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本工作在凝血酶活化的大鼠血小板上，观察ＲＧＤＳ肽对血小板聚集，蛋白磷酸化及丝裂素活化蛋白激酶（ＭＡＰＫ）活性的影响，结果发现，ＩＵ／ｍＬ凝血酶明显引起血小板聚集，９５和６６ｋＤ蛋白磷酸化及ＭＡＰＫ活性的增加，应用５０、１００、２００μｍｏｌ／ＬＲＧＤＳ肽共向孵育，呈浓度依赖地抑制凝血酶引起的血小板聚集和ＭＡＰＫ活性，且两者呈正相关（ｒ＝０．８１，Ｐ＜０．０１）。ＲＧＤＳ肽亦呈浓度依赖地抑制凝血酶诱导的９５和６６ＫＤ蛋白磷酸化，与其抑制ＭＡＰＫ活性呈明显正相关（ｒ＝０．４１，Ｐ＜０．０５和ｄ．５３，Ｐ＜０．０１）。提示，ＭＡＰＫ系统参与了凝血酶引起的Ｗ小板聚集，ＲＧＤＳ肽抑制血小板聚集机理之一可能是通过干预血小板内信号传导途径所致。
This work on thrombin-activated rat platelets observed RGDS peptide on platelet aggregation, protein phosphorylation and mitogen-activated protein kinase (MAPK) activity and found that IU / mL thrombin caused platelet aggregation, 95 And phosphorylation of 66kD protein and MAPK activity. Co-incubation with 50, 100 and 200μmol / L LRGDS peptide inhibited the thrombin-induced platelet aggregation and MAPK activity in a concentration-dependent manner, and both were positively correlated (r = 0.81 , P <0.01). RGDS peptide also inhibited thrombin-induced phosphorylation of 95 and 66KD protein in a concentration-dependent manner, which was positively correlated with its inhibition of MAPK activity (r = 0.41, P <0.05 and d.53, P <0.01) . It is suggested that the MAPK system is involved in thrombin-induced W plate aggregation. One of the mechanisms by which RGDS peptide inhibits platelet aggregation may be due to the intervention of the intraplatelet signal transduction pathway.