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IL-17 enhances oxidative stress in hepatocytes through Nrf2/keap1 signal pathway activation.

Hepatic disease is common worldwide. As apoptosis of hepatocytes is a hallmark of hepatic disease, strategies targeting apoptosis are an effective way to prevent and treat the disease. Oxidative stress is a classic pathway of apoptosis. Increased expression of IL-17 has been found in diverse human liver diseases. The aim of this research was to investigate whether the function of IL-17 influenced hepatocyte-induced H2O2. We found that the expression of IL-17 was enhanced in hepatocyte-induced H2O2 and that IL-17 was down-regulated by siRNA. A TUNEL assay showed that apoptosis was decreased in ΔIL-17-mutant hepatocyte-induced H2O2. Additionally, the ratio of Bax/Bcl-2 was decreased in ΔIL-17-mutant hepatocyte-induced H2O2. Finally, Nrf2/keap1 signal pathway was analyzed, the expression of Nrf2 and keap1 was decreased in ΔIL-17-mutant hepatocyte-induced H2O2. These results suggest that oxidative stress-induced apoptosis was induced and that IL-17 could enhance oxidative stress-induced apoptosis by the Nrf2/keap1 signal pathway in hepatocytes.