Naringin Attenuates D-galactose-Induced Brain Aging Via Regulation Of Oxidative Stress Markers TNF-α, NF-κβ And Modulation Of The Neurotrophic Markers PGC1-α, NT-3 AGEs, And GFAP In Vivo

Document Type : Original Article

Authors

1 pharmacology, NRC

2 Medical Biochemistry Department, National Research Centre

3 National research center

Abstract

Abstract

Aging is a global issue that we all deal with on a daily basis. The level of reliance among elderly persons everywhere increases as a result of brain aging and cognitive dysfunction. Naringin is a natural compound that showed various medicinal applications and is commonly used as an anticancer, antioxidant, and anti-inflammatory properties. The current research evaluated naringin infleunce on D-galactose (D-gal) stimulated brain aging in vivo. Mice were distriputed randomely to 4 groups (10 mice/ group): Normal group, D-gal group, Groups 3& 4: Naringin (150&300 mg/kg; orally) concurrent with D-gal for 8 weeks. Behavioral, brain biochemical, and histopathological changes were assessed. Results: Naringin treatment increased rate of discrimination in recognizing of objects , Y Maze percent fluctuation, locomotive activity, and brain levels of AMPK, LKB1, PGC1-α, nerve growth factor (neurotrophin-3; NT-3), dopamine, and serotonin with a significant decrement of brain contents of TNF-α, NF-κβ, AGEs, and GFAP compared to D-gal-treated mice. In addition, naringin ameliorated neuron degeneration. In conclusion, naringin ,with its anti-inflammatory effects , has stimulated mitochondrial biogenesis and modulated neurotrophic factors and neurotransmitters regulating nerve regeneration. Yet , naringin could be a promising drug with potential neuroprotective action against brain aging stimulated neurodegeneration.

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