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目的探讨黄芩苷对新西兰大白兔颈动脉粥样硬化(AS)的影响及潜在的分子机制。方法健康雄性新西兰大白兔30只,随机分为5组:空白对照组(NC组)、安慰剂对照组(PC组)、阿托伐他汀治疗组(AT组)、黄芩苷预防组(BP组)和黄芩苷治疗组(BT组),每组6只。后4组均在高脂饮食后,进行右侧颈动脉球囊拉伤,构建AS模型。在第2周末和第10周末测定各组血脂水平。第10周末处死大白兔,采用实时荧光定量PCR及Western blot检测各组5-脂氧合酶(5-LO)、5-脂氧合酶活化蛋白(FLAP)和白三烯B4受体(BLTR)基因及蛋白水平表达变化,HE染色测量颈动脉内膜变化情况。结果与NC组比较,PC组TC、TG、LDL-C、5-LO、FLAP和BLTR mRNA及蛋白表达明显增高(P<0.05)。AT组、BP组和BT组较PC组TC、TG、LDL-C水平、内膜与中膜厚度比值(1.76±0.97,1.04±0.11,1.83±0.17 vs 2.54±0.18)及5-LO、FLAP和BLTR mRNA及蛋白水平明显降低(P<0.05)。结论黄芩苷可以通过调脂、抑制5-LO炎症途径,发挥抗AS的作用。
Objective To investigate the effect of baicalin on carotid atherosclerosis (AS) in New Zealand white rabbits and its underlying molecular mechanism. Methods Thirty healthy male New Zealand white rabbits were randomly divided into five groups: blank control group (NC group), placebo control group (PC group), atorvastatin treatment group (AT group), baicalin prevention group (BP group ) And baicalin treatment group (BT group), 6 in each group. After 4 groups were in high-fat diet, right carotid balloon injury, the construction of AS model. Blood lipid levels in each group were measured on the 2nd weekend and the 10th weekend. Rabbits were sacrificed at the end of the 10th week. The expression of 5-lipoxygenase, 5-lipoxygenase-activating protein (FLAP) and leukotriene B4 receptor (BLTR) were detected by real- ) Gene and protein expression changes, carotid artery endometrial changes measured by HE staining. Results Compared with NC group, the mRNA and protein expressions of TC, TG, LDL-C, 5-LO, FLAP and BLTR in PC group were significantly increased (P <0.05). The levels of TC, TG and LDL-C in AT, BP and BT groups were significantly higher than those in PC group (1.76 ± 0.97,1.04 ± 0.11,1.83 ± 0.17 vs 2.54 ± 0.18), and 5-LO, FLAP And BLTR mRNA and protein levels were significantly lower (P <0.05). Conclusion Baicalin can play an anti-AS role by regulating lipid metabolism and inhibiting 5-LO inflammatory pathways.