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痰湿壅盛证高血压大鼠模型的建立与评价

发布时间:2018-08-13 08:34
【摘要】:目的观察痰湿壅盛证高血压模型大鼠的证候表现、理化指标及可能的病理机制。方法 50只Wistar大鼠采用高脂饲料饲养的方法制备痰湿壅盛证大鼠模型,同时设对照组(10只),给予普通饲料饲养。两组均持续饲养25周后,选取造模大鼠中体重、血压均超过对照组平均值25%的大鼠纳入模型组(22只)。检测两组大鼠体重、血压、血脂及相关血清学指标;观察靶器官形态变化;采用实时荧光定量PCR(q-PCR)检测主动脉中瘦素受体(leptin receptor,LepR)、Janus蛋白络氨酸激酶2(Janus kinase2,Jak2)、信号转导子和转录激活子3(signal transducer and activator of transcription 3,Stat3)、细胞因子信号抑制蛋白-3(suppressor of cytokine signaling-3,Socs3)、血管紧张素Ⅱ1型受体(angiotensinⅡreceptor type 1,AT1)、AT 2、磷脂酰肌醇3-激酶(phosphatidylinositol 3 kinase,PI3K)、丝苏氨酸蛋白激酶(serine threonine kinase,Akt)、核转录因子kBp65(nuclear factor of kappa B,NF-κBp65)、核因子kB激酶抑制蛋白α(inhibitor of nuclear factor kappa-B kinaseα,IKKα)、核因子kB抑制蛋白β亚基(NF-kappa-B inhibitorβ,IKKβ)、核因子kB抑制蛋白α亚基(NF-kappa-B inhibitorα,IKBα)和磷酸腺苷活化蛋白激酶(AMP-activated protein kinase,AMPK)mRNA表达水平。根据qPCR结果,分别采用免疫组化和Western blot检测主动脉中AT1、LepR的表达。结果与对照组比较,模型组大鼠体重、血压、血脂升高,血清Lep、AngⅡ、同型半胱氨酸(Hcy)、内皮素1(ET-1)、TNF-α、IL-6、β_2微球蛋白(β_2-MG)升高,NO下降,差异均有统计学意义(P0.05,P0.01)。模型组大鼠主动脉内皮损伤、平滑肌细胞增生,伴发心、肾损害。与对照组比较,模型组大鼠主动脉中LepR、Jak2、Stat3、Socs3、AT1、PI3K、Akt、NF-κB p65、IKKβ、IKBα、AMPK mRNA表达上调(P0.05),IKKα下调(P0.05)。免疫组化显示:模型组AT1和LepR棕黄色沉积明显增多、阳性部位分布更加广泛。Western blot显示:与对照组比较,模型组大鼠主动脉中AT1和LepR蛋白表达增加(P0.05)。结论模型大鼠呈现典型的证候特征,体重增加,呈腹形肥胖状态,毛色黯淡,纳呆嗜睡,活动度下降,饮食减少,便溏,舌黯红,苔白厚腻。瘦素可作为评价痰湿壅盛证高血压大鼠模型的客观指标之一。
[Abstract]:Objective to observe the syndromes, physicochemical indexes and possible pathological mechanism of hypertensives with phlegm and dampness. Methods 50 Wistar rats were fed with high fat diet to make the rat model of phlegm-dampness syndrome, and the control group (10 rats) was fed with common diet. After 25 weeks of continuous feeding, 22 rats with body weight and blood pressure higher than the average of the control group were included in the model group (22 rats). The body weight, blood pressure, blood lipid and relative serological indexes were measured, and the morphological changes of target organs were observed. Real-time quantitative PCR (q-PCR) was used to detect Janus protein complex kinase 2 (Janus kinase 2), signal transducers and activators of transcription (3 (signal transducer and activator of transcription 3 (signal transducer and activator of transcription 3), cytokine signal suppressor protein 3 (suppressor of cytokine signaling-3 (Socs3), angiotensin II type 1 in aorta. Angiotensin 鈪,

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