發(fā)布時間：2018-03-10 12:08

  本文選題：內(nèi)皮　切入點：血管　出處：《廣西醫(yī)科大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：目的:探討LPS誘導(dǎo)大鼠血管組織急性損傷后,其主動脈組織中Rho相關(guān)的卷曲蛋白激酶1(ROCK1)、縫隙連接蛋白(Cx)43和小窩蛋白(Cav)1表達(dá)的變化。Rho激酶抑制劑鹽酸法舒地爾(HF)對脂多糖(lipopolysaccharide,LPS)誘導(dǎo)的大鼠主動脈組織中ROCK1、Cx43、Cav1表達(dá)變化的影響,闡明HF的抗炎作用及機制。方法:采用隨機數(shù)字表法將24只雄性Sprague Dawley大鼠分為對照組(不做特殊處理)、HF組(腹腔注射HF 30 mg/kg)、脂多糖組(尾靜脈注射脂多糖1 mg/kg)和脂多糖+HF組(腹腔注射HF 30 mg/kg半小時后,尾靜脈注射脂多糖1 mg/kg),每組大鼠均為6只。LPS作用8 h后處死,提取主動脈組織。分別采用實時熒光定量PCR、Western blot和免疫組織化學(xué)法檢測主動脈組織中ROCK1、Cx43和Cav1的m RNA和蛋白表達(dá)水平。結(jié)果:(1)實時熒光定量PCR顯示,脂多糖組ROCK1(2.67±0.03)、Cx43(1.73±0.03)和Cav1(1.85±0.04)的m RNA表達(dá)水平均高于對照組中ROCK1(1.0±0.04)、Cx43(1.00±0.08)和Cav1(1.0±0.03)的m RNA表達(dá)水平及HF組ROCK1(0.77±0.04)、Cx43(0.91±0.01)和Cav1(0.82±0.03)的m RNA表達(dá)水平(P均0.05);而脂多糖+HF組ROCK1(0.38±0.02)、Cx43(0.58±0.02)和Cav1(0.27±0.01)的m RNA表達(dá)水平均低于脂多糖組(P均0.05)。(2)Western blot顯示,脂多糖組中ROCK1(3.46±0.82)、Cx43(0.33±0.09)和Cav1(3.45±0.74)的蛋白表達(dá)水平均高于對照組中ROCK1(2.19±0.56)、Cx43(0.21±0.09)和Cav1(2.25±0.91)的蛋白表達(dá)水平及HF組中ROCK1(1.57±0.38)、Cx43(0.18±0.07)和Cav1(2.06±0.40)(P均0.05);而脂多糖+HF組ROCK1(1.09±0.52)、Cx43(0.11±0.06)和Cav1(2.06±0.40)的蛋白表達(dá)水平均低于脂多糖組(P均0.05)。(3)免疫組織化學(xué)法顯示,脂多糖組ROCK1(84.1±0.9)、Cx43(99.1±2.1)和Cav1(167.0±6.4)的蛋白表達(dá)水平均高于對照組中ROCK1(53.7±2.9)、Cx43(46.2±0.8)和Cav1(84.9±1.0)的蛋白表達(dá)水平及HF組中ROCK1(40.1±0.9)、Cx43(35.1±0.6)和Cav1(74.4±0.5)的蛋白表達(dá)水平(P均0.05);而脂多糖+HF組ROCK1(30.4±0.6)、Cx43(21.4±1.3)和Cav1(55.8±2.8)的蛋白表達(dá)水平均低于脂多糖組(P均0.05)。結(jié)論:ROCK1、Cx43和Cav1均與LPS導(dǎo)致的血管內(nèi)皮功能障礙相關(guān)。LPS可以通過上調(diào)ROCK1、Cx43和Cav1的表達(dá),而發(fā)揮其致炎作用。HF可以通過直接抑制Rho A/ROCK1信號通路,降低ROCK1、Cx43的表達(dá)。同時也可能通過抑制Cav1的表達(dá)而調(diào)控Rho A/ROCK1信號通路的活性,改善LPS誘導(dǎo)的血管內(nèi)皮的炎性損傷,從而發(fā)揮其抗炎作用。
[Abstract]:Objective: to investigate the acute vascular injury induced by LPS in rats. Changes in the expression of Rho associated convoluted protein kinase 1 (ROCK1), creating-junction protein (CxF43) and fossa protein (Cav1) in aorta. Effects of Rho kinase inhibitor, fasudil hydrochloride, on the expression of ROCK1Cx43 Cav1 in rat aorta induced by lipopolysaccharide polysaccharide (LPS). Methods: 24 male Sprague Dawley rats were randomly divided into control group (30 mg / kg intraperitoneal injection of HF 30 mg / kg), lipopolysaccharide group (1 mg / kg lipopolysaccharide). Lipopolysaccharide HF group (30 mg/kg after intraperitoneal injection of HF), Lipopolysaccharide (LPS) 1 mg / kg was