本文選題：鹽誘導(dǎo)高血壓 + 左心室重構(gòu)　； 參考：《廣西醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的探討螺內(nèi)酯對鹽誘導(dǎo)高血壓大鼠左室心肌間質(zhì)纖維化及白介素17A(IL-17A)的影響。方法80只5周齡Wistar大鼠,隨機(jī)分為正常對照組、2%氯化鈉組、3%氯化鈉組、2%氯化鈉干預(yù)組和3%氯化鈉干預(yù)組每組16只;正常對照組、2%氯化鈉組和3%氯化鈉組分別給予蒸餾水、2%和3%氯化鈉飼養(yǎng)10周,2%氯化鈉干預(yù)組、3%氯化鈉干預(yù)組分別用2%和3%氯化鈉飼養(yǎng)5周后,給予螺內(nèi)酯20mg/(g·d)灌胃再飼養(yǎng)5周;每周尾袖法測動脈血壓1次,飼養(yǎng)10周后全部麻醉并處死,抽腹主動脈血和留取左心室心肌組織待檢測,HE染色觀察左心室心肌細(xì)胞形態(tài),Masson染色觀察心肌膠原纖維并計算膠原容積分?jǐn)?shù)(CVF),免疫組化、酶聯(lián)免疫吸附法(ELISA)分別檢測IL-17A、TNF-α、MMP-9、TGF-β1在心肌組織和血漿中的表達(dá)水平。結(jié)果(1)全部大鼠飼養(yǎng)10周后,死亡8只,死亡率10%(8/80),成模51只,成模率79.69%(51/64),其中2%氯化鈉組成模率75%(12/16),死亡率12.5%(2/16),3%氯化鈉組成模率81.3%(13/16),死亡率12.5%(2/16),2%氯化鈉+螺內(nèi)酯組成模率87.5%(14/16),死亡率12.5%(2/16)和3%干氯化鈉+螺內(nèi)酯組成模率75%(12/16),死亡率12.5%(2/16)。(2)與正常對照組相比,2%氯化鈉組、3%氯化鈉組、2%氯化鈉+螺內(nèi)酯組和3%氯化鈉+螺內(nèi)酯組大鼠的平均收縮壓及平均舒張壓均顯著增高(均P0.05),與2%和3%氯化鈉組相比,兩螺內(nèi)酯組的平均收縮壓明顯降低(均P0.05);但2%和3%氯化鈉組之間、兩螺內(nèi)酯組之間收縮壓水平無差異(P0.05)。(3)與正常對照組相比,2%和3%氯化鈉組大鼠的左室內(nèi)徑均顯著增大(均P0.05);與2%和3%氯化鈉組相比,螺內(nèi)酯干預(yù)5周后兩螺內(nèi)酯組的平均左室內(nèi)徑均顯著下降(均P0.01);但2%和3%氯化鈉組之間、兩螺內(nèi)酯組之間差別不明顯(P0.05)。(4)與正常對照組相比,2%和3%氯化鈉組大鼠心肌和血漿中IL-17A、TNF-α、MMP-9和TGF-β1的水平顯著增高(均P0.05),2%和3%氯化鈉干預(yù)組大鼠的血漿和心肌組織中IL-17A、TNF-α、MMP-9和TGF-β1的水平顯著下降(均P0.05),但2%和3%氯化鈉組間及2%和3%氯化鈉+螺內(nèi)酯組間上述指標(biāo)均無明顯差異。(5)與正常對照組相比,2%和3%氯化鈉組大鼠的CVF(P0.05)均顯著增高;但螺內(nèi)脂干預(yù)5周后2%和3%氯化鈉組CVF均明顯降低,但2%氯化鈉+螺內(nèi)酯組較3%氯化鈉+螺內(nèi)酯組降低更明顯(P0.05)(6)相關(guān)分析發(fā)現(xiàn):IL-17A與TNF-α、MMP-9、TGF-β1表達(dá)呈正相關(guān)(r=0.5、0.4、0.5,均P0.05);CVF與IL-17A、TNF-α、MMP-9、TGF-β1均呈正相關(guān)(r=0.4、0.6、0.7、0.8;均P0.01)。(7)心肌組織HE和Masson染色:成模大鼠心肌細(xì)胞增生肥大、灶性溶解,纖維組織增多;螺內(nèi)酯干預(yù)組大鼠心肌細(xì)胞增生、肥大、灶性溶解程度較輕,纖維組織顯著減少。結(jié)論鹽誘導(dǎo)高血壓大鼠的IL-17A表達(dá)明顯增高,與TNF-α、MMP-9、和TGF-β1表達(dá)呈正相關(guān);螺內(nèi)酯干預(yù)后IL-17A、TNF-α、MMP-9、TGF-β1和CVF均顯著降低;提示螺內(nèi)酯可能通過調(diào)控IL-17A、TNF-α、MMP-9和TGF-β1等因子的表達(dá)而逆轉(zhuǎn)左室間質(zhì)纖維化。
[Abstract]:Objective to investigate the effect of spironolactone on left ventricular interstitial fibrosis and interleukin 17 A (IL 17 A) induced by salt in hypertensive rats.Methods 80 5-week-old Wistar rats were randomly divided into 2% sodium chloride group (n = 16) and 3% sodium chloride group (n = 16).Normal control group (2% sodium chloride group) and 3% sodium chloride group (3% sodium chloride group) were fed with distilled water 2% and 3% sodium chloride for 10 weeks respectively. The 3% sodium chloride intervention group was fed with 2% and 3% sodium chloride for 5 weeks, and then fed with spironolactone 20mg/(g for 5 weeks.Arterial blood pressure was measured by cuff method once a week. After feeding for 10 weeks, all patients were anesthetized and executed.Extraction of abdominal aorta blood and left ventricular myocardial tissue to be detected by HE staining to observe left ventricular cardiomyocytes morphology and Masson staining to observe myocardial collagen fiber and calculate collagen volume fraction CVFFI, immunohistochemistry,Enzyme linked immunosorbent assay (Elisa) was used to detect the expression of IL-17An TNF- 偽-偽 -MMP-9 and TGF- 尾 1 in myocardium and plasma.Results 1) after 10 weeks of feeding, 8 rats died, and the mortality rate was 10% / 80%, 51 rats were modelled.79.69% 51 / 64%, of