香芹酚通过抑制氧化应激反应抑制大鼠急性肺损伤

摘要

目的：探讨香芹酚（CAR）对大鼠急性肺损伤的作用，及其相关作用机制。方法60只大鼠随机分为5组，对照组，模型组，香芹酚（10 mg/ kg），香芹酚（20 mg/ kg），香芹酚（40 mg/ kg），每组12只。香芹酚组分别通过灌胃给药香芹酚10 mg/ kg、20 mg/ kg 和40 mg/ kg，每日一次，连续一周，末次给药1 h 后进行造模。给予20%酵母混悬液5 ml/kg 腹腔注射，12 h 后再次注射20%酵母混悬液5 ml/ kg 诱导急性肺损伤模型。对照组只注射同等体积生理盐水。24 h后检测肺组织水肿指数，ELISA 法检测丙二醛（MDA）、过氧化氢酶（CAT）、过氧化物歧化酶（SQD）、谷胱甘肽过氧化物酶（GSH），化学定量法检测一氧化氮（NQ）含量和总一氧化氮合酶（eNQS）活性；Western blot 法检测 eNQS 蛋白相对表达。结果模型组大鼠肺水肿指数显著高于对照组，而香芹酚组则明显低于模型组（ P ＜0.05）；模型组 MDA、NQ 含量、eNQS 活性显著高于对照组，香芹酚显著抑制 MDA、NQ 含量剂 eNQS 活性，并呈剂量依赖趋势（ P ＜0.05）；模型组CAT、SQD 和 GSH 活性则显著低于对照组，香芹酚可明显提高其活性，呈剂量依赖趋势（ P ＜0.05）；Western blot 显示，香芹酚可显著抑制 eNQS 蛋白表达，呈剂量依赖趋势（ P ＜0.05）。结论香芹酚可通过抑制氧化应激反应从而发挥对大鼠急性肺损伤的保护作用。%Objective To explore the protective effects of carvacrol on acute lung injury and its potential mechanism. Methods 60 SD rats were divided into 5 groups,the control group,model group,CAR(10 mg/ kg),CAR(20 mg/ kg)and CAR(40 mg/ kg). Carvacrol group was administrated 10 mg/ kg,20 mg/ kg and 40 mg/ kg of carvacrol by intragastric administration once a day for one week and lasted for 1 h. The acute lung injury rat model was induced through intraperitoneal injection with 20% yeast suspension every 12 h for twice. In the control group,on-ly the same volume of saline was injected. After 24 h,lung tissues were removed and the wet and dry proportion,Catalase(CAT),superoxide dis-mutase(SQD),glutathione - peroxidase(GSHPx)and malonaldehyde(MDA)in lung tissue were determined,the content of NQ and eNQS were also detected by elisa. Results Carvacrol significantly suppressed the watern content in acute lung injury( P < 0. 05). Meanwhile,the content of MDA,NQ and eNQS were markedly higher in model group compared with the control group,showing a dose - dependent trend( P < 0. 05), while carvacrol effectively suppressed them. The activities of CAT,SQD and GSH in model group were significantly lower than that in the control group( P < 0. 05),while carvacrol effectively increased them,showing a dose - dependent trend( P < 0. 05). Western blot showed that carva-crol significantly suppressed the relative protein expression of eNQS,showing a dose - dependent trend( P < 0. 05). Conclusion Carvacrol could protect the acute lung injury probably through the anti - oxidative stress pathway.