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Rice bran extract ameliorates metal mixture induced cerebral cortex dysfunction: implicating the Nrf-2/HMOX-1/BDNF
Baridoo Donatus Dooka1, Chinna N Orish2, Anthonet N Ezejiofor1
1African Centre of Excellence for Public Health and Toxicological Research (ACE-PUTOR), University of Port Harcourt, PMB, 5323, Choba, Port Harcourt, Nigeria.
Summary
Rice bran extract (RBE) protects the brain from heavy metal mixtures (MM) by reducing oxidative stress, inflammation, and apoptosis. RBE reverses heavy metal-induced neurotoxicity through antioxidant and anti-inflammatory pathways.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Heavy metal mixtures (MM) pose significant public health risks due to neurotoxic effects.
- Rice bran extract (RBE) possesses known antioxidant, anti-inflammatory, and antiapoptotic properties.
Purpose of the Study:
- To evaluate the neuroprotective potential of RBE against MM-induced cerebral dysfunction.
- To elucidate the underlying cellular mechanisms of RBE's neuroprotection.
Main Methods:
- Rats were exposed to MM (Pb, Al, Mn) alone or co-administered with varying doses of RBE for 90 days.
- Cerebral cortex analysis included antioxidants, lipid peroxidation, inflammation markers (cyclooxygenase-2), and protein levels of occludin, amyloid precursor proteins (Aβ40, Aβ42), caspase-3, HMOX-1, BDNF, and Nrf-2.
Main Results:
- RBE co-administration reversed MM-induced decreases in antioxidants and occludin, while decreasing lipid peroxidation, cyclooxygenase-2, and caspase-3 levels.
- MM exposure increased heavy metal bioaccumulation, Aβ40/42, and Nrf-2, while decreasing BDNF and HMOX-1.
- RBE treatment normalized these MM-induced changes, indicating reversal of neurotoxicity.
Conclusions:
- RBE effectively mitigates heavy metal-induced neurotoxicity, oxidative stress, inflammation, and apoptosis in the cerebral cortex.
- The neuroprotective effects of RBE are mediated through the regulation of amyloid precursor proteins, BDNF, and HMOX-1 via Nrf-2 dependent pathways.
