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Bradykinin-induced inositol 1,4,5-triphosphate in neonatal rat cardiomyocytes is activated by endotoxin.

机译:Bradykinin-induced肌醇1 4 5-triphosphate新生大鼠心肌细胞被激活内毒素。

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We studied the effect of endotoxin on bradykinin-induced inositol 1,4,5-triphosphate (IP3) production and the relationship between IP3 and phospholipase A2 or thromboxane A2. When exposed with 0.1, 1.0, and 10 microg ml(-1) lipopolysaccharide (LPS) for short-term (60 min), 100 nmol L(-1) bradykinin-induced IP3 production was stimulated in a dose-dependent manner from 569.2+/-42.4 in absence of LPS to 714.3+/-52.8, 804.5+/-42.6, and 894.1+/-62.6 pmol mg protein(-1). Treatment of 100 micromol L(-1) ACA (a phospholipase A2 inhibitor) and 10 micromol L(-1) BM13.177 (a thromboxane A2 inhibitor) significantly decreased bradykinin-induced IP3 production and LPS (1.0 microg mL(-1)) modulation of bradykinin-induced IP3 formation from 804.5+/-42.6 to 217.4+/-12.7 and 208.6+/-17.1 pmol mg protein(-1), respectively. LPS modulation of bradykinin-induced IP3 production was significantly blocked by 1 micromol L(-1) TMB-8 (an intracellular Ca2+ antagonist) from 804.5+/-42.6 to 507.8+/-33.4 pmol mg protein(-1). LPS modulation of bradykinin-induced IP3 production was significantly inhibited from 804.5+/-42.6 to 397.4+/-30.3 pmol mg protein(-1) by treatment of 10 micromol L(-1) indomethacin. In conclusion, short-term administration of LPS stimulates bradykinin-induced IP3 formation through activation of phospholipase A2 and thromboxane A2 and the stimulation is associated with an elevation of intracellular Ca2+.
机译:我们研究内毒素的作用bradykinin-induced肌醇1,4,5-triphosphate(IP3)生产和IP3之间的关系和磷脂酶A2或血栓素A2。暴露与0.1、1.0和10 microg毫升(1)脂多糖(LPS)短期(60分钟),100 nmol L (1) bradykinin-induced IP3生产在剂量依赖性的方式刺激的569.2 + -42.4 /缺乏有限合伙人为714.3 + / - -52.8,804.5 + / - -42.6和894.1 + / - -62.6 pmol毫克蛋白质(1)。(磷脂酶A2抑制剂)和10 micromolL (1) BM13.177(血栓素A2抑制剂)显著降低bradykinin-induced IP3生产和有限合伙人(1.0 microg毫升(1))调制的bradykinin-induced IP3的形成804.5 + / - -42.6到217.4 + / - -12.7和208.6 + / - -17.1分别pmol毫克蛋白(1)。的bradykinin-induced IP3生产明显被1 micromol L (1) TMB-8(一种细胞内钙离子拮抗剂)804.5 + / - -42.6到507.8 + / - -33.4 pmol毫克蛋白(1)。有限合伙人的调制bradykinin-induced IP3产量显著抑制804.5 + / - -42.6到397.4 + / - -30.3 pmol毫克蛋白(1)通过治疗10 micromol L(1)吲哚美辛。总之,短期管理有限合伙人刺激bradykinin-induced IP3形成通过激活磷脂酶A2和血栓素A2和相关的刺激细胞内钙离子的海拔。

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