In vivo and in vitro studies of protective effect of CDPS onacute aging mouse model induced by D-galactose
10.3969/j.issn.1001-1978.2017.07.009
- VernacularTitle:肉苁蓉多糖对D-半乳糖所致急性衰老模型保护作用研究
- Author:
Yan WU
;
Hong ZHANG
;
Ren BU
;
Hui MA
;
Miao SU
;
Gang LI
- Keywords:
CDPS;
CAMP/PKA/CREB;
BDNF;
Neurotransmitters;
anti-aging;
D-galactose
- From:
Chinese Pharmacological Bulletin
2017;33(7):927-933
- CountryChina
- Language:Chinese
-
Abstract:
Aim To study the protective effect of CDPS on acute aging mouse model induced by D-galactose (D-gal) and its mechanism.Methods (1) The acute aging mouse model was induced by D-gal.After CDPS (25、50、100 mg·kg-1) treatment, the improving effect on learning and memory in mice was examined in vivo.(2) We also established the aging model on PC12 cells in vitro.After CDPS treatment (150、200 mg·L-1), the level of p-CREB in the nucleus was detected by Western blot, and the content of cAMP, PKA and brain derived neurotrophic factor (BDNF) levels were examined by the Elisa kits.Moreover, cAMP, PKA and BDNF were detected in PC12 cells under the condition that H89, the inhibitor of PKA, co-cultured with PC12 cells after CDPS treatment.(3) The UPLC/Q Exactive MS method was developed for determining the concentration of glutamic acid, dopamine and norepinephrine, which secreted in PC12 cells after CDPS treatment.Results (1) In vivo, CDPS significantly improved the memory impairment in aging mice induced by D-gal in the Morris assay.(2) In vitro, CDPS could significantly increase the expression of p-CREB (P<0.05), PKA, cAMP and BDNF (P<0.05).The H-89 abolished the increase of p-CREB (P<0.05), PKA, cAMP and BDNF (P<0.05) in PC12 aging cells induced by D-gal after CDPS treatment.(3) CDPS increased the release of dopamine, norepinephrine, and glutamate secreted in PC12 cells.Conclusion CDPS could significantly improve the learning and memory ability on aging mouse model in vivo, and reversed the damage in PC12 cells induced by D-gal by activating cAMP/PKA/CREB signal cascade, increase the expression of BDNF, and increasing modestly the release of excitatory neurotransmitter.
