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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Myocardial NOS activity and connexin-43 expression in untreated and omega-3 fatty acids-treated spontaneously hypertensive and hereditary hypertriglyceridemic rats.
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Myocardial NOS activity and connexin-43 expression in untreated and omega-3 fatty acids-treated spontaneously hypertensive and hereditary hypertriglyceridemic rats.

机译:未经处理和omega-3脂肪酸处理的自发性高血压和遗传性高甘油三酯血症大鼠的心肌NOS活性和连接蛋白43表达。

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The purpose of this study is to investigate myocardial nitric oxide synthase (NOS) activity and connexin-43 (Cx43) expression in young and old spontaneously hypertensive rats (SHR), adult hereditary hypertriglyceridemic (HTG) rats, and age-matched healthy rats without and with omega-3 PUFA supplementation for 2 months. Results showed that comparing to healthy rats the myocardial NOS activity was significantly increased in young SHR (8.2 +/- 1.16 vs. 1.37 +/- 0.67 pmol/min/mg) as well as old SHR (3.21 +/- 0.75 vs. 2.22 +/- 0.56 pmol/min/mg) and to much lesser extent in HTG rats, i.e., 1.87 +/- 0.42 vs. 1.34 +/- 0.1 pmol/min/mg. In parallel, there was a significant decline of total and phosphorylated forms of Cx43 in both groups of SHR while not in HTG rat hearts in which phosphorylated form of Cx43 was increased. Elevated NOS activity was suppressed (P < 0.05) in young and old SHR supplemented with omega-3 PUFA and it was associated with up-regulation of Cx43. In contrast to SHR, elevation of NOS activity in HTG rat hearts was not affected by treatment with omega-3 PUFA. However, increase of phosphorylated form of Cx43 was suppressed. In conclusion, there is an inverse relationship between myocardial NOS activity and Cx43 expression in SHR while not HTG rat hearts and omega-3 PUFA modulate both NOS activity and Cx43 expression. Whether over-expression of inducible NOS might account for down-regulation of myocardial Cx43 and whether its up-regulation is associated with an increase of endothelial NOS should be explored in further study.
机译:这项研究的目的是调查年轻和老龄自发性高血压大鼠(SHR),成年遗传性甘油三酸酯(HTG)大鼠和年龄匹配的健康大鼠的心肌一氧化氮合酶(NOS)活性和连接蛋白43(Cx43)表达并补充2个月的omega-3 PUFA。结果显示,与健康大鼠相比,年轻SHR(8.2 +/- 1.16 vs. 1.37 +/- 0.67 pmol / min / mg)和老SHR(3.21 +/- 0.75 vs. 2.22)的心肌NOS活性均显着增加。 (+/- 0.56 pmol / min / mg),而在HTG大鼠中的程度要小得多,即1.87 +/- 0.42对1.34 +/- 0.1 pmol / min / mg。同时,两组SHR的总Cx43和磷酸化形式均显着下降,而在HTG大鼠心脏中Cx43的磷酸化形式却没有增加。在补充omega-3 PUFA的年轻和老年SHR中,NOS活性升高被抑制(P <0.05),并且与Cx43的上调相关。与SHR相反,HTG大鼠心脏中NOS活性的升高不受omega-3 PUFA治疗的影响。但是,Cx43磷酸化形式的增加被抑制。总之,在SHR中,心肌NOS活性与Cx43表达之间存在反比关系,而HTG大鼠心脏和omega-3 PUFA却不能调节NOS活性和Cx43表达。诱导型NOS的过度表达是否可能解释了心肌Cx43的下调,以及其上调是否与内皮型NOS的增加有关。

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