Salvianolic acid a inhibits platelet activation and aggregation in patients with type 2 diabetes mellitus.

BACKGROUND: Platelets in patients with type 2 diabetes mellitus (DM2) are characterized by increased activation and aggregation, which tends to be associated with a high morbidity and mortality due to cardiovascular disease (CVD). Moreover, a large proportion of DM2 patients show an inadequate response to standard antiplatelet treatments, contributing to recurrent cardiovascular events. In our previous study, we indicated that Salvianolic acid A (SAA) presents an antiplatelet effect in healthy volunteers. However, whether it can inhibit "activated platelets" with a pathologic status has not been explored. Therefore, this study was designed to investigate the antiplatelet effect of SAA and its diabetic complication-related difference in DM2. METHODS: Forty patients diagnosed with DM2 from January 2018 to April 2018 were recruited. Fibrinogen-binding (PAC-1) and P-selectin (CD62p) flow cytometry reagents were measured under resting and stimulated conditions by flow cytometry, while agonist-induced platelet aggregation was conducted by light transmission aggregometry. Before all these measurements were conducted, all platelet samples were preincubated with a vehicle or SAA for 10 min. Additionally, the diabetic complication-related difference in the antiplatelet effect of SAA was further studied in enrolled patients. RESULTS: The expressions of PAC-1 and CD62p were elevated in DM2, as well as the maximal platelet aggregation. In addition, SAA decreased the expressions of PAC-1 and CD62p, which were enhanced by ADP and thrombin (all P < 0.01). It also reduced the platelet aggregation induced by ADP (P < 0.001) and thrombin (P < 0.05). Comparing the antiplatelet effect of SAA on DM2, with and without diabetic complications, no statistically significant difference was found (all P > 0.05). CONCLUSIONS: The present study demonstrated that SAA can inhibit platelet activation and aggregation in patients with DM2, and the inhibition did not abate for the existence of diabetic complications.

[A method of primary cell culture of rat pulmonary artery smooth muscle cells and effects of platelet-derived growth factor induced proliferation and migration].

OBJECTIVE: To establish an easy, not depending on advanced laboratory apparatus method to isolate and culture rat pulmonary artery smooth muscle cells (PASMCs), and to explore the effects of platelet-derived growth factor (PDGF) on cell proliferation and migration. METHODS: The right ventricle was perfused with the mixture of iron, agarose, and the PASMCs and iron could adhere to agarose. The iron-con-taining tissue would move to side of the tube next to the magnet and could be digested by collagenase I. By the method, vessel-containing tissue could be attained. With 3-4 weeks' purification, the PASMCs could be obtained. The PASMCs morphology was observed by an inverted micro-scope, and identified by immunocytochemistry and immunofluorescence. The effects of PDGF on cell proliferation and migration was detected by MTT assay and scratch wound assay. RESULTS: 14 days、21 days and primary culture after isolation, the PASMCs was identified, and the re-sult showed that isolation and primary culture of the cells were PASMCs. Compared with the cells with no stimulation, the proliferation of PASMCs exposed to PDGF was increased significantly(P<0.05), and scratch wound assay demonstrated that PDGF induced the significant increase of migration of PASMCs. CONCLUSIONS: This method to isolate and culture rat PASMCs is simple, not depending on advanced laborato-ry. PDGF can promote the proliferation and migration of PASMCs.