Anticancer Effect and Mechanism of Plumbagin on Lewis Lung Carcinoma in Vitro and in Vivo / 中国药学杂志

ABSTRACT

OBJECITVE To study the inhibitive effect of plumbagin on Lewis lung cancer. METHODS: Cell proliferation was determined by CCK8 assay. Apoptosis was determined by flow cytometry. The expression of Bcl-2 and VEGF protein was studied by Western blot assay. The model of C57BL/6 mice bearing Lewis lung cancer was established by subcutaneous seeding of Lewis lung cancer cells, and randomly divided into 5 groups (n = 6). Tumor-bearing mice were injected with normal saline, plumbagin(low, medium, high dose) or cyclophosphamide (CTX) in each group. The tumor volume was measured. All mice were sacrificed on Day 22nd under aseptic condition for the tumor collection. The transplanted tumors were weighed for calculation of the tumor inhibition rate; Immunohistochemical method was applied to assessing the VEGF expression in tumor tissue. RESULTS CCK-8 assay showed that plumbagin had an obvious inhibition on Lewis lung carcinoma cells line in a dose-dependent manner(r = 0.953, P < 0.05). Plumbagin significantly increased cell apoptosis rate(P<0.05). The protein levels of Bcl-2 and VEGF were significantly reduced by plumbagin (0, 2.5, 5, 10 μmol·L-1) treatment(P < 0.05). In plumbagin(low, medium, high dose) groups and CTX group, the tumour volume, tumour weight and the expression of VEGF were significantly less than those in the control group (P < 0. 05). CONCLUSION: The plumbagin effectively inhibits Lewis lung carcinoma cells proliferation and tumor growth of Lewis lung carcinoma cells in mice. The mechanism involved is down-regulating the expression of Bcl-2, VEGF and inducing cell apoptosis.