Modulatory Role of Curcumin on Cobalt-Induced Memory Deficit, Hippocampal Oxidative Damage, Astrocytosis, and Nrf2 Expression.
Rademene S OriaGodson E AnyanwuEmmanuel A EsomJohnson N NtoAmechi U KatchyAugustine U AguOmamuyovwi Meashack IjomonePublished in: Neurotoxicity research (2023)
Chemical overexposure is a growing environmental risk factor for many medical issues. Cobalt toxicity from environmental, industrial, and medical exposure has previously been linked to neurological impairment. Hence, the current study looked into the neuroprotective potential of curcumin, a natural polyphenol contained in the spice turmeric, against cobalt-induced neurotoxicity. Adult rats were randomly divided into six groups as follows: control, 40 mg/kg cobalt chloride (CoCl 2 ) only, 240 mg/kg curcumin only, 120 mg/kg or 240 mg/kg curcumin, or 100 mg/kg vitamin C co-administered with CoCl 2 . The administration was via oral route daily for 4 weeks. After that, neurobehavioral tests were undertaken to evaluate short-term spatial memory. Biochemical investigation was performed to determine the hippocampal levels of status via measures of SOD, CAT, GST, and LPO. Furthermore, immunohistochemical assessment of the expression of GFAP and Nrf2 in the hippocampus was carried out. In the CoCl 2 group, the results showed altered behavioral responses, a decrease in antioxidant activities, increased expression of GFAP and the number of activated astrocytes, and decreased immunoexpression of Nrf2. These effects were mitigated in the curcumin- and vitamin C-treated groups. These results collectively imply that curcumin enhances memory functions in rats exposed to cobalt possibly by attenuating oxidative responses, mitigating astrocytosis, and modulating Nrf2 signaling.
Keyphrases
- oxidative stress
- poor prognosis
- diabetic rats
- reduced graphene oxide
- cerebral ischemia
- working memory
- healthcare
- carbon nanotubes
- metal organic framework
- human health
- long non coding rna
- physical activity
- heavy metals
- gold nanoparticles
- risk assessment
- signaling pathway
- brain injury
- drug induced
- subarachnoid hemorrhage
- young adults
- blood brain barrier
- endothelial cells
- amyotrophic lateral sclerosis
- stress induced