摘要
目的：探讨肌肽（carnosine）对H9N2亚型猪流感病毒（H9N2-SIV）诱导的急性肺损伤（ALI）肺组织抗氧化的效果.方法：选用6～8周龄SPF级雌性BALB/c小鼠150只,随机分为对照组、模型组和肌肽干预组,每组50只,分别给予正常鸡胚尿囊液、H9N2-SIV和肌肽＋H9N2-SIV.实验第2、4、6、8和14天,每组分别处死8只小鼠,观察肺组织的病理变化,测定肺组织匀浆中丙二醛（MDA）的含量、超氧化物歧化酶（SOD）和髓过氧化物酶（MPO）的活性及肺湿/干重比值（W/D）.结果：肌肽可减轻H9N2-SIV造成的小鼠临床症状,降低死亡率.肌肽干预于第6、8天明显改善了肺组织的水肿程度（W/D降低,P＜0.05）并减轻了肺部的病理变化;实验至第6、8天可见肺组织MDA含量显著降低（P＜0.05）,SOD活性显著提高（P＜0.05）;于实验第4、第6和第8天可见肺组织MPO活性显著降低（P＜0.05,P＜0.01）.结论：肌肽可改善H9N2-SIV感染后肺组织的水肿程度,降低肺组织MDA含量和MPO活性,提高SOD活性,抑制自由基和脂质过氧化反应,从而减轻小鼠肺损伤的程度,降低死亡率.
AIM： To investigate the antioxidant effect of caruosine on H9N2 swine influenza virus （H9N2- SIV）-induced acute lung injury （ALI）. METHODS： One hundred and fifty SPF female BALB/c mice （6 to 8 weeks old） were randomly divided into control group, ALI group and carnosine intervention group with 50 each. The mice in control group were inoculated intranasally with normal allantoic fluid of chick embryos. The mice in ALI group were inoculated in- tranasally with allantoic fluid containing H9N2-SIV. The mice in carnosine group were treated with HgN2-SIV plus carnosine. On the 2rid, 4th, 6th, 8th and 14th days after treatment, 8 mice in each group were killed to observe tile patho- logical changes of the lung. Meanwhile, the activity of superoxide dismutase （SOD） and myeloperoxidase （ MPO）, the content of malondialdehyde （MDA） and the wet weight/dry weight ratio （W/D） of the lung tissues were determined. RE- SULTS： Carnosine alleviated the symptom of the mice induced by H9N2-SIV infection, and increased the viability of the mice. In carnosine intervention group, edema degree of the lung （W/D） was apparently reduced （P 〈 0.05）. The patho- logical changes were alleviated on the 6th and 8th days of the experiment. On the same days, the content of MDA was lower obviously （P 〈 0.05） and the activity of SOD was improved remarkably （ P 〈 0.05 ）. On the 4th day of the experiment, the activity of MPO was reduced apparently （P 〈 0.05） and continuously decreased on the 6th and 8th days （P 〈 0.05）. CONCLUSION： Carnosine protects the mice from acute lung injury induced by H9N2-SIV infection and increases the via- bility by reducing the content of MDA, lowering the activity of MPO, increasing the activity of SOD and inhibiting the pro- duction of free radicals and lipid peroxidation.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2013年第12期2235-2239,共5页
Chinese Journal of Pathophysiology
基金
河北省自然科学基金资助项目(No.C2011405002)
河北省教育厅自然科学研究计划项目(No.Q2012043
No.ZD20131045)
河北北方学院校级重大课题(No.ZD201306)
