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机构地区:[1]宁夏医科大学,银川750004 [2]宁夏医科大学总医院中医科,银川750004
出 处:《宁夏医科大学学报》2013年第6期635-639,3,共6页Journal of Ningxia Medical University
基 金:国家自然科学基金(81160432)
摘 要:目的研究清脉饮及其拆方含药血清对肿瘤坏死因子α(TNF-α)诱导的肠系膜下动脉血管内皮细胞Ealy926的保护作用。方法制备含药血清;对体外培养的Ealy926细胞,随机分为正常对照组、低剂清法组(5%、10%、15%)、中剂清法组(5%、10%、15%)、高剂清法组(5%、10%、15%)、活血组、全方组、软坚组、西药组、TNF-a损伤组等。不同浓度含药血清与TNF-α共同处理24h后,MTT比色法检测Ealy926细胞增殖变化,流式细胞术Annexin V/PI双标法测定Ealy926细胞凋亡。结果与正常对照组比较,TNF-a损伤组细胞增殖显著降低(P<0.05),细胞凋亡率显著增加(P<0.05);其他含药血清组与TNF-a损伤组比较细胞增殖明显增加(P<0.05),细胞凋亡率显著降低(P<0.05);各含药血清组之间两两比较,10%中剂清法组细胞增殖率明显高于活血组(P<0.01)。结论清脉饮及其拆方含药血清可提高TNF-α损伤的血管内皮细胞的增殖,降低其细胞的凋亡率,其机制可能与抑制TNF-a的促炎症作用有关。Objective To explore the protective effect of Qingmaiyin and its decomposed formulas medicated serum on the inferior mesenteric artery endothelial cell(Ealy926) induced by tumor necrosis factor-α(TNF-α).Methods Preparation medicated serum;Ealy926 cells were incubated in vitro and divided into 15 groups of normal control group,the low dose Qingfa group(5%,10%,15%),the normal dose Qingfa group (5%,10%,15%),the high dose Qingfa group(5%,10%,15%).activating blood group,all -party group, Ruanjian group,medicine group,TNF-αinjury group.Different concentrations of medicated serum activated with TNF-αfor 24 hours,Ealy926 cell proliferation was detected by MTT method and Ealy926 cell apoptosis was detected by Annexin V/PI double labled flow cytometry.Results Compared with the normal control group,the cell viability of TNF-αinjury group decreased significantly(P < 0.05) and the rate of apoptosis was significantly increased(P<0.05).Compared with TNF-αinjury group,the cell viability of the other medicated serum was significantly increased(P <0.05) and the rate of apoptosis was significantly lower(P < 0.05).Pairwise comparisons between each medicated serum showed that proliferation rate in 10%detergent Qingfa group was significantly higher than that in the blood group(P <0.01).Conclusion Qingmaiyin and its decomposed formulas medicated serum can increase the proliferation and reduce the apoptosis rate of endothelial cells in TNF-αinjury,by which its mechanism may be related to the inhibition of TNF-αpro - inflammatory role.
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