Dihydromyricetin attenuates D-galactose-induced brain aging of mice via inhibiting oxidative stress and neuroinflammation

Aging-related especially brain aging-related diseases are heavy health care burdens worldwide. Natural products with antioxidant and anti-inflammatory properties have been studied to prevent brain aging pathogenesis. In the present study we investigated the potential mechanism of dihydromyricetin (DMY), isolated from Ampelopsis grossedentata, against D-galactose (D-Gal)-triggered brain aging of mice. Mice were randomly assigned into five groups (n = 20): control group, D-gal (150 mg/kg) group, D-gal (150 mg/kg) + Puerarin group, D-gal (150 mg/kg) + DMY (168 mg/kg) and D-gal (150 mg/kg) + DMY (42 mg/kg). Morris water maze (MWM) was used to assess spatial cognition and oxidative stress and inflammation index such as advanced glycation end products (AGEs), malondialdehyde (MDA), IL-2 and IL-6 were detected by ELISA. Cellular senescence marker was detected by Western blotting analysis. We found that DMY (42 mg/kg) showed strong neuroprotective effects, evidenced by improved spatial cognition and might be attributed to the alleviated damage of hippocampal neurons. In addition, DMY also suppressed the D-Gal-induced senescence of hippocampal neurons by inhibiting the expressions of p53, p21, and p16. Furthermore, DMY restored the activity of catalase and exhibited a potent inhibitory effect on lipid peroxidation, AGEs and MDA of D-Gal-exposed mice. Moreover, DMY decreased the abundance of IL-6 but increased the abundance of IL-2 of D-Gal-exposed mice. These findings indicated that DMY might protect against brain aging caused by chronic D-Gal exposure by modulating oxidative stress and inflammation-related senescence of hippocampal neurons.

Automated summary

The study showed that dihydromyricetin (DMY) exhibited strong neuroprotective effects against D-galactose (D-Gal)-triggered brain aging in mice, improving spatial cognition and alleviating damage to hippocampal neurons. DMY also suppressed D-Gal-induced senescence of hippocampal neurons, restored catalase activity, and showed potent inhibitory effects on oxidative stress and inflammation-related factors.