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Mechanisms of the active components from Korean pine nut preventing and treating d-galactose-induced aging rats

Jianmei Zhang1, Weiwei Lin1, Ruijun Wu1

  • 1The State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|April 22, 2018
PubMed

Insights

Korean pine nut extract (UPNO-1) shows neuroprotective effects against d-galactose-induced aging and oxidative stress in rats. UPNO-1 reduced neuronal apoptosis and improved metabolic profiles, demonstrating its potential for preventing and treating age-related neurodegeneration.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Age-related neuronal injury and oxidative damage are key factors in neurodegenerative diseases like Alzheimer's disease.
  • D-galactose (d-gal) administration is a model for inducing such age-related changes.
  • Korean pine nut components, specifically UPNO-1, are investigated for their potential therapeutic benefits.

Purpose of the Study:

  • To determine if chronic d-galactose administration induces neuronal injury and oxidative stress.
  • To evaluate the neuroprotective and antioxidative effects of UPNO-1 from Korean pine nut.
  • To elucidate the metabolic disturbances caused by d-galactose and UPNO-1's impact on them.

Main Methods:

  • Rats were administered d-galactose with or without UPNO-1/fish oil (preventive) or UPNO-1/selegiline (therapeutic) for 8-12 weeks.
  • Histopathological examination and apoptosis assays were performed on brain tissues.
  • Metabolic profiling of hippocampus, cortex, and plasma was conducted using comprehensive analysis.

Main Results:

  • Chronic d-galactose administration led to histopathological changes, increased neuronal apoptosis, and decreased antioxidant enzyme activities (T-SOD, CAT, T-AOC).
  • Metabolic profiling revealed significant alterations in fatty acid, glycerolphospholipid, and arachidonic acid pathways.
  • UPNO-1 treatment significantly reduced neuronal apoptosis, improved histopathology, and restored T-SOD and CAT activities, while also normalizing specific plasma metabolites.

Conclusions:

  • Chronic d-galactose administration effectively models age-related neurotoxicity and oxidative stress.
  • UPNO-1 demonstrates significant neuroprotective and antioxidative effects, ameliorating d-galactose-induced damage.
  • UPNO-1 holds promise for preventing and treating neurodegenerative conditions associated with aging and oxidative stress.
Keywords:
MetabolomicsNeurotoxicityOxidative stressPrevention and treatmentUPNO-1d-Galactose

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