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作 者:乔星[1] 刘黎明 马少林[1] 赵阳[1] 秦涛[1]
机构地区:[1]新疆医科大学第一附属医院烧伤整形科,乌鲁木齐830054
出 处:《新疆医科大学学报》2017年第12期1592-1597,共6页Journal of Xinjiang Medical University
基 金:新疆维吾尔自治区医学联合项目(2015211C062)
摘 要:目的探讨维药异常黑胆质成熟剂(abnormal savdamunziq,ASMq)对体外培养萎缩性瘢痕细胞增殖的抑制作用及其通过TGF-β1/Smad通路介导的作用机制,为萎缩性瘢痕的治疗提供理论依据。方法对酶消法消化手术切取的萎缩性瘢痕细胞进行培养,将其分成空白对照组和ASMq处理组(0.25、0.5、0.75和1.0mg/mL的药物干预处理),用倒置显微镜观察其细胞形态及数量变化;应用CCK-8法检测各组细胞增殖情况;采取QtimePCR和Western blot法检测TGF-β1/Smad通路相关mRNA及蛋白的表达。结果与空白对照组比较,AMSq处理组在浓度为0.25mg/mL至1.0mg/mL的范围内,随着浓度的递增,细胞数不断减少;TGF-β1、CollagenⅠ和CollagenⅢmRNA表达量呈递减趋势,Smad7mRNA的表达逐渐增多,差异有统计学意义(P<0.05);与空白对照组比较,随着ASMq浓度增加,TGF-β1、CollagenⅠ和CollagenⅢ蛋白表达量减少,随着ASMq浓度逐渐增加,抑制性Smad7蛋白表达量增多,差异有统计学意义(P<0.05)。结论 ASMq可通过增强负反馈因子Smad7在TGF-β1/Smad通路中的作用,起到抑制萎缩性瘢痕细胞增殖及其表达各类胶原效应。Objective To study the inhibited effect of abnormal savda munziq(ASMq)on atrophic scar cell proliferation in vitro and the mechanism mediated by TGF-β1/Smad pathway,and provide a new evidence for the clinical treatment of atrophic scar.Methods In vitro atrophic scar fibroblasts were digested by type I collagenase,and they were divided into blank control group(serum-free DMEM medium)and ASMq groups(0.25,0.5,0.75 1.0 mg/mL drug intervention)to determine the changes in cell proliferation with CCK-8 assay;the relative mRNA and protein levels of TGF-β1/Smad pathway were detected by QtimePCR and Western Blot assay.Results Compared with the blank control group,the cell viability was decreasing at the concentration of 0.25 mg/ml to 1.0 mg/ml of AMSq.Compared with the blank control group,the mRNA and protein expression levels of TGF-β1,collagenⅠand collagenⅢreduced gradually in dose-dependent manner,whereas the mRNA and protein expression level of Smad7 mRNA elevated gradually in dose-dependent manner,which the difference was statistically significant(P <0.05).Conclusion Compared with the blank group,ASMq suppressed fibroblast proliferation and atrophic scar through enhanced the role of Smad7(negative feedback factor)in the pathway.
关 键 词:异常黑胆质成熟剂 萎缩性瘢痕 TGF-β1/Smad通路
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