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Study on the effect and mechanism of total saponins of panax notoginseng on late-life anxiety |
DU Yao1,2 LI Xin1 ZHANG Guixian1 YUAN Yajin1 ZHOU Ningna1 |
1.Yunnan University of Traditional Chinese Medicine, Yunnan Province, Kunming 650500, China;
2.the First People′s Hospital of Qujing, Yunnan Province, Qujing 655000, China |
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Abstract Objective To explore the effect and mechanism of total saponins of Panax notoginseng leaves (tSPNL) on late-life anxiety. Methods Fifty aging male mice (12 months) were reared in group (n = 15, normal control group) or isolation (n = 60) according to the random number table method. After 4 weeks, the isolated rearing animal were then randomly divided into model group (vehicle), Diazepam (BDZ) group, tSPNL 500 group (500 mg/kg tSPNL) and tSPNL 100 group (100 mg/kg tSPNL). All mice were intragastrically administered desired compounds once a day for consecutive 14 days. The anxiety-like behaviors were evaluated by elevated plus maze (EPM), and levels of GABA and BDNF in hippocampus were determined by enzyme linked immunosorbent assay after the behavior test. In another set, aging male mice (n = 135) were rearing isolated for 4 weeks and were then randomly divided into model (vehicle), BDZ group, fluoxetine group, tSPNL 500 group. After administration of desired compounds intragastrically once a day for 14 days, animals underwent intraventricular injection of either BDNF receptor TrkB antagonist K252a or GABAA receptor antagonist Bicuculline (Bic), and the anxiety-like behaviors were measured by EPM 1 hour later. Results Compared with model group, the percentage of open arm time (OT%) increased significantly in tSPNL 500 group (P < 0.01), and the levels of BDNF and GABA also increased in hippocampus significantly (P < 0.05 or P < 0.01). After intraventricular injection of K252a and Bic, OT% in tSPNL 500 group decreased significantly (P < 0.05). Conclusion tSPNL can alleviate the anxiety-like behaviors in aging mice, and the mechanism is involved in BDNF-GABA signaling pathway, which may restore the GABAergic plasticity by increasing BDNF levels, thereby reducing the anxiety susceptibility of aging mice.
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