女贞子多糖对H22荷瘤小鼠的抗肿瘤作用及机制研究OA

Objective:To investigate the antitumor effect and mechanism of Ligustrum lucidum polysaccharide in H22 tumor-bearing mice.Methods:The mouse model of H22 hepatocellular carcinoma was established.After 14 days of continuous administration,mice were dissected and tumor weights were measured to calculate the tumor inhibition rate.Serum levels of tumor necrosis factor(TNF)-α,interleukin(IL)-6,and interferon(IFN)-γ were determined by ELISA.Annexin-V-PE/7AAD dual-staining flow cytometry was employed to assess tumor cell apoptosis and expression of the au-tophagy and apoptosis marker microtubule-associated protein 1 light chain 3 A/B(LC3A/B).Western blot was em-ployed to evaluate the expression levels of the anti-apoptotic protein B-cell lymphoma 2(Bcl2),the pro-apoptotic protein Bcl2-associated X protein(Bax),LC3Ⅱ/Ⅰ,beclin1,protein kinase B(AKT),and mammalian target of rapamycin(mTOR).Results:L.lucidum polysaccharide exhibited significant antitumor activity,achieving a tumor inhibition rate of 50.83%.Compared with the model group,the L.lucidum polysaccharide(20 mg/kg)group showed decline serum levels of TNF-α,IL-6,and IFN-γ(P<0.01 or P<0.05),increased tumor cell apoptosis,up-regulated Bax expression,and down-regulated Bcl2 expression(P<0.05).In addition,this group showed increases in the percentage of LC3A/B and LC3Ⅱ/Ⅰ,and the expression levels of beclin1,reduces in the expression levels of AKT and mTOR(P<0.05,P<0.01).Conclusion:L.lucidum polysaccharide can inhibit the tumor growth and promote the tumor cell apoptosis and auto-phagy in H22 tumor-bearing mice by inhibiting the AKT-mTOR signaling pathway.