Feng Hui, Wang Zhipeng, Wang Changsong, Zhu Xinyi, Liu Zhigang, Liu Hongmei, Guo Ming, Hou Qian, Chu Zhenrong
Department of Traditional Chinese Medicine, Zhongda Hospital Affiliated to Southeast University, Nanjing, China.
Evid Based Complement Alternat Med. 2019 Jun 23;2019:9107847. doi: 10.1155/2019/9107847. eCollection 2019.
. To investigate the effect of Furostanol Saponins from Allium Macrostemon Bunge Bulbs (FSAMB) on platelet aggregation rate of rats with coronary heart disease and discuss the mechanism of FSAMB affecting the platelet aggregation rate through PI3K/Akt pathway. We established the rat models with coronary heart disease (CHD) and prepared the platelet-rich plasma. The effect of different concentrations of FSAMB on platelet aggregation in SD rats induced by ADP was observed in vitro and in vivo. And Lactate Dehydrogenase (LDH), Creatine Kinase-MB Form (CK-MB), and Cardiac Troponin I (cTnI) are detected in the blood to know the level of damage to heart cells. The expansion of platelets in the immobilized fibrinogen in different concentrations of FSAMB was observed. Western blot was conducted to detect the phosphorylation level of protein kinase B (also known as Akt) and the expression level of phosphoinositide 3-kinase (PI3K). We found that FSAMB had a significant inhibitory effect on the ADP-induced platelet aggregation in vitro. Intragastric administration of FSAMB also inhibited platelet aggregation induced by ADP in rats. LDH, CK-MB, and cTnI levels in serum of rats in FSAMB (672 mg/kg) group were lower than those in the model control group after the intervention (P<0.01 or P<0.05). FSAMB inhibited the expansion of platelets on immobilized fibrinogen. Also, FSAMB inhibited ADP-induced platelet PI3K expression and Akt phosphorylation. The inhibition of Akt phosphorylation by FSAMB was more obvious after the inhibition of the expression of PI3K. This study demonstrated that FSAMB can reduce the degree of myocardial cell damage and inhibit ADP-induced platelet aggregation in SD rats, possibly by inhibiting platelet PI3K/Akt signaling pathway in vitro and in vivo.
研究薤白呋甾烷醇皂苷（FSAMB）对冠心病大鼠血小板聚集率的影响，并探讨FSAMB通过PI3K/Akt途径影响血小板聚集率的机制。我们建立了冠心病大鼠模型并制备富血小板血浆。观察不同浓度FSAMB对体外及体内ADP诱导的SD大鼠血小板聚集的影响。检测血液中的乳酸脱氢酶（LDH）、肌酸激酶同工酶（CK-MB）和心肌肌钙蛋白I（cTnI），以了解心肌细胞损伤程度。观察不同浓度FSAMB对固定化纤维蛋白原中血小板伸展的影响。进行蛋白质免疫印迹法检测蛋白激酶B（又称Akt）的磷酸化水平和磷酸肌醇3激酶（PI3K）的表达水平。我们发现，FSAMB对体外ADP诱导的血小板聚集有显著抑制作用。灌胃给予FSAMB也可抑制大鼠体内ADP诱导的血小板聚集。干预后，FSAMB（672mg/kg）组大鼠血清中LDH、CK-MB和cTnI水平低于模型对照组（P<0.01或P<0.05）。FSAMB抑制固定化纤维蛋白原上血小板的伸展。此外，FSAMB抑制ADP诱导的血小板PI3K表达和Akt磷酸化。在抑制PI3K表达后，FSAMB对Akt磷酸化的抑制作用更明显。本研究表明，FSAMB可能通过在体外和体内抑制血小板PI3K/Akt信号通路，减轻SD大鼠心肌细胞损伤程度并抑制ADP诱导的血小板聚集。
