Xiaokai Zhang1, Jianwei Jiang2, Zhiwei Chen3, Mingrong Cao4. 1. Department of General Surgery, The First People's Hospital of Nanyang City, Nanyang, Henan 473000, China. Electronic address: huojiege_md@163.com. 2. Department of Biochemistry, Medical College, Jinan University, Guangzhou, Guangdong 510630, China. 3. Department of General Surgery, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong 510630, China. 4. Department of General Surgery, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong 510630, China. Electronic address: panyingying_md@126.com.
Abstract
BACKGROUND: Previous investigation have indicated Silibinin induces apoptosis and JNK/SAPK in human pancreatic cancer cells. This study aims to evaluate the further mechanism of Silibinin in pancreatic cancer treatment. MATERIALS AND METHODS: Human pancreatic cancer cell lines SW1990 was treated with Silibinin and/or JNK/SAPK inhibitor SP600125 followed by measurement of cell viability, apoptosis, autophagy, ROS and ATP, and western blotting. RESULTS: Silibinin promoted cell viability and promoted cell apoptosis. The expression of ROS and ATP associated with mitochondrial function was also promoted by the treatment of silibinin. Silibinin also promoted autophagy in pancreatic cancer cells. All these biological effects of Silibinin can be reversed by JNK/SAPK inhibitor. CONCLUSIONS: The biological effects regulated by Silibinin can be mediated by JNK/SAPK signaling. This provides a solid theoretical basis for the role of Silibinin in the treatment of pancreatic cancer.
BACKGROUND: Previous investigation have indicated Silibinin induces apoptosis and JNK/SAPK in humanpancreatic cancer cells. This study aims to evaluate the further mechanism of Silibinin in pancreatic cancer treatment. MATERIALS AND METHODS:Humanpancreatic cancer cell lines SW1990 was treated with Silibinin and/or JNK/SAPK inhibitor SP600125 followed by measurement of cell viability, apoptosis, autophagy, ROS and ATP, and western blotting. RESULTS:Silibinin promoted cell viability and promoted cell apoptosis. The expression of ROS and ATP associated with mitochondrial function was also promoted by the treatment of silibinin. Silibinin also promoted autophagy in pancreatic cancer cells. All these biological effects of Silibinin can be reversed by JNK/SAPK inhibitor. CONCLUSIONS: The biological effects regulated by Silibinin can be mediated by JNK/SAPK signaling. This provides a solid theoretical basis for the role of Silibinin in the treatment of pancreatic cancer.