Therapeutic potential of CDP-choline against paracetamol-induced injury in rats

Abstract

Paracetamol overdose is a leading cause of acute liver failure worldwide, necessitating alternative therapeutic agents. Cytidine 5′-diphosphocholine (CDP-choline, CDPC) exerts neuroprotective effects and may offer hepatoprotection via membrane-stabilizing, anti-inflammatory, and anti-apoptotic actions. This study aimed to evaluate the structural hepatoprotective potential of CDPC in a rat model of acute paracetamol toxicity. Randomized, controlled experimental animal study. Twenty-four male Wistar albino rats were randomized into four groups ( n = 6 /group): vehicle control, toxicity control (paracetamol 4 g/kg followed by saline at 6 h), and two CDPC treatment groups (250 and 500 mg/kg CDPC administered 6 h after paracetamol). Liver tissues were harvested 48 h post-dosing for histopathological scoring of hepatocyte degeneration, sinusoidal congestion, centrilobular necrosis, and parenchymal hemorrhage. High-dose CDPC (500 mg/kg) significantly reduced the incidence and severity of hepatocyte degeneration and sinusoidal congestion ( p < 0.001 ). Severe lesions were absent in the 500 mg/kg group. Centrilobular necrosis and parenchymal hemorrhage showed a non-significant decreasing trend with CDPC treatment. CDPC, particularly at 500 mg/kg, exhibits protective potential against paracetamol-induced structural liver injury. Further independent preclinical studies with biochemical and mechanistic endpoints are required to characterize its therapeutic efficacy. Not applicable.