【摘要】：目的觀察痰濕壅盛證高血壓模型大鼠的證候表現(xiàn)、理化指標及可能的病理機制。方法 50只Wistar大鼠采用高脂飼料飼養(yǎng)的方法制備痰濕壅盛證大鼠模型,同時設(shè)對照組(10只),給予普通飼料飼養(yǎng)。兩組均持續(xù)飼養(yǎng)25周后,選取造模大鼠中體重、血壓均超過對照組平均值25%的大鼠納入模型組(22只)。檢測兩組大鼠體重、血壓、血脂及相關(guān)血清學(xué)指標;觀察靶器官形態(tài)變化;采用實時熒光定量PCR(q-PCR)檢測主動脈中瘦素受體(leptin receptor,LepR)、Janus蛋白絡(luò)氨酸激酶2(Janus kinase2,Jak2)、信號轉(zhuǎn)導(dǎo)子和轉(zhuǎn)錄激活子3(signal transducer and activator of transcription 3,Stat3)、細胞因子信號抑制蛋白-3(suppressor of cytokine signaling-3,Socs3)、血管緊張素Ⅱ1型受體(angiotensinⅡreceptor type 1,AT1)、AT 2、磷脂酰肌醇3-激酶(phosphatidylinositol 3 kinase,PI3K)、絲蘇氨酸蛋白激酶(serine threonine kinase,Akt)、核轉(zhuǎn)錄因子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亞基(NF-kappa-B inhibitorβ,IKKβ)、核因子kB抑制蛋白α亞基(NF-kappa-B inhibitorα,IKBα)和磷酸腺苷活化蛋白激酶(AMP-activated protein kinase,AMPK)mRNA表達水平。根據(jù)qPCR結(jié)果,分別采用免疫組化和Western blot檢測主動脈中AT1、LepR的表達。結(jié)果與對照組比較,模型組大鼠體重、血壓、血脂升高,血清Lep、AngⅡ、同型半胱氨酸(Hcy)、內(nèi)皮素1(ET-1)、TNF-α、IL-6、β_2微球蛋白(β_2-MG)升高,NO下降,差異均有統(tǒng)計學(xué)意義(P0.05,P0.01)。模型組大鼠主動脈內(nèi)皮損傷、平滑肌細胞增生,伴發(fā)心、腎損害。與對照組比較,模型組大鼠主動脈中LepR、Jak2、Stat3、Socs3、AT1、PI3K、Akt、NF-κB p65、IKKβ、IKBα、AMPK mRNA表達上調(diào)(P0.05),IKKα下調(diào)(P0.05)。免疫組化顯示:模型組AT1和LepR棕黃色沉積明顯增多、陽性部位分布更加廣泛。Western blot顯示:與對照組比較,模型組大鼠主動脈中AT1和LepR蛋白表達增加(P0.05)。結(jié)論模型大鼠呈現(xiàn)典型的證候特征,體重增加,呈腹形肥胖狀態(tài),毛色黯淡,納呆嗜睡,活動度下降,飲食減少,便溏,舌黯紅,苔白厚膩。瘦素可作為評價痰濕壅盛證高血壓大鼠模型的客觀指標之一。
[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，

本文編號：2180441