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Angiopoietin-like protein 2 expression is suppressed by angiotensin II via the angiotensin II type 1 receptor in rat cardiomyocytes

机译:血管紧张素II通过大鼠心肌细胞中的1型血管紧张素II受体抑制血管生成素样蛋白2的表达

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The present study aimed to determine the inhibitory effects of angiotensin II (AngII) on angiopoietin-like protein 2 (Angptl2) in rat primary cardiomyocytes, and to investigate the potential association between angiotensin II type 1 receptor (AT1R) and these effects. Cardiomyocytes were isolated from 3-day-old Wistar rats, and were cultured and identified. Subsequently, the expression levels of Angptl2 were detected following incubation with various concentrations of AngII for various durations using western blotting, reverse transcription-quantitative polymerase chain reaction, enzyme-linked immunosorbent assay and immunofluorescence. Finally, under the most appropriate conditions (100 nmol/l AngII, 24 h), the cardiomyocytes were divided into six groups: Normal, AngII, AngII + losartan, normal + losartan, AngII + PD123319 and normal + PD123319 groups, in order to investigate the possible function of AT1R in Angptl2 suppression. Losartan and PD123319 are antagonists of AT1R and angiotensin II type 2 receptor, respectively. The statistical significance of the results was analyzed using Student's t-test or one-way analysis of variance. The results demonstrated that Angptl2 expression was evidently suppressed (P<0.05) following incubation with 100 nmol/l AngII for 24 h. Conversely, the expression levels of Angptl2 were significantly increased in the AngII + losartan group compared with the AngII group (P<0.01). However, no significant difference was detected between the AngII + PD123319, normal + losartan or normal + PD123319 groups and the normal group. The present in vitro study indicated that AngII was able to suppress Angptl2 expression, whereas losartan was able to significantly reverse this decrease by inhibiting AT1R.
机译:本研究旨在确定血管紧张素II(AngII)对大鼠原代心肌细胞中血管生成素样蛋白2(Angptl2)的抑制作用,并研究血管紧张素II 1型受体(AT1R)与这些作用之间的潜在联系。从3天大的Wistar大鼠中分离出心肌细胞,并进行培养和鉴定。随后,使用蛋白质印迹,逆转录定量聚合酶链反应,酶联免疫吸附测定和免疫荧光法,在各种浓度的AngII中孵育不同的时间后,检测Angptl2的表达水平。最后,在最合适的条件下(100 nmol / l AngII,24小时),将心肌细胞分为六组:正常,AngII,AngII +氯沙坦,正常+氯沙坦,AngII + PD123319和正常+ PD123319组,以便研究AT1R在Angptl2抑制中的可能功能。 Losartan和PD123319分别是AT1R和2型血管紧张素II受体的拮抗剂。结果的统计显着性使用Student t检验或单向方差分析进行了分析。结果表明,在与100 nmol / l AngII孵育24小时后,Angptl2表达被明显抑制(P <0.05)。相反,AngII +氯沙坦组的Angptl2表达水平明显高于AngII组(P <0.01)。然而,在AngII + PD123319,正常+氯沙坦或正常+ PD123319组和正常组之间未检测到显着差异。目前的体外研究表明,AngII能够抑制Angptl2表达,而氯沙坦能够通过抑制AT1R显着逆转这种下降。

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