摘要
Objective： To investigate the possible mechanism through which Artemisinin induced apoptosis in pancreatic cell line. Methods： Column chromatography, thin layer chromatography （TLC） and proton NMR spectroscopy were used to purify Artemisinin. The flowcytometry was employed to detect apoptosis and reactive oxygen species （ROS）. Results： The results indicated that 50% inhibiting concentration （ICso value） for pancreatic cell line （RIN） was 45 μmol/L of Artemisinin. Artemisinin had no cytotoxic effect on the growth of peripheral blood lymphocytes. The mechanism of apoptosis was evaluated by measuring intraceliular ROS. It was shown that Artemisinin-induced apoptosis occurred independently of the binding of CD95L to CD95 receptor in the RIN cells. Moreover, Artemisinin, in a dose-dependent manner, could significantly increase the level of ROS. Conclusion： Artemisinin can induce apoptosis in the RIN cells via the generation of ROS and triggering the intrinsic pathway of cell death.
Objective： To investigate the possible mechanism through which Artemisinin induced apoptosis in pancreatic cell line. Methods： Column chromatography, thin layer chromatography （TLC） and proton NMR spectroscopy were used to purify Artemisinin. The flowcytometry was employed to detect apoptosis and reactive oxygen species （ROS）. Results： The results indicated that 50% inhibiting concentration （ICso value） for pancreatic cell line （RIN） was 45 μmol/L of Artemisinin. Artemisinin had no cytotoxic effect on the growth of peripheral blood lymphocytes. The mechanism of apoptosis was evaluated by measuring intraceliular ROS. It was shown that Artemisinin-induced apoptosis occurred independently of the binding of CD95L to CD95 receptor in the RIN cells. Moreover, Artemisinin, in a dose-dependent manner, could significantly increase the level of ROS. Conclusion： Artemisinin can induce apoptosis in the RIN cells via the generation of ROS and triggering the intrinsic pathway of cell death.
