Objective To observe the expression changes of 3-nitrotyrosine (3-NT), inducible nitric oxide synthase (iNOS), and nitric oxide (NO) in brain tissues of ischemia-reperfusion rats treated with different doses of hydroxysafflor yellow A (HSYA) by intravenous injection.Methods The healthy adult male SD rats were randomly divided into the sham operation group, model group, low-dose HSYA group, medium-dose HSYA group and high-dose HSYA group.In the sham operation group, rats' common carotid artery, internal carotid artery and external carotid artery were exposed, and then sutured.The other rats were subjected to a 60-min middle cerebral artery occlusion and 24-h reperfusion (MCAO/R).The rats in the low-dose, medium-dose and high-dose HSYA groups were injected with 2.5, 5 and 10 mg/kg HSYA, respectively, in the tail vein at 60 min after ischemia, and the same volume of Tris buffer was injected into the tail vein of rats in sham operation group and model group.All rats were continued to raise for 24 h.The expression of 3-NT and iNOS in the rat brain tissues after ischemia-reperfusion in each group was examined by Western blotting.The NO level was also detected by Griess assay.Results The absolute gray values of 3-NT in the sham operation group, the model group, the low-dose HSYA group, the medium-dose HSYA group and the high-dose HSYA group after ischemia-reperfusion were (2.81±1.37)×103, (46.86±4.75)×103, (44.51±4.13)×103, (13.88±2.98)×103, and (6.38±2.66)×103, respectively;the absolute gray values of iNOS of each group were (2.25±0.32)×103, (79.67±4.73)×103, (75.29±4.08)×103, (27.31±2.77)×103, (19.19±1.86)×103, respectively.In the model group and low-dose, medium-dose, and high-dose HSYA groups, the levels of NO were (16.50±2.20), (15.40±1.44), (10.33±1.30), and (6.80±0.73) nmol/mg.The levels of 3-NT, iNOS and NO in brain tissues of the model group, low-dose HSYA group, medium-dose HSYA group and high-dose HSYA group were higher than those of the sham operation group (all P<0.05).The levels of 3-NT, iNOS and NO in the brain tissues of rats in the low-dose HSYA group were not significantly different from those in the model group (P>0.05).The levels of 3-NT, iNOS, NO in the medium-dose and high-dose HSYA groups were lower than those in the model group and low-dose HSYA group (all P<0.05), and the levels of 3-NT, iNOS and NO in brain tissues of high-dose HSYA group were lower than those in medium-dose HSYA group (all P<0.05).Conclusion HSYA can inhibit the expression of 3-NT, iNOS, and NO in rat brain tissues after ischemia-reperfusion.The higher the HSYA dose is, the more obvious the effect will be.

Objective To study the inhibitory effect of panax notoginseng saponins (PNS) on 3-nitrotyrosine (3-NT) formation in brain induced by heme/NO2 -/H2O2 or ONOO - pathways in vitro. Methods According to the two major pathways of 3-NT formation in vivo, the models of protein nitration induced by heme/NaNO2/H2O2 or ONOO-system were established, respectively, in vitro. Bovine serum albumin (BSA)/rat plasma protein or rat brain homogenate protein were utilized as reactive substrates in both systems. Samples were divided into blank-control group, 3-NT group and PNS group (including low-, medium-and high-concentration subgroups). In 3-NT group, samples were exposed to heme/NaNO2/H2O2 or ONOO-system, respectively, at 37℃for 30 min, whereas in PNS group, samples were pre-incubated with PNS (at final concentrations of 50 mg/L, 100 mg/L, and 200 mg/L) at 37℃for 5 min before the nitrating system exposure. The 3-NT level in each group was detected by Western blot assy. Results Compared with the blank-control group, both heme/NaNO2/H2O2 and ONOO-system can induce significant 3-NT generation in BSA/rat plasma protein or rat brain homogenate protein (P<0.05). Compared with model group, PNS pre-treatment markedly inhibited 3-NT expression in BSA/rat plasma protein in a dose-dependent manner (P<0.05), the inhibitory effect of low intervention on the level of 3-NT in rat brain homogenate protein was not significant (P>0.05). Medium- and high-concentrations of PNS pre-treatment markedly inhibited 3-NT accumulation, with maximum effect at the concentration of 200 mg/L (P<0.05). Conclusion Medium- and high-concentrations of PNS can inhibit 3-NT formation in brain tissue mediated by either heme/NO2-/H2O2 or ONOO-pathways, implying that potential neuroprotective action against 3-NT involves pathological conditions, like trauma, stroke, and neurodegenerative diseases.

目的 探讨前循环同侧短暂性脑缺血发作(TIA)对后续脑梗死的影响及可能机制.方法 选取113例前循环脑梗死患者,分为单纯脑梗死组87例和进展脑梗死组26例,分别比较2组早期神经功能恶化(END)、美国国立卫生研究院卒中量表(NIHSS)评分、3个月改良Rankin量表(mRS)评分、脑梗死体积、高敏C反应蛋白(hs-CRP)及其他相关危险因素.结果 与单纯脑梗死组比较,进展脑梗死组发生END比例1j(11.5％ vs 31.0％)、出院NIHSS评分[(1.85±2.31)分vs (3.30±3.65)分]、3个月mRS评分[(0.90±0.83)分 vs(1.78±1.77)分、hs-CRP[(2.52±3.23)mg/L vs (6.21±32.23)mg/L]、脑梗死体积[(3.92±8.05)cm3 vs(9.15±15.07)cm3均明显减小(P＜0.05);脑梗死前7～14 d TIA发生2～3次、TIA持续时间＞10 min的患者上述指标的变化最为显著;hs-CRP与END(r=0.311,P=0.014)、入院NIHSS评分(r=0.455,P=0.000)及脑梗死体积呈正相关(r=0.524,P=0.000).结论 TIA对后续脑梗死具有缺血预处理作用,其作用可能与hs-CRP水平下降有关.