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Ginsenoside Rg1 cerebral ischemia on the expression of pJNK
PAGE \* MERGEFORMAT 11
Ginsenoside Rg1 cerebral ischemia on the expression of pJNK
[Abstract] Objective ginsenoside Rg1 on cerebral ischemia reperfusion rat brain c-jun N-terminal kinase (pJNK Express and its significance. Methods Rats were randomly divided into sham operation group, ischemia-reperfusion group, ginsenoside Rg1 10,20,40 mg / kg group, nimodipine 1 mg / kg group, using established by middle cerebral artery occlusion model of cerebral ischemia, using immunohistochemistry to detect cerebral ischemia 4h, pJNK expression. Results of the dose of ginsenoside Rg1 group pJNK expression in brain tissue were positive (23.89 + -6.77), (15.19 + -4.59), (9.15 + -4.77), were lower than ischemia reperfusion group (27.15 + -8.46). Conclusion ginsenoside Rg1 in rats during cerebral ischemia and reperfusion injury in rats by inhibiting the expression of brain pJNK, and the high dose is better.
[Keywords:] Ginsenosides Rg1 pJNK cerebral ischemia in rats
Abstract: Objective To discuss the effects of Ginsenoside Rg1 on the expressions of JNK in the rat s brain tissue after focal cerebral ischemia-reperfusion and its significance. Methods Rats were divided into the sham-operative group, Model group, Ginsenoside Rg1 groups of 10 mg / kg, 20 mg / kg, 40mg/kg, and Nimodipine group of 1 mg / kg at random. The method of middle cerebral artery occlusion (MCAO) in rats was adopted to establish the model of cerebral ischemia-reperfusion, and then the expressions of JNK after cerebral ischemia-reperfusion 6 h was tested based on the chemical method in immunity tissue. Results The positive rate of expression of rat s brain tissue in each of the Ginsenoside Rg1 groups is (23.89 + -6.77), (15.19 + -4.59), (9.15 + -4.77) respectively. Conclusions The results showed that the mechanism of Ginsenoside Rg1 to protect the brain cells from damage after cerebral ischemia-reperfusion injury may be associated with JNK expression to inhibit brain tissue, and it was more effectiv
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