【摘 要】
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Aim To investigate the antitumor activities and mechanisms of sodium rosmarinate against hepatocellular carcinoma.Methods Antitumor activities of sodium rosmarinate were measured on HepG2, HNE, K562,H
【机 构】
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Dept of Pharmacology,West China College of Preclinical and Forensic Medicine,Sichuan University,Chen
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Aim To investigate the antitumor activities and mechanisms of sodium rosmarinate against hepatocellular carcinoma.Methods Antitumor activities of sodium rosmarinate were measured on HepG2, HNE, K562,HCT116, and SW480 cells by MTT assay in vitro at 5 mg · L1, 25 mg · L1, and 50 mg · L1 Nude mice and H22 cells were employed to establish a liver tumorbearing murine model.Sodium rosmarinate were intraperitoneally administered at 25 mg · kg1 and 50 mg · kg1 for 10 days.Body weights, organ indexes, white blood cells,lymphocytes, and neutrophils of peripheral blood were measured.Murine tumors were histologically stained.TNFα and IFNγin serum were detected by ELISA.Expressions of Caspase3, Bcl2, Bax, Sirtl, NFκB p65, NFκB p50, and pIκBo were measured by realtimePCR and Western blot.Results Sodium rosmarinate showed obvious inhibition on proliferation of HepG2 cells at 5 mg · L1.But no inhibition effects were observed on HNE,K562, HCT116, and SW480 cells.Body weights and organ indexes of nude mice with H22 ceils were not changed by sodium rosmarinate.But sodium rosmarinate showed significant inhibition rate at 25 mg· kg1 (45.67%) and50 mg· kg1 (52.82%).Necrosis was aggregated by sodium rosmarinate as shown by H&E staining.TNFα and IFNγin murine serum were significantly increased by sodium rosmarinate at both doses (P < 0.05).Expressions of caspase3 were significantly increased (P < 0.01).Sodium rosmarinate were shown to increase expressions of Bax, decrease expressions of Bcl2, and significantly decrease Bacl2/Bax ratio to induce apoptosis.Expressions of Sirt1, NFκB p65, NFκB p50, and pIκBα were all decreased dosedependently.Discussion Sodium rosmarinate were demonstrated to inhibit hepatocellular carcinoma in vivo and in vitro through upregulating TNFα, IFNγ, Bcl2/Bax ratio, and downregulating Sirt1 and NFκB related genes dose dependently, which may be developed a promising drug for treatment of hepatocellular carcinoma.
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