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机构地区:[1]广东省人民医院/广东省医学科学院药学部,广州510080
出 处:《中国药房》2016年第34期4811-4813,共3页China Pharmacy
摘 要:目的:探讨紫草多糖是否通过诱导自噬而抑制H_(22)肝癌实体瘤细胞的增殖。方法:将40只KM小鼠随机分为模型组、环磷酰胺组(阳性药物,30 mg/kg,ip,每4 d给药1次)和紫草多糖低、高剂量组(100、300 mg/kg,ig,每天给药1次),每组10只。各组小鼠均腋下接种H_(22)细胞株复制H_(22)肝癌实体瘤模型,造模同时各给药组小鼠给予相应药物,模型组小鼠ig等体积生理盐水。末次给药后,记录并测定小鼠体质量、瘤质量系数和胸腺、脾脏指数;采用实时荧光定量聚合酶链式反应法测定小鼠瘤组织中自噬相关基因Atg5、Beclin1 m RNA表达水平;Western blot法测定瘤组织中自噬微管相关蛋白1轻链3A/B(LC3A/B)蛋白表达水平。结果:紫草多糖可显著降低H_(22)实体瘤小鼠的瘤质量系数,抑瘤率达34.7%;可显著上调瘤组织中自噬相关基因Atg5、Beclin1 m RNA的表达和LC3A/B蛋白的表达,较模型组差异均有统计学意义(P<0.05或P<0.01)。结论:紫草多糖通过促进肝癌细胞的自噬,从而抑制H_(22)肝癌实体瘤细胞的增殖、延缓肿瘤生长。OBJECTIVE:To investigate whether Lithospermum erythrorhizon polysaccharide inhibit the proliferation of H22 hepatoma solid tumor cells in mice through inducing autophagy.METHODS:40 KM mice were randomly divided into model group,cyclophosphamide group(30 mg/kg,ip,once for every 4 d),L.erythrorhizon polysaccharide low-dose and high-dose groups(100,300 mg/kg,ig,once a day),with 10 mice in each group.H22 hepatoma solid tumor model was induced of mice in each group by incubating H22 cell line.Treatment groups were given relevant medicine during modeling,and model group was given constant volume of normal saline intragastrically.After last medication,body weight,tumor weight coefficient,thymus and spleen index were recorded and determined.The m RNA expression of autophagy related genes,such as Atg5 and Beclin1,were measured by using Real-time PCR.The protein expression of autophagic microtubule-associated protein 3A/B(LC3A/B) was detected by Western blot assay.RESULTS:L.erythrorhizon polysaccharide could significantly reduce tumor weight coefficient of H22 solid tumor,with tumor inhibitory rate of 34.7%;it also significantly up-regulated the m RNA expression of autophagy related genes Atg5 and Beclin1 and the protein expression of LC3A/B,with statistical significance compared to model group(P〈0.05 or P〈0.01).CONCLUSIONS:L.erythrorhizon polysaccharide can inhibit the proliferation of H22 hepatoma solid tumor cells and slow down the growth of tumor through promoting hepatoma cell autophagy.
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