Anti-tumor activity of tanshinone IIA in combined with cyclophosphamide against Lewis mice with lung cancer

ABSTRACT

Objective To explore the anti-tumor activity of tanshinone IIA in combined with cyclophosphamide against Lewis mice with lung cancer and the effect on cellular immune function. Methods Lewis tumor cells were inoculated subcutaneously into the right armpit of mice in each group (n = 20) to establish Lewis lung cancer mice model. After model establishment, mice in the model group were given normal saline by lavage, qd. Mice in treatment I group were given intraperitoneal injection of Tan IIA, 15 mg/kg, qd. Mice in treatment II group were given intraperitoneal injection of CTX, 25 mg/kg, qd. Mice in treatment III group were given intraperitoneal injections of Tan IIA and CTX, in which the administration method of Tan IIA was the same as in treatment I group, continuously for 2 weeks, and the dosage of CTX was the same as in treatment II group, 24 h after model establishment, every other day. Mice were sacrificed 2 weeks after establishment. The tumor tissues were collected to calculate the anti-tumor rate. Immunohistochemistry was used to detect the expressions of Bcl-2, Bax, VEGF, Angiostatin, and Endostatin. FCM was used to detect T lymphocyte subsets in spleen and liver of mice. Results The tumor weight in treatment I, II, and III groups was significantly lower than that in the model group (P < 0.05). The tumor weight in treatment III group was significantly lower than that in treatment I and II groups (P < 0.05). The anti-tumor rate in treatment II and III groups was significantly higher than that in treatment I group (P < 0.05). Bcl-2 expression in the tumor tissues of treatment I, II, and III groups was significantly lower than that in the model group (P < 0.05), while Bax expression was significantly higher than that in the model group (P < 0.05). Bcl-2 expression in the tumor tissues of treatment I and II groups was significantly higher than that in treatment III group (P < 0.05), while Bax expression was significantly lower than that in treatment III group (P < 0.05). CD4