To investigate the effects of icariin （ICA） on angiotensin Ⅱ（Ang Ⅱ）-induced injury in human umbilical vein endothelial cells line （ECV-304）. The ECV-304 cells were cultured in vitro. After 24 h incubating with icariin, the model of AngⅡ-induced injury in ECV-304 was established. The cell viability （MTT method）, Lactate dehydrogenase （LDH） release and Nitric oxide （NO） production in the medium, the capacity of scavenging superoxide anion radicals （O2^-） and hydroxyl radicals （.OH） were measured. The activities of superoxide dismutase （SOD）, total nitric oxide synthase （T-NOS）, inducible nitric oxide synthase （iNOS） and constitutive nitric oxide synthase （cNOS） in the cells were determined. Compared with the Ang Ⅱ-treated group, ICA can significantly raise the viability of EC, increase the activities of SOD, T-NOS and cNOS, increase the production of NO, enhance the capacity of scavenging superoxide anion radicals （ O2^- ） and hydroxyl radicals（.OH）, and lower LDH leakage and iNOS activity. The results suggest that ICA can protect endothelial cells （ECV-304） from Ang II-induced injury.
目的：探讨注射用尼莫地平脂质体对大鼠局灶性脑缺血再灌注损伤的影响。方法：70只SD大鼠分为注射用尼莫地平脂质体（nimodipine liposomes for injection，NDLI）1．00mg／kg组、NDLI0．50mg／kg组、NDLI0．25mg／kg组、尼莫地平组（1．00mg／kg）、溶媒组（10mL／kg）、假手术组和缺血模型组。复制大鼠大脑中动脉闭塞模型。对各组大鼠进行行为学评分，检测梗死灶体积、脑含水量、脑匀浆生化指标和脑组织学。结果：NDLI1．00mg／kg、0．50mg／kg和0．25mg／kg均能够显著改善局灶性脑缺血大鼠的行为学评分，缩小梗死灶体积，减少脑含水量，提高脑组织内Na＋，K＋-ATP酶、Ca2＋-ATP酶、谷胱甘肽和超氧化物歧化酶活性，降低丙二醛、乳酸和一氧化氮含量，并能改善脑组织损伤。结论：NDLI对大鼠局灶性脑缺血再灌注损伤有保护作用。
