Synergy nerve protective effect and its mechanism of sodium ferulate and ginseng saponins Rg1
10.3760/cma.j.issn.1673-4246.2013.10.009
- VernacularTitle:阿魏酸钠与人参皂苷Rg1协同神经保护作用及其机制
- Author:
Fengxia HOU
- Publication Type:Journal Article
- Keywords:
Sodium Ferulate;
Ginseng saponins Rg1;
Ischemia-reperfusion;
Peroxidase proliferation of activated receptor γ
- From:
International Journal of Traditional Chinese Medicine
2013;35(10):896-899
- CountryChina
- Language:Chinese
-
Abstract:
Objective Observe the synergy nerve protective effect and its mechanism of Sodium Ferulate (SF) and Ginseng saponins Rg1.Methods Ischemia-reperfusion injury models of rats were copied.The effects of SF,Ginsengsaponins Rg1 and the combination on infarction volume,lectin markers positive cells,peroxidase proliferation of activated receptorγ(PPAR-γ) mRNA expression,SOD activity and MDA content were observed.Results The blank control group didn't show infarction areas under TTC staining,and the cerebral infarction volume percentage of model control group,sodium ferulate group,ginsenoside Rg1 group and combination group was 44.2％,25.0％,20.4％,6.2％ respectively.The lectin positive cells number of blank control group,model control group,sodium ferulate group,ginsenoside Rg1 group and combination group were 11.4,44.6,27.8,23.0,13.4/500μm2 respectively; the PPAR-γmRNA expression were1883,1022,1473,1537,1843 respectively; the MDA content was 1.52,3.50,2.62,2.38,1.66 mmol/mg respectively; and the SOD acitivity was 71.54、73.14、81.72、82.22、91.10 U/mg respectively.Compared with model control group,sodium ferulate group,ginsenoside Rg1 group and combination group reduced the volume of cerebral infarcts (P＜0.01),inhibited the microglia activation(P＜0.01),increased the p PPAR-γ mRNA expression(P＜0.01),decreased the MDA content(P＜0.01) and increased SOD activity(P＜0.05,P＜0.01)significantly,and the effect of combination group was better than either sodium ferulate group or ginsenoside Rg1 group(P＜0.05,P＜0.01).Conclusion SF and Ginseng saponins Rg1 had collaborative neural protection and its activation on PPAR-γ may be one of the mechanisms.
