目的 探讨莱菔硫烷（sulforaphane， SFN）对高糖（high glucose， HG）诱导人血小板凋亡的保护作用及机制。 方法 将不同浓度（5、10、20 μmol/L）的SFN或溶剂对照（0.05% DMSO）与健康人纯化血小板在体外共同孵育40 min，然后加入normal glucose（NG， 5 mmol/L）或HG（25 mmol/L）的葡萄糖溶液干预血小板90 min，用流式细胞术检测血小板线粒体膜电位（ΔΨm）去极化、磷脂酰丝氨酸（phosphatidylserine， PS）暴露和胞内总活性氧（reactive oxygen species， ROS）生成水平，用蛋白免疫印迹法检测PI3K、Akt蛋白磷酸化水平。 结果 与NG组相比，HG可显著增加血小板ΔΨm去极化和PS暴露水平（P < 0.001），且可被不同浓度的SFN显著抑制（P < 0.001）。机制上，与溶剂对照组相比，SFN显著下调HG诱导的血小板PI3K（P < 0.01）和Akt（P < 0.05）蛋白的磷酸化水平，显著降低HG诱导的胞内总ROS生成水平（P < 0.001）；PI3K的特异性激动剂740 Y-P可完全逆转SFN对HG诱导的PI3K和Akt蛋白磷酸化的抑制作用，部分逆转SFN对总ROS生成、ΔΨm去极化和PS暴露的抑制作用。 结论 SFN在体外具有保护HG诱导健康人血小板凋亡的作用，其作用机制可能是下调PI3K/Akt介导的信号通路。

Objective To investigate the protective effects of Sulforaphane （SFN） against high glucose （HG）?induced human platelet apoptosis and elucidate the underlying mechanisms in vitro. Methods Purified platelets obtained from healthy individuals were pre?incubated with various concentrations of SFN （5， 10， or 20 μmol/L） or a vehicle control （0.05% DMSO） for 40 minutes at 37 ℃. Subsequently， the platelets were stimulated with normal glucose （NG， 5 mmol/L） or high glucose （HG， 25 mmol/L） for an additional duration of 90 minutes. Flow cytometry was employed to assess platelet mitochondrial membrane potential depolarization （Δψm）， exposure of phosphatidylserine （PS）， and generation of total intraplatelet reactive oxygen species （ROS）. Phosphorylation levels of PI3K and Akt were determined using Western blot. Results Compared to NG?treated human platelets， HG significantly induced depolarization of platelet Δψm and exposure of PS （P < 0.001）. These effects of HG were markedly attenuated by various concentrations of SFN （P < 0.001）. Mechanistically， SFN down?regulated the phosphorylation levels of PI3K （P < 0.01） and Akt （P < 0.05）， which were increased by HG when compared to the vehicle control， and substantially reduced total intracellular ROS levels （P < 0.001）. The inhibitory effects of SFN on HG?induced phosphorylation of PI3K and Akt， as well as its efficacy on total intracellular ROS generation， Δψm depolarization， and PS exposure in HG?stimulated human platelets were completely reversed by a specific agonist for PI3K， 740 Y?P. Conclusions The current study demonstrates that SFN exerts a protective effect on platelet apoptosis induced by HG， potentially through the down?regulation of the PI3K/Akt?mediated pathway in human platelets in vitro. These findings suggest that SFN may hold promise for improving thrombosis in diabetes mellitus and related chronic metabolic diseases.