本文選題：趨化因子CCL + 心肌梗死��； 參考：《解放軍醫(yī)學(xué)雜志》2017年05期

【摘要】：目的探討CC趨化因子配體2(CCL2)在殘余血小板高反應(yīng)中的作用及其調(diào)控血小板的可能機(jī)制。方法納入ST段抬高型心肌梗死(STEMI)患者40例,采用Verify Now法檢測(cè)P2Y12反應(yīng)單元(PRU),根據(jù)檢測(cè)結(jié)果將40例患者分為殘余血小板高反應(yīng)組(高反應(yīng)組,n=24)和殘余血小板正常反應(yīng)組(正常反應(yīng)組,n=16)。ELISA檢測(cè)兩組患者血漿中CCL2的表達(dá),Western blotting檢測(cè)血小板中CCL2和CCR2的表達(dá),ARY003B蛋白芯片篩選經(jīng)外源性CCL2刺激后血小板中磷酸化水平發(fā)生變化的激酶。Western blotting驗(yàn)證經(jīng)CCL2刺激,或經(jīng)CCR2拮抗劑(RS 102895)、p38MAPK信號(hào)通路抑制劑(SB 203580)預(yù)處理后血小板中p38MAPK和HSP27的磷酸化變化。結(jié)果高反應(yīng)組血漿中CCL2濃度、血小板中CCL2和CCR2表達(dá)均明顯高于正常反應(yīng)組。經(jīng)外源性CCL2刺激后,芯片篩選發(fā)現(xiàn)p38α、HSP27的磷酸化水平增高。在CCL2刺激前,應(yīng)用RS 102895或SB 203580預(yù)處理血小板,Western blotting檢測(cè)顯示p38MAPK和HSP27的磷酸化水平下降。結(jié)論 CCL2以自分泌/旁分泌的方式參與殘余血小板高反應(yīng),CCL2可能通過(guò)p38MAPK-HSP27通路調(diào)控血小板。
[Abstract]:Objective to investigate the role of CC chemokine ligand 2 (CCL 2) in the hyperresponsiveness of residual platelet and its possible mechanism. Methods 40 patients with ST-segment elevation myocardial infarction (STEMI) were included. P2Y12 reaction unit (PRU) was detected by Verify now method. According to the results, 40 patients were divided into two groups: high response group (high response group) and normal reaction group (n = 16). Elisa was used to detect CCL2 in plasma of two groups. The expression of CCL2 and CCR2 in platelets was detected by Western blotting. The protein chip ARY003B was used to screen the kinase. Western blotting showed that the phosphorylation of platelet was stimulated by CCL2. Or the phosphorylation of p38 MAPK and HSP27 in platelets were pretreated with CCR2 antagonist (RS 102895) and p38 MAPK signaling pathway inhibitor (SB 203580). Results the levels of CCL2 in plasma and the expression of CCL2 and CCR2 in platelets in high response group were significantly higher than those in normal reaction group. After stimulation with exogenous CCL 2, the phosphorylation level of p38 偽 -HSP27 was found to be increased by microarray screening. Before CCL2 stimulation, the phosphorylation of p38 MAPK and HSP27 was decreased after pretreatment with RS 102895 or SB 203580. Conclusion CCL2 is autocrine / paracrine involved in the hyperresponsiveness of residual platelet. CCL2 may regulate platelet by p38MAPK-HSP27 pathway.
【作者單位】： 沈陽(yáng)軍區(qū)總醫(yī)院全軍心血管病研究所;
【基金】：國(guó)家自然科學(xué)基金面上項(xiàng)目(81670340);國(guó)家自然科學(xué)基金青年項(xiàng)目(81500282)~~
【分類號(hào)】：R542.22

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