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作 者:郑纪阳[1] 戴新建[1] 王万铁[2] 鲍小欧[1] 许益笑[2] 邱晓晓
机构地区:[1]温州市第二人民医院呼吸内科,浙江温州325000 [2]温州医学院病理生理学教研室,浙江温州325035
出 处:《中国呼吸与危重监护杂志》2009年第3期238-241,共4页Chinese Journal of Respiratory and Critical Care Medicine
基 金:温州市科技计划重点资助项目(编号:Y20060061)
摘 要:目的观察盐酸氨溴索对油酸诱导的ALI兔肺组织细胞凋亡的影响,探讨盐酸氨溴索对ALI的作用及其机制。方法健康日本大耳白兔24只,随机分为3组:正常对照组(NC组)、ALI组和盐酸氨溴索治疗组(AMB组)。复制兔油酸型ALI模型。光镜观察各组干预后6h肺组织病理改变,肺组织细胞凋亡指数(AI)以及肺组织匀浆Caspase-3活性,检测各组干预前及干预后6h血清超氧化物歧化酶(SOD)活性和丙二醛(MDA)、IL-1β及TNF-α含量。结果AMB组肺组织病理损伤较ALI组明显减轻,AI显著低于ALI组(P<0.01),但显著高于NC组(P<0.01);AMB组肺组织匀浆Caspase-3活性显著低于ALI组(P<0.05);AMB组干预后6h血清SOD活性显著高于ALI组,而血清MDA、IL-1β及TNF-α含量显著低于ALI组(P<0.01)。结论盐酸氨溴索有一定的抗ALI的作用,其机制可能与抑制氧化应激,从而抑制细胞因子合成、减少Caspase-3的活化、抑制肺组织细胞凋亡有关。Objective To observe the protective effects of ambroxol hydrochloride (AMB) on rabbit model of acute lung injury (ALI) induced by oleic acid and explore its mechanisms. Methods The ALI model of rabbit was induced by oleic acid. Twenty-four Japanese white rabbits were divided into three groups randomly,ie, a normal saline group (NC group), an ALI group and an ALI plus ambroxol injection group (AMB group). The pathological changes and apoptotic index (AI) in lung tissue, Caspase-3 activity in lung tissue homogenate were observed 6 hours after the intervention. Serum activity of superoxide dismutase (SOD) and serum levels of malonaldehyde (MDA), interleukin-1 β (IL-1 β), and tumor necrosis factor-α (TNF-α) were measured simutanously. Results The pathological injury of lung in the AMB group was milder than that in the ALI group. Both the AI in lung tissue and Caspase-3 activity in homogenate in the AM B group were lower than those in the ALI group significantly (P 〈 0. 01, P 〈 0. 05 respectively), but were higher than those in the NC group( both P 〈 0. 01 ). The activity of SOD in serum measured 6 hours after AMB intervention was higher while the serum levels of MDA, IL-1β and TNF-α in serum were lower ( P 〈 0. 01 ) than those in the ALI group significantly ( all P 〈 0. 01 ). Conclusions Ambroxol hydrochloride has protective effects on oleic acid-induced acute lung injury. The mechanisms may be related to inhibition of oxidative stress and suppression of cytokines synthesis ( IL-1β and TNF-α), the activity of the Caspase-3, and the apoptosis of lung tissue.
关 键 词:急性肺损伤 盐酸氨溴索 细胞凋亡 细胞因子 半胱氨酸天冬氨酸蛋白酶3
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