Calcium ion (Ca²⁺) signaling in endometriosis (ENDO) is associated with increased neutrophil activation and oxidative stress. A Ca²⁺ signaling modulator and antioxidant actions of cabergoline (CBG) in some cells were recently reported. TRPM2 cation channel is activated by reactive oxygen species (ROS). Antioxidant action of CGB via inhibition of ROS may modulate the channel. We aimed to investigate the effect of CBG on TRPM2 inhibition in serum and neutrophils of patients with ENDO. The serum and neutrophil samples were grouped into healthy samples (no treatment), ENDO and ENDO + CBG treated groups (n = 10 in each). In some experiments, the neutrophils were also incubated with TRPM2 (ACA) and PARP-1 (PJ34) blockers. The values of intracellular ROS, Ca²⁺ concentration, mitochondrial membrane depolarization, lipid peroxidation, apoptosis, and caspase − 3, caspase − 9, PARP-1 and TRPM2 expressions were high in the neutrophils of patients with ENDO, although antioxidant levels (reduced glutathione, glutathione peroxidase, vitamin A, and vitamin E) were low in the neutrophils and serum from these patients. However, markers for apoptosis, oxidative stress, and mitochondrial dysfunction were reduced with CBG, ACA and PJ34 treatments, although the antioxidant levels were increased in the serum and neutrophils following treatment with CBG. Taken together, our current results suggest that CBG are useful antagonists against apoptosis and mitochondrial oxidative stress via inhibition of TRPM2 in neutrophils of patients with ENDO.

子宫内膜异位症（ENDO）中的钙离子（Ca ²⁺）信号传导与中性粒细胞活化和氧化应激增加有关。最近报道了一些细胞中Ca ²⁺的Ca ²⁺信号传导调节剂和抗氧化作用。TRPM2阳离子通道被活性氧（ROS）激活。通过抑制ROS，CGB的抗氧化作用可以调节通道。我们旨在研究CBG对ENDO患者血清和中性粒细胞TRPM2抑制的影响。将血清和中性粒细胞样品分为健康样品（未治疗），ENDO和ENDO + CBG治疗组（每组n = 10）。在某些实验中，中性粒细胞也与TRPM2（ACA）和PARP-1（PJ34）阻断剂一起孵育。细胞内ROS，Ca ²⁺的值浓度，线粒体膜去极化，脂质过氧化，细胞凋亡和caspase-3，caspase-9，PARP-1和TRPM2的表达在ENDO患者的中性粒细胞中较高，尽管抗氧化剂水平（谷胱甘肽，谷胱甘肽过氧化物酶，维生素A和这些患者的中性粒细胞和血清中维生素E）含量低。然而，CBG，ACA和PJ34处理可降低凋亡，氧化应激和线粒体功能障碍的标志物，尽管CBG处理后血清和中性粒细胞的抗氧化剂水平增加。两者合计，我们目前的结果表明CBG是通过抑制ENDO患者嗜中性粒细胞中TRPM2来对抗细胞凋亡和线粒体氧化应激的有效拮抗剂。