摘要
目的研究氯胺酮对哮喘模型大鼠氧化应激反应及相关蛋白表达的影响。方法51只Brown-Norway大鼠随机分成不同浓度氯胺酮雾化吸入组(K1组、K2组、K3组,每组8只)、不同剂量氯胺酮腹腔注射组(V1组、V2组,每组6只)、卵蛋白组(A组,8只)和对照组(C组,7只)。采用鸡卵蛋白(OVA)辅以百日咳杆菌菌苗和氢氧化铝为佐剂注射致敏大鼠。雾化吸入OVA激发。K1、K2、K3组大鼠在激发前分别给予12.5、25及50 mg/ml浓度的氯胺酮雾化吸入,V1、V2组在激发前分别给予50和100 mg/kg氯胺酮腹腔注射。A组在激发前给予PBS雾化吸入,C组采用PBS替代OVA进行雾化吸入。最后一次激发后取血和肺组织,检测一氧化氮(NO)、过氧化氢(H2O2)的量及c-Jun氨基末端激酶(JNK)蛋白的表达。结果与C组相比,A组的NO及H2O2的量均增高(P<0.01);氯胺酮处理组测得的NO及H2O2量明显低于A组(P<0.05或P<0.01)。与C组相比,A组JNK的激活程度(pJNK/JNK)增高(P<0.01)。JNK的激活程度在氯胺酮处理组均降低,其中K1、K2、K3、V1、V2组明显低于A组(P<0.05或P<0.01)。结论氯胺酮通过全身用药和局部雾化吸入均可抑制哮喘模型大鼠增高的氧化应激反应,并抑制JNK蛋白的激活。
Objective To investigate the effect of nebulized ketamine inhalation and ip. injection on oxidative stress in the lungs of asthmatic rats. Methods Fifty-one Brown-Norway rats were randomly assigned to seven groups, with 6-8 rats each： control group （C）, asthma group （ A）, ketamine inhaled groups（K1 ,K2 ,K3 ） and ketamine ip. injection groups（V1 ,V2 ）. The rats in group A, K1, K2, K3, V1, V2, asthma was induced by subcutaneous injection of ovalbumia and aluminum hydroxide in PBS,and followed by inhaling nebulized 1% OVA in PBS. The rats in group K1, K2 and K3 ,the sensitized rats were exposed to 12. 5 mg/ml （group K1 ）, 25 mg/ml （group K2 ）, 50 mg/ml （group K3 ）of nebulized ketamine before OVA inhalation. The rats in group V1 and V2, the sensitized rats were ip. injected 50 mg/kg ketamine（V1 ） or 100 mg/kg （V2） before inhaling nebulized OVA. Blood and lung samples were taken for the measurements of nitrus monoxide（NO）, H2 O2 and JNK. Results The blood levels of NO and H2 O2 of group A were higher than those of group K1,K2 and V1 （P〈0.01）and K3 and V2 （P〈0.05）,which were significantly higher in group A than those in group C （P〈0.01）. Compared with group C, the activation of JNK of group A was significantly increased （P〈0.01）, and was higher than that of group K1, K2 and V1 （P〈 0. 01） and K3, V2 （P〈0.05）. Conclusion Inhalation of nebulized ketamine and ip. injecting ketamine can reduce the oxidative stress reaction and the activation of JNK in the lungs in asthmatic rats.
出处
《临床麻醉学杂志》
CAS
CSCD
2008年第10期895-897,共3页
Journal of Clinical Anesthesiology
