Moscatilin suppresses the inflammation from macrophages and T cells
Ying Zhang, Yugang Xu, Xiujie Jing, Wenkui Lu, Fusen Zhang, Chengkun Qin
Abstract
Abstract In this study, we aim to investigate moscatilin in alleviating symptoms of autoimmune liver disease (ALD) in a concanavalin A (ConA)-induced liver injury mouse model and elucidate the underlying mechanisms. ALD mouse models were constructed by intravenous injection of ConA (20 mg/kg) and the serum level of alanine aminotransferase (ALT) was measured using an enzyme-linked immunosorbent assay. Moscatilin in various doses was administered for two days starting from a day before the ConA injection. We showed that moscatilin dose-dependently decreased ALT levels in liver tissue of ALD mouse models. Ifng and Tnfa also showed significant downregulation in liver tissues. Macrophages only showed significant Tnfa downregulation and CD4 + T cells only showed significant Ifng downregulation at high moscatilin doses. In vivo administration of moscatilin induced interleukin-37 upregulation in hepatic tissues. In vitro , moscatilin also induced IL-37 upregulation in hepatic stellate cell line JS-1 rather than immune cells represented by RAW264.7 and CTLL-2 cell lines, suggesting that the hepatic stellate cell is majorly responsive to moscatilin treatment in terms of interleukin (IL)-37 upregulation. Our data indicate that moscatilin could alleviate liver injury in ConA-induced ALD mouse models through anti-inflammatory activities, warranting further development of moscatilin as a new drug in treating ALD.