Sharma_2025_Neuromolecular.Med_27_39

Organophosphate insecticides like malathion, though less toxic than other compounds in the same class, remain a significant public health concern due to their widespread use and potential neurotoxic effects. Prolonged exposure to malathion can lead to environmental contamination and neurobehavioral issues such as anxiety, depression, and cognitive impairment, mediated through cholinergic and non-cholinergic pathways. Cynodon dactylon (L.), a medicinal herb renowned in traditional and Ayurvedic medicine, exhibits anti-inflammatory, antioxidant, anti-diabetic, and neuroprotective properties. Evidence suggests that it can mitigate neurotoxicity and improve brain antioxidant status in rodent models. Therefore, this study explored the protective effects of the hydro-alcoholic extract of Cynodon dactylon (HAECD) on malathion-induced neurotoxicity, emphasizing its impact on behavior, biochemistry, and brain structure. Forty-two Swiss mice were randomly assigned to six groups, each containing seven mice. One group received normal saline (control), while another was given malathion (100 mg/kg, orally). Three groups received HAECD (250, 500, or 1000 mg/kg daily) alongside malathion, and the final group received only HAECD (1000 mg/kg, orally). Behavioral tests, including the elevated plus maze, light-dark test, and Morris water maze to assess the anxiety-depression-like behaviors, and cognitive function. Biochemical analyses measured acetylcholinesterase activity, lipid peroxidation, antioxidant enzymes (superoxide dismutase and catalase), and brain-derived neurotrophic factor (BDNF). Inflammatory markers and hippocampal histopathology were also examined. Results indicated that HAECD significantly alleviated anxiety and cognitive dysfunction while reducing oxidative stress markers, restoring antioxidant enzyme levels, and modulating brain-derived neurotrophic factor and inflammatory responses. These findings highlight the potential of HAECD in protecting the brain from malathion-induced neurotoxicity.