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目的观察抑制Janus激酶-信号转导子与转录激活子(janus kinases-singnal transducers and activatorsof transcription,JAK/STAT)信号通路对大鼠心肌缺血再灌注(I/R)损伤的影响。方法选择健康Wistar大鼠24只,随机分为假手术组、I/R组、JAK抑制剂组、STAT抑制剂组,每组各6只。JAK抑制剂组、STAT抑制剂组于I/R前30 min腹腔内分别注射AG490(8 mg/kg)、西罗莫司(0.4 mg/kg)。I/R组、JAK抑制组、STATR抑制组以穿线法结扎左冠状动脉前降支制备心肌I/R大鼠模型,假手术组仅穿线不结扎。采用免疫印迹法检测大鼠心肌p-JAK2、p-STAT1及p-STAT3的表达情况。结果假手术组p-JAK2、p-STAT1、p-STAT3均有少量表达。与假手术组比较,I/R组p-JAK2、p-STAT1、p-STAT3和STAT抑制剂组p-JAK2、p-STAT1表达明显增加,差异均有统计学意义(P<0.01)。与I/R组比较,JAK抑制剂组p-JAK2、p-STAT1、p-STAT3表达均减少,STAT抑制剂组p-STAT3表达减少,差异均有统计学意义(P<0.05)。I/R组和STAT抑制剂组p-STAT1的表达均高于同组p-STAT3的表达,差异有统计学意义(P<0.05)。结论 JAK/STAT信号通路参与心肌I/R,应用AG490抑制JAK/STAT后信号通路激活可减轻心肌损伤,但STAT抑制剂在心肌I/R中的作用有待进一步探讨。
Objective To observe the effect of Janus kinase-signal transducers and activators of transcription (JAK / STAT) signaling pathway on myocardial ischemia-reperfusion (I / R) injury in rats. Methods Twenty-four healthy Wistar rats were randomly divided into sham-operated group, I / R group, JAK inhibitor group and STAT inhibitor group, 6 rats in each group. JAK inhibitor group and STAT inhibitor group were injected AG490 (8 mg / kg) and sirolimus (0.4 mg / kg) intraperitoneally 30 minutes before I / R respectively. I / R group, JAK inhibition group and STATR inhibition group were ligated to ligate the left anterior descending coronary artery to establish myocardial I / R rat model. Western blotting was used to detect the expression of p-JAK2, p-STAT1 and p-STAT3 in rat myocardium. Results The sham group had a small amount of p-JAK2, p-STAT1 and p-STAT3. Compared with the sham group, the expressions of p-JAK2 and p-STAT1 in p-JAK2, p-STAT1, p-STAT3 and STAT inhibitor group were significantly increased in I / R group, the difference was statistically significant (P <0.01). Compared with I / R group, the expression of p-JAK2, p-STAT1, p-STAT3 in JAK inhibitor group decreased and the STAT inhibitor group decreased. The difference was statistically significant (P <0.05). The expression of p-STAT1 in I / R group and STAT inhibitor group was higher than that in the same group, the difference was statistically significant (P <0.05). Conclusions JAK / STAT signaling pathway is involved in myocardial I / R. Activation of AGA490 by inhibiting JAK / STAT signaling pathway may reduce myocardial injury. However, the role of STAT inhibitor in myocardial I / R remains to be further explored.