Modulation of High-Fat Diet-Induced Brain Oxidative Stress by Ferulate-Rich Germinated Brown Rice Ethyl Acetate Extract

The oxidative stress resulting from the production of reactive oxygen species plays a vital role in inflammatory processes and is associated with neurodegenerative changes. In view of the ability of germinated brown rice (GBR) to improve learning and memory, this present study aimed to investigate the mechanistic basis of GBR's neuroprotection in a high-fat diet (HFD)-induced oxidative changes in adult Sprague-Dawley rats. Ferulate-rich GBR ethyl acetate extract (GBR-EA; 100 mg/kg and 200 mg/kg body weight) was supplemented orally for the last 3 months of 6 months HFD feeding during the study. GBR-EA supplementation was found to improve lipid profile and serum antioxidant status, when compared to the HFD group. Elevated mRNA expressions of SOD1, SOD2, SOD3, Catalase, and GPX were demonstrated in the frontal cortex and hippocampus of GBR-EA treated animals. The pro-inflammatory changes induced by HFD in the hippocampus were attenuated by GBR-EA through the downregulation of CRP and TNF- alpha and upregulation of PPAR-gamma. GBR also reduced the hippocampal mRNA expression and enzyme level of acetylcholinesterase. In conclusion, this study proposed the possible transcriptomic regulation of antioxidant and inflammation in neurodegenerative processes resulting from high cholesterol consumption, with an emphasis on GBR's potential to ameliorate such changes.

Automated summary

This study investigates the neuroprotective effect of germinated brown rice ethyl acetate extract (GBR-EA) on oxidative changes induced by a high-fat diet (HFD) in rats. GBR-EA supplementation improves lipid profile and serum antioxidant status, regulates the expression of antioxidant and inflammatory genes, and attenuates pro-inflammatory changes in the hippocampus. This study highlights the potential of GBR-EA to ameliorate neurodegenerative processes resulting from high cholesterol consumption.