Lee Yuan Yee, Akram Abdul Wahab, Kim Young-Hee, Irfan Muhammad, Kim Sung Dae, Saba Evelyn, Kim Tae Wan, Yun Bong-Sik, Rhee Man Hee
Department of Veterinary Medicine, Kyungpook National University, Daegu, Republic of Korea.
Department of Animal and Avian Sciences, University of Maryland, College Park, MD, United States.
Front Pharmacol. 2025 Jun 26;16:1538417. doi: 10.3389/fphar.2025.1538417. eCollection 2025.
Traditionally, Thunb. (GJ) extract has been used to treat headaches and dizziness. We hypothesize that GJ exhibits anti-platelet activity that may prevent ischemic events to alleviate these symptoms. In this study, we investigated the anti-platelet activity of GJ as a potential mechanism for enhancing blood flow and preventing vessel occlusion.
Platelets were stimulated with collagen, adenosine diphosphate (ADP) or thrombin. Platelet aggregation was carried out using a platelet aggregometer with washed platelets from Sprague-Dawley rats. We observed the mobilization of calcium ions using Fura-2AM and adenosine triphosphate (ATP) release via a luminometer. The activation of integrin αIIbβ3 and population of platelet-neutrophil aggregates (PNAs) were investigated using flow cytometry. Platelet shape change was observed using scanning electron microscopy and transmission electron microscopy.
GJ extract inhibited collagen, ADP and thrombin-induced platelet aggregation. It effectively prevented the mobilization of calcium ions, ATP secretion, and serotonin release while thromboxane B2 levels did not change. Moreover, GJ inhibited the inside-out and outside-in signaling of integrin αIIbβ3. Notably, GJ treatment led to elevated expression of cyclic guanine monophosphate (GMP) (but not cyclic adenosine monophosphate). The protein expressions in the PI3K/Akt pathway were inhibited and platelet shape change was prevented. Finally, GJ treatment resulted in a decreased population of PNAs .
GJ exhibits potent anti-platelet activity acting by upregulating cGMP. It holds promise as a potential candidate for supplementation in patients with cardiovascular disease and thrombosis.
传统上，[植物名称]（GJ）提取物一直用于治疗头痛和头晕。我们假设GJ具有抗血小板活性，可能预防缺血性事件以缓解这些症状。在本研究中，我们研究了GJ的抗血小板活性，将其作为增强血流和预防血管闭塞的潜在机制。
用胶原蛋白、二磷酸腺苷（ADP）或凝血酶刺激血小板。使用血小板聚集仪对来自Sprague-Dawley大鼠的洗涤血小板进行血小板聚集实验。我们使用Fura-2AM观察钙离子的动员，并通过发光计检测三磷酸腺苷（ATP）的释放。使用流式细胞术研究整合素αIIbβ3的激活和血小板-中性粒细胞聚集体（PNA）的数量。通过扫描电子显微镜和透射电子显微镜观察血小板形状变化。
GJ提取物抑制胶原蛋白、ADP和凝血酶诱导的血小板聚集。它有效地阻止了钙离子的动员、ATP分泌和5-羟色胺释放，而血栓素B2水平没有变化。此外，GJ抑制整合素αIIbβ3的内向和外向信号传导。值得注意的是，GJ处理导致环磷酸鸟苷（cGMP）（而非环磷酸腺苷）表达升高。PI3K/Akt途径中的蛋白表达受到抑制，血小板形状变化得到阻止。最后，GJ处理导致PNA数量减少。
GJ通过上调cGMP表现出强大的抗血小板活性。它有望成为心血管疾病和血栓形成患者补充剂的潜在候选物。
