Shin Jung-Hae, Kwon Hyuk-Woo, Rhee Man Hee, Park Hwa-Jin
Department of Biomedical Laboratory Science, College of Biomedical Science and Engineering, Inje University, Gimhae, Republic of Korea.
Department of Biomedical Laboratory Science, Far East University, Eumseong, Republic of Korea.
J Ginseng Res. 2019 Apr;43(2):236-241. doi: 10.1016/j.jgr.2017.12.007. Epub 2018 Jan 9.
Thromboxane A (TXA) induces platelet aggregation and promotes thrombus formation. Although ginsenoside Ro (G-Ro) from is known to exhibit a Ca-antagonistic antiplatelet effect, whether it inhibits Ca-dependent cytosolic phospholipase A (cPLA) activity to prevent the release of arachidonic acid (AA), a TXA precursor, is unknown. In this study, we attempted to identify the mechanism underlying G-Ro-mediated TXA inhibition.
We investigated whether G-Ro attenuates TXA production and its associated molecules, such as cyclooxygenase-1 (COX-1), TXA synthase (TXAS), cPLA, mitogen-activated protein kinases, and AA. To assay COX-1 and TXAS, we used microsomal fraction of platelets.
G-Ro reduced TXA production by inhibiting AA release. It acted by decreasing the phosphorylation of cPLA, p38-mitogen-activated protein kinase, and c-Jun N-terminal kinase1, rather than by inhibiting COX-1 and TXAS in thrombin-activated human platelets.
G-Ro inhibits AA release to attenuate TXA production, which may counteract TXA-associated thrombosis.
血栓素A(TXA)可诱导血小板聚集并促进血栓形成。虽然已知人参皂苷Ro(G-Ro)具有钙拮抗抗血小板作用,但其是否通过抑制钙依赖性胞质磷脂酶A(cPLA)活性来阻止TXA前体花生四烯酸(AA)的释放尚不清楚。在本研究中,我们试图确定G-Ro介导的TXA抑制作用的潜在机制。
我们研究了G-Ro是否能减弱TXA的产生及其相关分子,如环氧合酶-1(COX-1)、TXA合酶(TXAS)、cPLA、丝裂原活化蛋白激酶和AA的水平。为了检测COX-1和TXAS,我们使用了血小板微粒体部分。
G-Ro通过抑制AA释放来减少TXA的产生。在凝血酶激活的人血小板中,它通过降低cPLA、p38丝裂原活化蛋白激酶和c-Jun氨基末端激酶1的磷酸化水平起作用,而不是通过抑制COX-1和TXAS。
G-Ro抑制AA释放以减弱TXA的产生,这可能抵消与TXA相关的血栓形成。