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目的研究脑肠肽Ghrelin对血管紧张素Ⅱ(AngⅡ)诱导的大鼠胸主动脉血管平滑肌细胞(VSMCs)胞内钙离子浓度上升的作用,并初步探讨其机制。方法采用细胞培养的方法获得大鼠胸主动脉VSMCs,经Fluo-4-AM染色后,采用激光共聚焦显微镜技术分别检测加入AngⅡ后,1×10-7mol·L-1和1×10-5mol·L-1的Ghrelin对胞内钙荧光强度(FI)的影响,以及腺苷酸环化酶抑制剂Sq22536对Ghrelin作用的影响。结果①2×10-8mol·L-1的AngⅡ可以使得VSMCs胞内钙FI上升到静息状态的(165±76)%;②随后加入1×10~(-7)mol·L-1的Ghrelin可以使FI下降到(117±34)%(P<0.01vs①);③加入1×10-5mol·L-1的Chrelin可以使FI下降到(87±22)%(P<0.01 vs①,P<0.05 vs②);④预先以1×10-5mol·L-1的Sq22536孵育,再加入2×10-8mol·L-1AngⅡ和1×10-7mol·L-1的Ghrelin,胞内FI为原来的(143±24)%(P<0.01 vs②)。结论 Ghrelin能够降低AngⅡ引起的大鼠胸主动脉VSMCs胞内钙离子升高作用,其机制可能与激活胞内CAMP/PKA信号通路有关。
Objective To investigate the effect of Ghrelin on the increase of intracellular Ca2 + concentration in rat thoracic aorta vascular smooth muscle cells (VSMCs) induced by angiotensin Ⅱ (Ang Ⅱ) and its mechanism. Methods Thoracic aorta VSMCs were obtained by cell culture. After staining with Fluo-4-AM, the expression of AngⅡ was detected by laser scanning confocal microscopy in the presence of 1 × 10-7mol·L-1 and 1 × 10-5mol Effect of L-1 Ghrelin on Intracellular Calcium Fluorescence Intensity (FI), and Effect of Adenylate Cyclase Inhibitor Sq22536 on Ghrelin. Results AngII at 2 × 10-8 mol·L-1 increased intracellular calcium FI to (165 ± 76)% at rest in VSMCs. Secondly, Ghrelin (1 × 10 -7 mol·L -1) (P <0.01 vs ①, P <0.01 vs ①, P <0.01 vs P <0.01 vs P <0.01 vs P <0.01); (3) Chlitin treated with 1 × 10-5mol·L-1 could decrease FI to (87 ± 22) 0.05 vs ②); ④ pre-incubated with 1 × 10-5mol·L-1 Sq22536, then added 2 × 10-8mol·L-1Ang Ⅱ and 1 × 10-7mol·L-1 Ghrelin, intracellular FI is the original (143 ± 24)% (P <0.01 vs ②). Conclusions Ghrelin can decrease the intracellular Ca2 + upregulation induced by Ang ¢ ò in rat aorta VSMCs, which may be related to the activation of intracellular CAMP / PKA signaling pathway.