Chlorogenic acid confers robust neuroprotection against arsenite toxicity in mice by reversing oxidative stress, inflammation, and apoptosis

[Display omitted] •Exposure to arsenic causes apoptosis, inflammation and oxidative stress in brain.•Chlorogenic acid inhibits arsenic-induced neurotoxicity in mice.•Chlorogenic acid has antioxidant, antiinflammatory and antiapoptotic activities. Arsenic is a potent neurotoxic xenobiotic found in drinking water, and food. Chlorogenic acid (CGA), an abundant polyphenol in coffee, potentially has a wide range of therapeutic benefits. This study aimed to explore the mechanism in detail the neuroprotection provided by CGA against arsenite-induced toxicity in mice and the underlying mechanisms involved. The mice were randomly divided into five groups; control, CGA (200 mg/kg), arsenite (5 mg/kg), CGA (100 mg/kg) + arsenite, and CGA (200 mg/kg) + arsenite. All animals were treated daily for four weeks. Arsenite exposure significantly lowered all brain functions (neurochemicals, AChE, and BDNF) as well as cellular antioxidant activities, increased inflammatory and oxidative stress biomarkers, and the antiapoptotic Bcl2 gene, and upregulated apoptotic Bax and Casp3 genes. Fortunately, CGA reversed all arsenite-induced brain alterations in a dose-dependent manner. Therefore, CGA is recommended for practice use as a natural safeguarding food additive.