摘要
目的:探讨缬沙坦对尼古丁损伤大鼠肠系膜动脉内皮依赖性舒张(EDR)功能的保护作用及其机制。方法:将30只大鼠分为5组,即正常对照、尼古丁损伤组(2mg.kg-1,ip)、缬沙坦低、中、高剂量组(nicotine2mg.kg-1,ip+valsartan3,10,30mg.kg-1,ig),6周后检测各组肠系膜动脉环EDR及主动脉匀浆中一氧化氮(NO)、丙二醛(MDA)含量,一氧化氮合成酶(NOS)、超氧化物歧化酶(SOD)活性变化。结果:尼古丁使肠系膜动脉环EDR明显降低(54.03%),并伴随主动脉匀浆NO含量,NOS、SOD活性的下降及丙二醛含量的升高;而缬沙坦(中、高剂量组)使其EDR得到明显改善(73.06%,82.95%),并且抑制了尼古丁诱导的NO含量,NOS、SOD活性的下降及MDA的升高(P<0.05,与尼古丁损伤组比较)。结论:缬沙坦对尼古丁所致的血管损伤具有明显保护作用,该作用可能与其抗氧化,促进内皮细胞合成、释放NO有关。
OBJECTIVE To examine whether valsartan exerts beneficial effects on the nicotine-induced impairment of endo thelium-dependent relaxation （EDR） in rat mesenteric arteries and explore the possible mechanisms underlying the observed protective effects of valsartaru METHODS A total of 30 rats were randomly divided into 5 groups： control group, nicotine group（2 mg·kg^-1 ,ip）, and 3 valsartan groups（3, 10 or 30 mg·kg^-1 , ig） consisting of 6 rats in each group. After 6 weeks, isometric tension recordings were used to assess EDR responses of mesenteric arteries. The NO, MDA contents and NOS, SOD activities in aorta homogenates were measured. RESULTS Administration of nicotine significantly inhibited EDR responses of mesenteric arteries （54. 03% ） and decreased the content of nitric oxide （NO） and nitric oxide synthase （NOS）, superoxide dismutase （SOD） activities and increased the content of malondialdehyde （MDA） in aorta homogenates when compared with that of the control group. However, chronic valsartan treatment（middle, high dose） significantly improved the vasodilator response （73. 06, 82.95%） and prevented the reduction in nitrite/nitrate levels, the activity of NOS, SOD and the increase of MDA in the aorta homogenates. CONCLUSION Valsartan can be used to attenuate nicotine-induced endothelial dysfunction, an effect that may be related not only to antioxidation, but also to enhancing NO production by preventing the decrease in NOS.
出处
《中国医院药学杂志》
CAS
CSCD
北大核心
2010年第18期1550-1552,共3页
Chinese Journal of Hospital Pharmacy
关键词
缬沙坦
尼古丁
内皮依赖性舒张
valsartan
nicotine
endothelium-dependent relaxation
