排序方式: 共有8条查询结果,搜索用时 15 毫秒
1
1.
2.
Objective To investigate the mechanism of telomere shortening through 8-methoxypsoralen(8-MOP)and subsequent ultraviolet A(UVA)irradiation-induced photoaging model in human dermal fibroblasts(HDFs).Methotis Photoaging model was established by 8-MOP+UVA in skin HDFs.Flow cytometer.enzyme eytochemistry,immunofluorescence,Westem blot and Real-time PCR were employed.Results The percentage of G1 blockage of 8-MOP+UVA group were higher than that of control group at 24、48、72 h and 7 d(61.4%±1.5% vs 32.8%±1.5%.69.5%±2.2% vs 44.9% ±2.3%.88.2%±1.6% vs 59.8%±1.4%,90.7%±2.5% vs 68.5%±2.6%.all P<0.01).The expression of SA-β-Gal of 8-MOP+UVA group were higher than that of control group at 24、48、72 h and 7 d(34.87%±0.59% vs 7.11%±0.78%,59.38%±0.46% vs 10.57%±0.47%.72.46%±0.98% vs 11.67%±0.87%,94.33%±0.13% vs 12.04%±0.12%,all P<0.01).8-MOP+UVA treatment could significantly aggravate the oxidative DNA damages,the percentage of 8-oxo-dG positive cell of 8-MOP+UVA group(95.78%±0.14%)were significantly higher than that of control group(7.69%±0.09%,P<0.01),8-MOP group(9.76%±0.11%,P<0.01)and UVA group(35.29%±0.14%,P<0.05).8-MOP+UVA treatment could accelerate the telomere shortening.the relative length of telomere of 8-MOP +UVA group were 2.57±0.05 lower than that of control group(6.63±0.12.P<0.01).The levels of P53,P21WAF-1 and P16INK-4a of 8-MOP+UVA group were higher than that of control group(3.00±0.88 vs 0.54±0.10,2.50±0.51 vs 0.42±0.06,2.21±0.34 vs 0.38±0.05,all P<0.01).Conclusion 8-MOP+UVA-induced photoaging of HDFs can be mediated though the regulation of telomere and subsequent P53-dependent signaling pathways. 相似文献
3.
目的:客观评价参芪扶正注射液治疗慢性肾功能衰竭(CRY)的疗效及安全性。方法:临床观察随机分组,治疗组(120例)给予参芪扶正注射液,对照组(60例)给予尿毒清;实验研究选取雌、雄性小鼠,随机分为正常对照组,模型组和参芪扶正注射液药物大、小剂量组,分别做负重游泳、灌胃急毒、动物模型治疗。结果:临床疗效治疗组明显优于对照组;实验动物无急性毒性反应,大剂量能显著提高小鼠抗疲劳能力及免疫功能,能较好地改善肾功能。结论:参芪扶正注射液无毒副作用,能维护和改善肾功能,从而延缓慢性肾功能衰竭的进程和延长病人的寿命。 相似文献
4.
5.
6.
1928年,美国微生物学家弗莱明发现了青霉素,并于20世纪40年代在美国研制成功,投入市场,从此进入了抗生素时代。半个多世纪以来,人类不断地研究、生产各种抗生素,而微生物(主要为细菌)也不断对抗生素产生耐药。肿瘤药人由于本身体质的原因,加上放疗、化疗以及免疫抑制剂的使用,极易出现由条件致病菌或耐药菌造成的院内感染,甚至出现院内感染暴发流行,严重威胁病人的健康和生命。为了使抗感染治疗获得最佳疗效。减少耐药菌株的产生。降低院内感染率,加强对抗生素的合理使用至关重要。按照卫生部《医院感染管理规范》的要求,我们对肿瘤病人抗生素的使用情况进行了摸底调查。 相似文献
7.
EGCG对中波紫外线诱导HaCaT细胞p53基因和蛋白表达的实验研究 总被引:1,自引:0,他引:1
目的:研究表没食子儿茶素没食子酸酯(EGCG)对中波紫外线(UVB)照射诱导永生化角质形成细胞株-HaCaT细胞的p53 mRNA和p53蛋白表达的影响。方法:以一定剂量UVB照射HaCaT细胞,并以200μg/mL EGCG处理照射后的HaCaT细胞,分别用RT-PCR法和Western blot方法检测各处理条件下p53 mRNA和/或p53蛋白的表达水平。结果:30 mJ/cm2的UVB照射后HaCaT细胞的p53 mR-NA和p53蛋白表达逐渐增加,4 h达到峰值,4 h后随照射剂量增加而增加,24 h后有所恢复;加入EGCG可下调UVB诱导的表达作用。结论:UVB照射对HaCaT细胞p53 mRNA和p53蛋白的诱导表达有时效性与量效性,EGCG可下调UVB照射的这种诱导作用。 相似文献
8.
Objective To investigate the mechanism of telomere shortening through 8-methoxypsoralen(8-MOP)and subsequent ultraviolet A(UVA)irradiation-induced photoaging model in human dermal fibroblasts(HDFs).Methotis Photoaging model was established by 8-MOP+UVA in skin HDFs.Flow cytometer.enzyme eytochemistry,immunofluorescence,Westem blot and Real-time PCR were employed.Results The percentage of G1 blockage of 8-MOP+UVA group were higher than that of control group at 24、48、72 h and 7 d(61.4%±1.5% vs 32.8%±1.5%.69.5%±2.2% vs 44.9% ±2.3%.88.2%±1.6% vs 59.8%±1.4%,90.7%±2.5% vs 68.5%±2.6%.all P<0.01).The expression of SA-β-Gal of 8-MOP+UVA group were higher than that of control group at 24、48、72 h and 7 d(34.87%±0.59% vs 7.11%±0.78%,59.38%±0.46% vs 10.57%±0.47%.72.46%±0.98% vs 11.67%±0.87%,94.33%±0.13% vs 12.04%±0.12%,all P<0.01).8-MOP+UVA treatment could significantly aggravate the oxidative DNA damages,the percentage of 8-oxo-dG positive cell of 8-MOP+UVA group(95.78%±0.14%)were significantly higher than that of control group(7.69%±0.09%,P<0.01),8-MOP group(9.76%±0.11%,P<0.01)and UVA group(35.29%±0.14%,P<0.05).8-MOP+UVA treatment could accelerate the telomere shortening.the relative length of telomere of 8-MOP +UVA group were 2.57±0.05 lower than that of control group(6.63±0.12.P<0.01).The levels of P53,P21WAF-1 and P16INK-4a of 8-MOP+UVA group were higher than that of control group(3.00±0.88 vs 0.54±0.10,2.50±0.51 vs 0.42±0.06,2.21±0.34 vs 0.38±0.05,all P<0.01).Conclusion 8-MOP+UVA-induced photoaging of HDFs can be mediated though the regulation of telomere and subsequent P53-dependent signaling pathways. 相似文献
1