ABSTRACT
Objective: To observe the antitumor effect of triptolide in the human pancreatic cancer tumor-bearing nude mice, and to explore its molecular mechanism. Methods: The healthy BALB/ c nude mice were selected and transplanted with the human pancreatic cancer SW1990 cells into the skin of the right hind limb to establish the tumor-bearing model of nude mice. The successful modeling nude mice were divided into model group, gemcitabine group and triptolide group, 10 in each group; another 10 healthy nude mice were selected as control group. The tumor tissue of SW1990 pancreatic cancer tumor-bearing nude mice were weighed and the inhibitory rate of tumor was calculated. The expressions of apoptosis-related proteins Bax and bcl-2 in the pancreas tissue of the nude mice in each group were detected by rmmunohistochemistry. The expression levels of Bax, bcl-2, Caspase-9 and Caspase-3 in the pancreas tissue of the nude mice in each group were detected by Western blotting method. Results: Compared with gemcitabine group, the inhibitory rate of tumor of SW1990 pancreatic cancer in triptolide group was significantly increased (P < 0. 05). The HE staining results showed that compared with model group, the proliferation of pancreatic cancer tumor cells in triptolide group was inhibited. The immunohistochemistry results showed that the expression level of Bcl-2 in the pancreas tissue and the Bcl-2 /Bax ratio of the nude mice in tripptolide group were lower than those in model group (P < 0 . 05). The Western blotting results showed that compared with model group, the expression levels of Bax, Caspase-9 and Caspase-3 in the pancreas tissue of the nude mice in triptolide group were significantly increased (P < 0 . 05), while the expression level of Bcl-2 was significantly decreased (P < 0 . 05). Conclusion: Triptolide can inhibit the growth of tumor tissue in the nude mice; its mechanism may be related to inhibiting the activation of Bcl-2 in pancreatic tumor tissue, promoting the expression of Bax, reducing the ratio of Bcl-2 /Bax, promoting the activation of Caspase-9 and Caspase-3, and inducing the apoptosis of pancreatic cancer transplanted tumor cells.