Paraquat (PQ), an environmental neurotoxicant, causes acute fatal poisoning upon accidental or intentional ingestion (suicidal cases) worldwide. To date, an effective remedy for PQ toxicity is not available. In this study, we have evaluated the therapeutic efficacy of Bacopaside-I (BS-I), an active compound found in the plant extract of Bacopa monnieri (Brahmi), against acute PQ intoxication using zebrafish as a model organism. Adult zebrafish were injected with a dose of either 30 mg/kg or 50 mg/kg PQ. PQ-intoxicated zebrafish showed an increased rate of mortality and oxidative imbalance in their brain. Also, the proliferation of neural cells in the adult zebrafish brain was inhibited. However, when BS-I pretreated zebrafish were intoxicated with PQ, the toxic effects of PQ were ameliorated. PQ treatment also affected the expression of particular genes concerned with the apoptosis and dopamine signaling, which was not altered by BS-I administration. Our results highlight the efficiency of BS-I as a novel therapeutic agent for PQ intoxication. It further compels us to search and evaluate the molecular mechanisms targeted by BS-I to develop a potent therapy for acute PQ intoxication.

百草枯 (PQ) 是一种环境神经毒物，在全球范围内因意外或故意摄入（自杀案例）而导致急性致命中毒。迄今为止，还没有针对百草枯毒性的有效补救措施。在这项研究中，我们评估了假马齿苋植物提取物中发现的活性化合物 Bacopaside-I (BS-I) 的治疗效果(Brahmi)，以斑马鱼为模式生物对抗急性百草枯中毒。成年斑马鱼注射剂量为 30 mg/kg 或 50 mg/kg PQ。PQ 中毒斑马鱼的大脑死亡率和氧化失衡率增加。此外，成年斑马鱼大脑中神经细胞的增殖也受到抑制。然而，当 BS-I 预处理的斑马鱼被百草枯中毒时，百草枯的毒性作用得到了改善。PQ 治疗还影响与细胞凋亡和多巴胺信号传导有关的特定基因的表达，BS-I 给药并未改变这些基因的表达。我们的结果强调了 BS-I 作为百草枯中毒的新型治疗剂的有效性。它进一步迫使我们搜索和评估 BS-I 靶向的分子机制，以开发一种有效的治疗急性百草枯中毒的方法。