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目的从中性粒细胞浸润的角度,探讨中药清肠栓治疗溃疡性结肠炎(UC)急性期的作用机理。方法 SD大鼠48只,分为正常组、模型组、清肠栓组和柳氮磺胺吡啶(SASP)组,每组各12只。用三硝基苯磺酸(TNBS)诱导大鼠UC急性期模型。造模后第3日开始给药,连续给药7d后处死。记录病变结肠组织损伤指数;组织病理学观察结肠黏膜病理变化及中性粒细胞浸润情况;Elisa检测血清及结肠组织中的髓过氧化物酶(MPO)、中性粒细胞弹性蛋白酶(NE)含量。结果动物模型病理观察有大量炎症细胞浸润(以中性粒细胞和淋巴细胞为主);清肠栓组及SASP组可见组织修复征象;血清中MPO含量各组差异无统计学意义;血清中NE含量正常组与模型组差异无统计学意义;组织上清中MPO及NE模型组较正常组明显增高,清肠栓组和SASP组较模型组降低。结论清肠栓对大鼠TNBS诱导的急性UC模型有治疗作用,能够减轻UC急性期结肠黏膜大量中性粒细胞浸润的状态,促进组织修复,并通过调节MPO、NE的蛋白表达,减少这两种物质对组织的损伤。 相似文献
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药穴结合治疗对溃疡性结肠炎患者血小板功能状态影响的临床观察 总被引:1,自引:0,他引:1
目的:观察药穴结合对溃疡性结肠炎(UC)患者血小板功能状态(CMP-140、TXB2)的影响。方法:将262例UC患者随机分为4组。中药组45例口服中药方【黄芪、蒲黄(包)、党参、茯苓、厚朴、荔枝核、白术、川芎、木香、三七粉(冲)】。耳穴组48例取脾、大肠、内分泌、交感、皮质下,以王不留行籽贴在耳穴上。药穴组89例在口服中药同时加耳穴贴压。对照组80例口服柳氮磺胺吡啶2.0g。分别测定治疗前后CMP一140、TXB:的含量。结果:药穴组CMP-140、TXB:治疗后显著降低,与治疗前比较,差异有非常显著性意义(P〈0.01);治疗后药穴组与对照组、中药组比较,差异有显著性意义(P〈0.05)。提示药穴组能明显降低CMP-140、TXB2含量。总有效率药穴组与中药组、耳穴组、对照组比较,差异均有显著性意义(P〈0.05);中药组、耳穴组、对照组3组比较,差异无显著性意义(P〉0.05)。提示药穴组疗效明显优于其他3组。结论:药穴结合能明显降低CMP-140、TXB:的含量,对UC有较好治疗作用。 相似文献
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Objective:To evaluate the effects of the ethanol extract isolated from Weiqi Decoction(胃祺饮,WQD-EE)on AGS cell proliferation and apoptosis.Methods:By using high-performance liquid chromatography with ultraviolet detectors(HPLC-UV)assay and MTT method,the main compounds in WQD-EE and cell viability were detected.And cell cycle distributions were determined by flow cytometry with propidium iodine(PI)staining while apoptosis was detected by flow cytometry with annexin V/Pl double staining.Finally,caspase-3 activities were measured by calorimetric method and protein expression was determined by Western blotting.Results:HPLC analysis showed that naringin(35.92μg/mg),nobiletin(21.98μg/mg),neohesperidin(17.98μg/mg)and tangeretin(0.756μg/mg)may be the main compounds in WQD-EE.WQD-EE not only inhibited AGS and MCF7 cell proliferation in a dose-dependent manner,but also blocked cell cycle progression at G_2/M stage as well as inducing cell apoptosis at concentrations triggering significant inhibition of proliferation and cell cycle arrest in AGS cells.While at 0.5 mg/mL,WQD-EE significantly increased caspase-3 activity by 2.75 and 7.47 times at 24 h and 48 h,respectively.Moreover,WQD-EE in one hand reduced protein expressions of p53 and cyclin B1,and in other hand enhanced protein expressions of cytochrome c and Bax.Protein levels of Bcl-2,Fas L and Fas were not significantly affected by WQD-EE.Conclusions:WQD-EE inhibits AGS cell proliferation through G_2/M arrest due to down-regulation of cyclin Bi protein expression,and promotes apoptosis by caspase-3 and mitochondria-dependent pathways,but not by p53-dependent pathway. 相似文献
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