which 2% sodium chloride composition is 75 / 12 / 16%, mortality rate is 12.55% / 2 / 16%, sodium chloride composition rate is 81.33 / 16%, mortality rate is 12.55% / 21% / 2% sodium chloride spironolactone composition module rate is 87.555% 14 / 16%, mortality rate 12.555% / 216%) and 3% dry sodium chloride spironolactone composition module rate 75 / 12 / 16%, mortality rate 12.555% / 22%.The mean systolic blood pressure and mean diastolic pressure of rats in 2% sodium chloride group and 3% sodium chloride spironolactone group were significantly higher than those in 2% sodium chloride group and 3% sodium chloride group (all P 0.05, compared with 2% and 3% sodium chloride groups).The mean systolic blood pressure of the two spironolactone groups decreased significantly (both P0.05N; but between the 2% and 3% sodium chloride groups),There was no difference in systolic blood pressure level between the two spironolactone groups (P 0.05).) the left ventricular diameter of rats in 2% and 3% sodium chloride groups increased significantly compared with the normal control group (P0.05%; compared with 2% and 3% sodium chloride group, respectively), the left ventricular diameter of the rats in the 2% and 3% sodium chloride groups was significantly higher than that in the control group (P < 0.05).The mean left ventricular diameter in the two spironolactone groups decreased significantly after 5 weeks of intervention (all P 0.01), but between the 2% and 3% sodium chloride groups,The levels of IL-17AnTNF- 偽, MMP-9 and TGF- 尾 1 in myocardium and plasma of rats in the 2% and 3% sodium chloride groups were significantly higher than those in the control group (both P0.05% and 3% sodium chloride intervention group) (both P0.05% and 3% sodium chloride intervention group). The levels of IL-17 ANF- 偽 TNF- 偽 MMP-9 and TGF- 尾 1 in the plasma and myocardium of the rats in the intervention group were significantly higher than those in the control group (both P0.05% and 3% sodium chloride group).The level of TGF- 尾 _ 1 decreased significantly (all P 0.05, but there was no significant difference between 2% and 3% sodium chloride groups and 2% and 3% sodium chloride spironolactone groups.) compared with the normal control group, the CVFFN P0.05 of rats in 2% and 3% sodium chloride groups were significantly higher than those in the control group.However, the CVF of 2% and 3% sodium chloride groups decreased significantly after 5 weeks of intraspirolide intervention.In the group treated with spironolactone, the cardiac myocytes proliferated, hypertrophy, the degree of focal dissolving was light, and the fibrous tissue decreased significantly.Conclusion the expression of IL-17A in salt-induced hypertensive rats was significantly increased, which was positively correlated with the expression of TNF- 偽 -MMP-9 and TGF- 尾 _ 1, and decreased significantly after the intervention of spironolactone, suggesting that spironolactone might reverse the left ventricular interstitial fibrosis by regulating the expression of IL-17A- TNF- 偽 MMP-9 and TGF- 尾 _ 1.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R544.1;R542.2

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