Parkinson’s disease (PD) is a neurodegenerative condition for which the exact causes remain elusive, and no effective treatments currently exist. The pathogenesis of PD is believed to involve oxidative stress, mitochondrial dysfunction, and lipid metabolism disorders. A benzodiazepine derivative JM-20 has demonstrated protective effects on mitochondria in both neurons and peripheral tissues of rats with rotenoneinduced Parkinson’s syndrome (PS). This study aimed to analyze bile composition and assess the impact of a new benzodiazepine derivative, methanindiazenone, on lipid metabolism in the liver of rats subjected to the rotenone model of PS. The results indicated that, compared to the control group, bile concentration of phospholipids, cholesterol, cholesterol esters, and triglycerides decreased by 24.3, 26.2, 25.8, and 27.5%, respectively. With methanindiazenone treatment at doses of 0.5 and 1.0 mg/kg, all these metrics reverted to the control level. However, in the rotenone+methanindiazenone 2.0 mg/kg group, the levels of phospholipids, cholesterol, and cholesterol esters (except for triglycerides) surpassed the control values by 33, 28.1, 28.4 and 33.5%, respectively. Methanindiazenone positively impacted the motor behavior of rats with the rotenone model of PS and enhanced their survival rates. Therefore, at doses of 0.5 and 1.0 mg/kg, methanindiazenone not only improved lipid metabolism in the liver but also the overall well-being of rats with the rotenone model of PS. However, a 2 mg/kg dose of methanindiazenone displayed toxic effects, as seen from the increased content of phospholipids, cholesterol, and cholesterol esters in bile. Hence, methanindiazenone holds potential as a therapeutic agent for PS and possibly other neurodegenerative diseases related to lipid metabolism impairment, but its use should be limited to doses of 0.5 and 1.0 mg/kg.