Objective To investigate the expression level of NF-κB and TNF-α of aorta in rabbit with chronic intermittent hy-poxia(CIH) ,to seek the possible existing relation between these two inflammatory factors and to observe the possible interventional effect of baicalin .Methods (1)The preparation of chronic-intermittent hypoxia rabbit model by atmospheric intermittent low oxy-gen tank :New Zealand rabbits in the blank control group were routinely fed and performed the gavage with normal saline at last 4 weeks .The experimental cycle was 8 weeks ;the CIH group was given intermittent hypoxia for maintaining for 8 weeks ;the baicalin intervention group was same to the CIH group and given the same 8-week intermittent hypoxia .Then the baicalin gavage interven-tion[100 mg/(kg · d)] was given at the last 4 weeks .(2)The morphological experimental detection :the aortal structure changes af-ter HE staining were observed by optical microscope ;the expressions of NF-κB and TNF-αprotein in aortal intima were qualitative-ly and semiquantitatively detected by SABC and immunohistochemistry .Results (1)The pathological changes of early arterial ath-erosclerosis of aorta in chronic intermittent hypoxia group appeared ,while the obvious early arterial atherosclerosis change in the baicalin intervention group did not appeared .(2)The expressions of NF-κB and TNF-αof aortal endothelial cells in the CIH group were significantly increased ;compared with the CIH group ,the expressions of NF-κB and TNF-α of aortal endothelial cells in the baicalin intervention group were obviously decreased .(3)There was positive relation between the expression of NF-κB and TNF-αin rabbit aortal endothelial cells (r=0 .702 ,P<0 .01) .Conclusion CIH can lead to early atherosclerosis in rabbits ,its mechanism is related to the activation of NF-κB and TNF-α.Baicalin may down-regulate TNF-α expression by alleviating endothelial cell NF-κB activation ,thus reaches the target for controlling vascular endothelial inflammatory reaction and anti-arterial atherosclerosis .%目的 探讨慢性间歇性缺氧兔主动脉核转录因子(NF)-κB和肿瘤坏死因子(TNF)-α的表达水平,寻求两炎性因子之间可能存在的联系,并观察黄芩苷的可能干预作用.方法 (1)利用常压间歇低氧舱制备慢性间歇性缺氧兔模型:空白对照组新西兰兔常规饲养,后4周予生理盐水灌胃,实验周期为8周;慢性间歇性缺氧组给予间歇性缺氧,总共维持8周;黄芩苷干预组同慢性间歇性缺氧组,持续予以相同间歇性缺氧8周,后4周给予黄芩苷灌胃干预[100 mg/(kg·d)].(2)形态学实验检测:光镜下观察HE染色后主动脉结构改变;SABC法行免疫组织化学后定性及半定量检测主动脉内膜NF-κB和TNF-α蛋白的表达.结果 (1)慢性间歇性缺氧组兔主动脉出现了早期动脉粥样硬化的病理改变.黄芩苷干预组未出现明显早期动脉粥样硬化改变;(2)慢性间歇性缺氧组兔主动脉内皮细胞中NF-κB和TNF-α的表达明显升高;黄芩苷干预组与慢性间歇性缺氧组相比,NF-κB、TNF-α在主动脉内皮的表达水平明显减弱.(3)兔主动脉内皮细胞NF-κB表达水平与TNF-α呈正相关(r=0.702,P<0.01).结论 慢性间歇性缺氧可导致兔早期动脉粥样硬化改变,其机制与激活NF-κB、TNF-α相关.黄芩苷可通过减轻内皮细胞NF-κB活性,下调TNF-α表达,达到控制血管内皮炎性反应、抗动脉粥样硬化的目的.
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