Dilanchian Galia, Rezvani Sichani Ziba, Nayeri Hashem, Asgary Sedigheh
Department of Biochemistry, Islamic Azad University, Falavarjan Branch, Isfahan, Iran.
Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran.
ARYA Atheroscler. 2025;21(4):36-43. doi: 10.48305/arya.2025.43452.3024.
Rivaroxaban, a direct Factor Xa inhibitor, primarily acts by disrupting the coagulation cascade. However, it may also influence oxidative stress. This effect likely stems from its ability to reduce thrombin-mediated reactive oxygen species (ROS) production and mitigate inflammation. The major aim of the present investigation was to assess the effects of Rivaroxaban on oxidative stress and antioxidant capacity in patients with heart failure.
This study included 39 patients (17 males and 22 females, aged 30-95 years) with Stage B heart failure (HF) who had never previously received Rivaroxaban. Patients were enrolled from Chamran Cardiovascular Hospital in Isfahan after providing written informed consent, approved by the Falavarjan University Ethical Committee (IR.IAU.FALA.REC.1398.029). All patients had structural cardiac abnormalities, including reduced left ventricular ejection fraction (LVEF < 40%) or diastolic dysfunction, but no clinical symptoms of HF. Rivaroxaban (20 mg/day) was administered orally to all patients for two months using a pre-post design. Blood samples were collected before and after treatment to assess oxidative stress and antioxidant biomarkers, including total antioxidant capacity (TAC), malondialdehyde (MDA), homocysteine (Hcy), and the enzymatic activities of paraoxonase-1 (PON1) and arylesterase. TAC, MDA, and enzyme activities were measured spectrophotometrically, while homocysteine levels were determined using ELISA.
The results showed a significant reduction in MDA levels (P < 0.001), indicating reduced oxidative stress after Rivaroxaban treatment. However, no statistically significant changes were observed in other biomarkers, including homocysteine, arylesterase, paraoxonase, and TAC (P > 0.05).
In conclusion, Rivaroxaban appears to effectively reduce oxidative stress, as evidenced by decreased MDA levels.
利伐沙班是一种直接的Xa因子抑制剂,主要通过破坏凝血级联反应发挥作用。然而,它也可能影响氧化应激。这种作用可能源于其降低凝血酶介导的活性氧(ROS)生成和减轻炎症的能力。本研究的主要目的是评估利伐沙班对心力衰竭患者氧化应激和抗氧化能力的影响。
本研究纳入了39例B期心力衰竭(HF)患者(17例男性和22例女性,年龄30 - 95岁),这些患者此前从未接受过利伐沙班治疗。在获得法拉瓦尔詹大学伦理委员会(IR.IAU.FALA.REC.1398.029)批准并提供书面知情同意书后,患者从伊斯法罕的查姆兰心血管医院招募。所有患者均有心脏结构异常,包括左心室射血分数降低(LVEF < 40%)或舒张功能障碍,但无HF临床症状。采用前后设计,对所有患者口服利伐沙班(20 mg/天)两个月。在治疗前后采集血样,以评估氧化应激和抗氧化生物标志物,包括总抗氧化能力(TAC)、丙二醛(MDA)、同型半胱氨酸(Hcy)以及对氧磷酶-1(PON1)和芳基酯酶的酶活性。TAC、MDA和酶活性采用分光光度法测量,而同型半胱氨酸水平采用酶联免疫吸附测定法测定。
结果显示MDA水平显著降低(P < 0.001),表明利伐沙班治疗后氧化应激减轻。然而,在其他生物标志物,包括同型半胱氨酸、芳基酯酶、对氧磷酶和TAC方面,未观察到统计学上的显著变化(P > 0.05)。
总之,如MDA水平降低所示,利伐沙班似乎能有效减轻氧化应激。