PKG信号通路在ACS患者PCI术后血管内皮损伤中作用

The Effect of PKG Signaling Pathway on Vascular Endothelial Injury Induced by PCI in ACS Patients

目的探讨急性冠脉综合征(acute coronary syndrome, ACS)患者经皮冠状动脉介入治疗(percutaneous coronary intervention, PCI)与血管内皮功能损伤的关系,以及蛋白激酶G (PKG)信号通路在其中的作用。方法纳入ACS患者52例,收集患者基线资料,根据是否接受PCI治疗将患者分为PCI组(n=33)和非PCI组(n=19),测定两组患者术前及术后24 h血流介导的血管舒张(FMD)数值,采用ELISA检测患者术前及术后6h血清中内皮型一氧化氮合酶(e NOS)、亚硝酸盐及蛋白激酶G (PKG)活性值。结果 PCI组和非PCI组两组患者基线特征差异无统计学意义(P>0.05)。术前两组FMD值、血清e NOS、亚硝酸盐和PKG浓度比较差异无统计学意义(P>0.05)。PCI组术后FMD值(10.78±1.44)%与(13.20±2.79)%,(P <0.05)、血清e NOS (132.78±12.44) ng/m L与(148.89±15.22) ng/m L,(P <0.05)、亚硝酸盐(73.55±17.53) mmol/L与(91.14±7.15)mmol/L,(P <0.01)和PKG浓度(10.32±1.93) ng/m L与(11.77±1.95) ng/m L,(P <0.05)均较非PCI组降低。PCI组患者术后血清e NOS (132.78±12.44) ng/m L与(157.67±18.20) ng/m L,(P <0.05)、亚硝酸盐(73.55±17.53) ng/m L与(92.11±17.94) ng/m L,(P <0.05)和PKG浓度(10.32±1.93) ng/m L与(11.65±2.58) ng/m L,(P <0.05)均较术前显著降低,而非PCI组术后亚硝酸盐浓度、PKG浓度较术前均无明显变化。PCI组术前的PKG浓度与术后FMD值呈正相关(r=0.478,P=0.005)。结论 ACS患者PCI术后FMD和血清e NOS、NO、PKG均降低,提示PCI术可导致血管内皮损伤,可能与e NOS/NO/PKG信号通路有关。

Objective The aim of the study is to explore the relation between the percutaneous coronary intervention(PCI) and vascular endothelial injury in acute coronary syndrome(ACS) patients, and to investigate the effect of PKG signaling pathway on endothelial dysfunction. Methods 52 patients with ACS were enrolled, and baseline data of patients were collected. Patients were divided into PCI group(n = 33) and non-PCI group(n = 19) according to whether they were treated with PCI. Flow-mediated dilation(FMD) was measured before and 24 hours after operation in both groups, and the serum levels of endothelial nitric oxide synthase(e NOS),nitrite,and protein kinase G(PKG) concentration were measured by ELISA before and 6 hours after operation in the two groups. Results The baseline characteristics of the two groups patients had no statistically significant difference(P>0.05). There were no differences in FMD values, serum concentration of e NOS, nitrite and PKG between the two groups before operation(P >0.05). After operation, FMD values(10.78±1.44) % vs(13.20±2.79) %,(P < 0.05) and the concentration of e NOS(132.78±12.44)ng/m L vs(148.89±15.22) ng/m L,(P < 0.05), nitrite(73.55±17.53) mmol/L vs(91.14±7.15)mmol/L,(P < 0.01) and PKG(10.32±1.93) ng/m L vs(11.77±1.95) ng/m L,(P < 0.05) in the PCI group were lower than those in the non-PCI group. In the PCI group, the concentration of e NOS(132.78±12.44)ng/m L vs(157.67 ±18.2) ng/m L,(P < 0.05), nitrite(73.55 ±17.53) ng/m L vs(92.11 ±17.94)ng/m L,(P < 0.05) and PKG(10.32±1.93) ng/m L vs(11.65±2.58) ng/m L,(P < 0.05) after operation significantly reduced compared with before PCI operation group. However, in non-PCI groups, there was no significant difference in the concentration of nitrite and PKG between pre-operation and post-operation groups. There was a positive correlation between PKG and FMD in PCI group(r = 0.478, P = 0.005). Conclusion FMD values and the serum concentration of e NOS, NO and PKG were decreased after PCI in patients with ACS, and it suggests that PCI could induce vascular endothelial dysfunction, which may be related to e NOS/NO/PKG signaling pathway.