increase in HO-1 mRNA expression was augmented. Nuclear factor-κB nuclear localization was inhibited by 1, and this compound limited the rate of mitochondrial swelling and the activation of caspases-3 and -8 observed in I/R rats. Rats treated with 1 had markedly fewer apoptotic cells than I/R rats. It was concluded that baicalin (1) exhibits antioxidant, anti-inflammatory, and antiapoptotic effects, which protect against hepatocellular I/R-induced damage.
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