injected into caudal vein. Six rats in each group were killed after exposure to LPS for 8 h. The expression levels of m RNA and protein of Rock1Cx43 and Cav1 in aortic tissue were detected by real-time fluorescence quantitative PCR Western blot and immunohistochemistry, respectively. The results showed that the expression of m RNA and protein in aortic tissue was detected by real-time fluorescence quantitative PCR. The expression level of m RNA in lipopolysaccharide group (ROCK1(2.67 鹵0.03Cx43C 1.73 鹵0.03) and Cav1(1.85 鹵0.04) was higher than that in control group (ROCK1(1.0 鹵0.04Cx43C 1.00 鹵0.08) and Cav1(1.0 鹵0.03), and the expression level of m RNA in HF group (ROCK1(0.77 鹵0.04Cx430.91 鹵0.01) and Cav1(0.82 鹵0.03) was lower than that in lipopolysaccharide group (ROCK1(0.38 鹵0.02Cx43C 0.58 鹵0.02) and Cav1(0.27 鹵0.01). In group A, P was 0.05 and P was 0. 05 and 0. 05, respectively. Western blot was used to display the results. The expression levels of ROCK1(3.46 鹵0.82Cx43C 0.33 鹵0.09 and Cav1(3.45 鹵0.74) in the lipopolysaccharide group were higher than those in the control group (ROCK1(2.19 鹵0.56Cx43C 0.21 鹵0.09) and Cav1(2.25 鹵0.91), ROCK1(1.57 鹵0.38Cx430.18 鹵0.07) and Cav1(2.06 鹵0.40P in the HF group, while the expression levels of ROCK1(1.09 鹵0.52Cx43C 0.11 鹵0.06 and Cav1(2.06 鹵0.40) in the lipopolysaccharide group were lower than those in the lipopolysaccharide group (P < 0.05). Histochemistry shows that. The expression levels of ROCK1(84.1 鹵0.9Cx4399.1 鹵2.1) and Cav1(167.0 鹵6.4) in lipopolysaccharide group were higher than those in control group (46.2 鹵0.8) and Cav1(84.9 鹵1.0), ROCK1(40.1 鹵0.9Cx43C 35.1 鹵0.6.1 and Cav1(74.4 鹵0.5) protein expression levels in HF group were lower than those in lipopolysaccharide HF group (ROCK1(30.4 鹵0.6Cx4321.4 鹵1.3) and Cav1(55.8 鹵2.8). Conclusion both Cav1 and Cx43 are related to vascular endothelial dysfunction induced by LPS. LPs can up-regulate the expression of Cx43 and Cav1. By directly inhibiting Rho A / ROCK1 signaling pathway and decreasing the expression of ROCK1Cx43, HF could also regulate the activity of Rho A / ROCK1 signaling pathway by inhibiting the expression of Cav1, and improve the inflammatory injury of vascular endothelium induced by LPS. In order to play its anti-inflammatory effect.
【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】：R54

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本文編號：1593269