Kaempferol Protects Against Acetaminophen-Induced Acute Liver Injury by Inhibiting Oxidative Stress, Inflammation and Apoptosis in Mice

Acetaminophen (APAP) is a widely used analgesic and antipyretic drug in the clinic, but excessive amounts of APAP can result in liver damage. However, APAP-induced acute liver injury lacks effective treatment. In this study, acetaminophen-treated mice were used as a model to explore the efficacy of kaempferol as an antioxidation, anti-inflammatory and anti-apoptotic agent and to explore its efficacy in the treatment of APAP-induced acute liver injury. In this study, 50 mice were randomly divided into 5 groups: group I, the negative control, was fed hydroxymethyl cellulose sodium; group II was treated with 300 mg/kg acetaminophen; group III was intraperitoneally injected with 20 mg/kg kaempferol; groups IV and V were injected and fed 20 mg/kg kaempferol, respectively, 1 h after receiving a dose of 300 mg/kg acetaminophen. We found that kaempferol could significantly inhibit the increase in ALT and AST in the serum and TNF-alpha and IL-6 in the liver. In addition, kaempferol up-regulated the mRNA expression levels of antioxidant factors SOD2 and Nrf2 and down-regulated the mRNA expression levels of TNF-alpha, IL-6 and TLR4 in the liver injury model. In addition, we found that kaempferol could reduce bax and increase bcl-2 and procaspase-3. These results suggest that kaempferol can protect against APAP-induced liver toxicity by inhibiting oxidative stress, inflammatory response, and apoptosis pathways.