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机构地区:[1]青岛大学公共卫生学院,山东青岛266021 [2]青岛市城阳区人民医院感染科 [3]青岛大学附属医院神经外科
出 处:《齐鲁医学杂志》2015年第4期423-425,429,共4页Medical Journal of Qilu
基 金:产学研合作引导计划:应用基础研究(10-3-4-3-11-jch)
摘 要:目的通过观察海兔素对小鼠脑胶质瘤异位移植瘤血管内皮生长因子(VEGF)、表皮生长因子受体(EGFR)及环氧化酶-2(COX-2)表达影响,探讨其对脑胶质瘤的抑制作用。方法将75只昆明种小鼠于左前腋下皮下接种1×10^9/L胶质瘤细胞悬液,24h后随机分为5组,每组15只。脑胶质瘤异位移植瘤模型组(A组)小鼠以等体积大豆色拉油灌胃,海兔素低剂量组(B组)以50 mg/(kg·d)剂量海兔素灌胃,海兔素中剂量组(C组)以100mg/(kg·d)剂量海兔素灌胃,海兔素高剂量组(D组)以150mg/(kg·d)剂量海兔素灌胃,替莫唑胺(TMZ)阳性对照组(E组)以20mg/(kg·d)剂量TMZ灌胃,每天灌胃1次,连续给药2周。末次灌胃24h后,称体质量,经眼球取血后处死小鼠。无菌条件下剥离肿瘤组织,免疫组化法测定肿瘤组织中VEGF、EGFR及COX-2的表达情况。结果与A组比较,B、C、D组随着海兔素剂量的增加,VEGF、EGFR、COX-2的表达均有逐渐降低趋势,各组间比较,除D组与E组差异无显著性外,其他各组间差异均有显著性(H=22.21~24.69,U=4.50~16.00,P〈0.05)。结论海兔素可抑制小鼠脑胶质瘤异位移植瘤生长,其作用机制可能与抑制小鼠脑胶质瘤异位移植瘤组织VEGF、EGFR及COX-2的表达有关。Objective To observe the inhibition of aplysin on the expressions of VEGF,EGFR and COX-2in glioma heterotopic transplanted tumor(GHTT)in mice. Methods Seventy-five Kunming mice were given subcutaneous inoculation of1×10^9 cell/L glioma-cell suspension on left armpit to create a GHTT model in mice and evenly randomized to five groups-group A(GHTT model group),the mice in this group were given equal-volume soybean salad oil;group B(low-dose aplysin group),aplysin 50mg/(kg·d);group C(medium-dose aplysin group),100 mg/(kg·d)aplysin;group D(high-dose aplysin group),150mg/(kg·d)aplysin;group E(temo-zolomide group),temo-zolomide(TMZ)20mg/(kg·d),all were given intragastrically,once a day for two weeks.After 24 hof the last gavage,the weight of mice was measured,blood was taken from eyeball.Tumors were dissected under sterile condition.The expressions of VEGF,EGFR and COX-2in tumor tissue were detected using immunohistochemical method. Results Compared with group A,the expressions of VEGF,EGFR and COX-2in groups B,C and D showed a gradual decline along with the increase of aplysin dose,the differences among each groups were significant,except that between groups D and E(H =22.21-24.69,U=4.50-16.00,P〈0.05). Conclusion Aplysin can inhibit the growth of glioma heterotopic transplantation tumor,its mechanism is likely to be associated with restraining the expressions of VEGF,EGFR and COX-2in mouse's glioma.
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