首页> 外文期刊>Journal of Thoracic Disease >Adiponectin protects rat heart from left ventricular remodeling induced by chronic intermittent hypoxia via inhibition of TGF-β/smad2/3 pathway
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Adiponectin protects rat heart from left ventricular remodeling induced by chronic intermittent hypoxia via inhibition of TGF-β/smad2/3 pathway

机译:脂联素通过抑制TGF-β/ smad2 / 3途径保护大鼠心脏免受慢性间歇性缺氧所致的左心室重构

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Objective: Obstructive sleep apnea syndrome (OSAS) is associated with many cardiovascular disorders. Chronic intermittent hypoxia (CIH) is the primary player in OSAS of the many associated factors. This study was in order to investigate the effects of the Adiponectin (Ad) on left ventricular remodeling induced by CIH. Methods: Forty-five rats were randomly divided into three groups: normal control (NC) group, CIH group and CIH plus Ad supplemented (CIH + Ad) group. After 35 days’ CIH exposure, masson analysis was used to detect the left ventricular fibrosis and western blot was used to measure the protein expression of collagen I, collagen III and TGF-β/smad2/3 pathway. Gene analysis by RT-PCR was used to study the MMP2 and TIMP2. Results: After CIH exposure, the fibrosis of left ventricular in CIH group was significantly remarkable than that in both NC and CIH + Ad groups (P0.05), although statistical difference existed between NC and CIH + Ad groups (P0.05). In addition, the protein expression of collagen I as well as collagen III and the ratio of mRNA levels of MMP2/TIMP2 were the highest in CIH group but the lowest in NC group, with CIH + Ad group in between. There was a significant difference among three groups (all P0.05). The TGF-β/smad2/3 pathway was activated obviously in CIH group, but less noticeably in CIH + Ad group (P0.05) with a significant difference in the two groups. Conclusions: The present study showed that Ad could ameliorate the left ventricular remodeling induced by CIH via inhibition of the expression of TGF-β/smad2/3 pathway.
机译:目的:阻塞性睡眠呼吸暂停综合症(OSAS)与许多心血管疾病有关。慢性间歇性缺氧(CIH)是许多相关因素中OSAS的主要因素。这项研究是为了调查脂联素(Ad)对CIH诱导的左心室重塑的影响。方法:45只大鼠随机分为三组:正常对照组(NC),CIH组和CIH加Ad补充组(CIH + Ad)。 CIH暴露35天后,用Masson分析检测左心室纤维化,Western blot检测I型胶原,III型胶原和TGF-β/ smad2 / 3途径的蛋白表达。通过RT-PCR进行基因分析以研究MMP2和TIMP2。结果:CIH暴露后,CIH组左心室纤维化明显高于NC和CIH + Ad组(P <0.05),尽管NC和CIH + Ad组之间存在统计学差异(P <0.05)。另外,CIH组胶原蛋白I和III的蛋白表达和MMP2 / TIMP2的mRNA水平之比在CIH组中最高,而在NC组中最低,介于CIH + Ad组之间。三组间差异有统计学意义(均P <0.05)。在CIH组中,TGF-β/ smad2 / 3途径被明显激活,而在CIH + Ad组中,则较不明显(P <0.05),两组之间有显着差异。结论:本研究表明,Ad可以通过抑制TGF-β/ smad2 / 3途径的表达来改善CIH引起的左心室重构。

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