Protective Role of Launaea taraxacifolia Against Cadmium Chloride-Induced Hippocampal and Cortical Damage: A Study of Nitric Oxide Dysregulation and Bax Immunoreactivity in Male Wistar Rats

Abstract

Background: Cadmium chloride (CdCl₂) is a pervasive environmental neurotoxin known to induce nitrosative stress, disrupt neuronal signaling, and trigger apoptotic pathways in the brain.
Objective: This study explored the neuroprotective potential of Launaea taraxacifolia aqueous extract against CdCl₂-induced hippocampal and cortical injury, emphasizing nitric oxide (NO) dysregulation and Bax-mediated apoptosis in Wistar rats.
Methods: 32 male Wistar rats were randomly divided into four groups, each consisting of eight animals. For 21 consecutive days, Group I received distilled water orally; Group II received cadmium chloride
(CdCl₂) at a dose of 5 mg/kg orally; Group III received Launaea taraxacifolia aqueous extract (LTAE) at 400 mg/kg orally; while Group IV received 5 mg/kg of CdCl₂ followed by 400 mg/kg of LTAE orally. Biochemical analysis (NO) and Bax immunostaining were performed to assess CdCl2-induced hippocampal and cortical damage.
Results: There was a significant increase (p<0.05) in NO activity and overexpression of Bax in the cerebral cortex and hippocampus of Wistar rats that received CdCl2. However, these changes were significantly (p<0.05) reversed by reduced NO activity and Bax expression in rats that received LTAE as a co-treatment with CdCl2 when compared with the CdCl2-treated rats.
Conclusion: These findings suggest that L. taraxacifolia provides neuroprotection by mitigating nitrosative stress and apoptosis through modulation of NO signaling and Bax-mediated pathways. Keywords: Cadmium Chloride, Launaea taraxacifolia, Cerebral cortex, Hippocampus