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Role of homocysteine and folic acid on the altered calcium homeostasis of platelets from rats with biliary cirrhosis

机译：同型半胱氨酸和叶酸对胆汁肝硬化大鼠血小板钙稳态的作用

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Previously, we have found that intracellular calcium homeostasis is altered in platelets from an experimental model of liver cirrhosis, the bile-duct ligated (BDL) rat; these alterations are compatible with the existence of a hypercoagulable state. Different studies indicate that cholestatic diseases are associated with hyperhomocysteinemia; thus, we hypothetized that it could contribute to those platelet alterations. In the present study, we have investigated the role of homocysteine (HCY) in platelet aggregation and calcium signaling in the BDL model. The effect of chronic folic acid treatment was also analyzed. Acute treatment with HCY increased the aggregation response to ADP and calcium responses to thrombin in platelets of control and BDL rats. Capacitative calcium entry was not altered by HCY. Chronic treatment with folic acid decreased platelet aggregation in control and BDL rats, but this decrease was greater in BDL rats. In folic acid-treated rats, thrombin-induced calcium entry and release were decreased in platelet of control rats but unaltered in BDL rats; however, capacitative calcium entry was decreased in platelets of control and BDL rats treated with folic acid. Reactive oxygen species were produced at higher levels by BDL platelets after stimulation with HCY or thrombin and folic acid normalized these responses. HCY plays a role in the enhanced platelet aggregation response of BDL rats, probably through an enhanced formation of ROS. Folic acid pretreatment normalizes many of the platelet alterations shown by BDL rats.
机译：在此之前，我们已经发现，在肝硬化实验模型——胆管结扎（BDL）大鼠的血小板中，细胞内钙稳态发生改变；这些改变与高凝状态的存在是一致的。不同的研究表明，胆汁淤积性疾病与高同型半胱氨酸血症有关；因此，我们假设它可能导致血小板的改变。在本研究中，我们研究了同型半胱氨酸（HCY）在BDL模型中血小板聚集和钙信号传导中的作用。还分析了慢性叶酸治疗的效果。同型半胱氨酸急性治疗增加了对照组和BDL大鼠血小板对ADP的聚集反应和对凝血酶的钙反应。同型半胱氨酸不改变钙离子的容量输入。在对照组和BDL大鼠中，叶酸慢性治疗降低了血小板聚集，但在BDL大鼠中这种降低更大。在叶酸处理的大鼠中，对照组大鼠血小板中凝血酶诱导的钙进入和释放减少，而BDL大鼠中则没有变化；然而，对照组和接受叶酸治疗的BDL大鼠的血小板中的容性钙进入降低。在用同型半胱氨酸或凝血酶和叶酸刺激后，BDL血小板产生更高水平的活性氧，使这些反应正常化。同型半胱氨酸在BDL大鼠增强的血小板聚集反应中发挥作用，可能是通过增强ROS的形成。叶酸预处理使BDL大鼠的许多血小板改变正常化。

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