Résumé
AIM To investigate protective effects and mechanism of tanshinones on ischemia-like injury models. METHODS Six ischemia models including hypoxia, hypoglucose, oxidant injury, caffeine injury, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti-ischemic roles of tanshinones in cultured primary cortex neurons. The changes of injuried cortex neurons were observed by the way of morphological examination, and live neurons of crystal violet staining were measured according to absorbent index. RESULTS It was found that tanshinones possessed obvious protective effects on primary neurons in injury models by the way of morphological examination. Crystal violet staining also indicated that tanshinones increased number of live neurons in injury models significantly. The protective effects of tanshinones on models of oxidant injury, caffeine injury and NMDA injury were superior to other injury models. CONCLUSIONS 83.0 μmol*L-1 tanshinones protected rat cortex cells from all injury models effectively in vitro.
Résumé
Aim To investigate protective effects and mechanism of TPG on ischemia_like injury models. Methods Six ischemia models including hypoxia, hypoglucose, oxidant injury, calcium overload, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti_ischemic roles of TPG in cultured primary cortex neurons. Results It was found that TPG possessed obvious protective effects on primary neurons in injury models by the way of morphological examination. Crystal violet staining also indicated that TPG increased number of life neurons in injury models significantly. Couclusions 50～200 ?g?ml-1 TPG protected rat cortex cells from all injury models effectively in vitro.
Résumé
Objective: To investigate the protective effect and mechanism of total peaony glycoside (TPG) on calium overloading injury of nerve cells in rat models. Methods: The nerve cells of cerebral cortex of primary rats were subject to tissue culture,and the calcuim-overloading injury models were induced by caffeine,KCl and NMDA respectively. Results:TPG possessed obvious protective effects on the nerve cells in rat models, increased the number of survival nerve cells and reduced the content of LDH released nerve cells.Conclusion: TPG can protect rat nerve cells with calium-overloading injuriy.
Résumé
Objective: To investigate the effects and mechanism of transhinone on calcium overloaded injuried models.Methods: Three injured models induced by caffeine, KCI, and NMDA, respectively, were used to assay the action of tanshinone in cultured primary cortex neurone of baby rats. Results: It was found that tanshinone possessed obvious protective effects on primary neurone in injured models by the way of morphological examination. Crystal violet staining and lactic dehydrogenase (LDH) measurement in supernate also indicated that tanshinone increased number of live neurone and reduced the extent of cell injury significantly.Conclusion: Tanshinone protected rat cortex cells from three kinds of calcium overloadied injured effectively in vitro.
Résumé
AIM To investigate protective effects and mechanism of tanshinones on ischemia-like injury models. METHODS Six ischemia models including hypoxia, hypoglucose, oxidant injury, caffeine injury, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti-ischemic roles of tanshinones in cultured primary cortex neurons. The changes of injuried cortex neurons were observed by the way of morphological examination, and live neurons of crystal violet staining were measured according to absorbent index. RESULTS it was found that tanshinones possessed obvious protective effects on primary neurons in injury models by the way of morphological e~nation. Crystal violet staining also indicated that tanshinones increased number of live neurons in injury models significantly. The protective effects of tanshinones on models of oxidant injury, caffeine injury and NMDA injury were superior to other injury models. CONCLUSIONS 83.0 ?mol? L- 1 tanshinones protected rat cortex cells fm all injury models effectively in vitro.