Homoplantaginin, a flavonoid derived from the traditional Chinese medicine Salvia plebeia, exhibits protective and therapeutic effects on hepatocyte injury and demonstrates potent inhibitory activities against influenza.

Homoplantaginin may be used for the prevention and treatment of endothelial dysfunction associated with insulin resistance, it ameliorates endothelial insulin resistance by inhibiting inflammation and modulating cell signalling via the IKKβ/IRS-1/pAkt/peNOS pathway.

Homoplantaginin displayed an antioxidant property in a cell-free system and showed IC(50) of reduction level of DPPH radical at 0.35 microg/ml. In human hepatocyte HL-7702 cells exposed to H(2)O(2), the addition of 0.1-100 microg/ml of Homoplantaginin, which did not have a toxic effect on cell viability, significantly reduced lactate dehydrogenase (LDH) leakage, and increased glutathione (GSH), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in supernatant. In vivo assay, we employed the model of Bacillus Calmette-Guérin (BCG)/lipopolysaccharide (LPS)-induced hepatic injury mice to evaluate efficacy of Homoplantaginin. Homoplantaginin (25-100mg/kg) significantly reduced the increase in serum alanine aminotranseferase (ALT) and aspartate aminotransferase (AST), decreased the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1). The same treatment also reduced the content of thiobarbituric acid-reactive substances (TBARS), elevated the levels of GSH, GSH-Px and SOD in hepatic homogenate. The histopathological analysis showed that the grade of liver injury was ameliorated with reduction of inflammatory cells and necrosis of liver cells in Homoplantaginin treatment mice.