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作 者:孙婧[1] 陈宁 张晓 姚晓燕 聂振宇 庄萍霞 黄为 张翠英[1] Sun Jing;Chen Ning;Zhang Xiao(Department of Physiology,Changzhi Medical College)
机构地区:[1]长治医学院生理学教研室,046000 [2]长治医学院临床医学系 [3]长治医学院护理学系 [4]长治医学院医学影像系 [5]长治医学院基础部
出 处:《长治医学院学报》2018年第2期81-84,共4页Journal of Changzhi Medical College
基 金:长治医学院大学生创新创业训练计划(D2016020);长治医学院科研启动基金项目(QDZ201604)
摘 要:目的:探讨N-乙酰半胱氨酸(NAC)和小檗碱(Ber)对博莱霉素(BLM)所致大鼠肺纤维化的作用及机制。方法:SD大鼠随机分为对照组(n=6)、BLM组(n=6)、NAC组(n=6)和Ber组(n=6),BLM组、NAC组及Ber组大鼠气管内缓慢注射博莱霉素生理盐水溶液(0.2~0.3mL,5mg/kg),对照组大鼠气管内注射等体积生理盐水。术后次日起,Ber组大鼠予200mg/(kg·d)Ber灌胃。NAC组大鼠于BLM处理前1周及此后每日经强饲法口服NAC[3mmol/(kg·d)]。各组于术后第14天处死大鼠,取出肺组织行HE染色,镜下观察肺组织病理改变,同时采用样本碱水解法检测羟脯氨酸(HYP),以黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)含量。结果:NAC和Ber组大鼠肺组织病理损伤较BLM组减轻,HYP含量低于BLM组(P<0.05),而SOD含量高于BLM组(P<0.05)。结论:NAC和Ber均能通过抗氧化作用减缓BLM诱导的肺纤维化。Objective:To observe the effect of NAC and Ber in pulmonary fibrosis in rats induced by bleomycin and explore its mechanism.Methods:SD rats were randomly divided into 4 groups:control group,BLM group,NAC group and Ber group with 6 rats in each group.The rats in the BLM group,NAC group and Ber group were intratracheally injected with bleomycin and physiological saline mixture solution(0.2~0.3 mL,5 mg/kg)slowly,and the rats in the control group were injected with the same volume physiological saline solution.Ber group were fed Ber 200 mg/(kg·d)from the second day.NAC group were fed with N-acetylcysteine every day for one week before the single intratracheal instillation of blemycin up to the day being executed on the 14th day.Their pulmonary pathological change was observed under HE staining.At the same time,contents of hydroxyproline(HYP),superoxide dismutase(SOD)in lung tissues were compared among the four groups.Results:Compared with model group,the pathological injury was obviously reduced after treatment with NAC or Ber.The content of HYP was decreased than the model group;and the content of SOD was increased in lung tissue on the 14th day in NAC and Ber treatd groups than that in BLM group(P<0.05).Conclusion:NAC and Ber inhibit pulmonary fibrosis induced by bleomycin in rats.The antioxygenation might be one of the mechanisms of their treatment in pulmonary fibrosis.
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