SK N SH cell glucoprival culture was used to establish the model of energy metabolic disturbance of nerve cells. The cytological and morphological indexes and lipid peroxide were measured to observe the preventing effects of PNS.
采用SK N SH细胞无糖培养方法 ,建立神经细胞能量代谢障碍模型 ,通过细胞学、形态学与脂质过氧化损伤指标的检测 ,观察中药三七皂甙 (PNS)对模型细胞的保护作用。
The present study was designed to explore the cause of mitochondrial energy metabolism dysfunction. The changes of ATPase6,8 genes and their expressions in a rat model of hemorrhagic shock were investgated.
Conclusions The method of injecting sodium azide into the rat's hippocampus could simply and rapidly establish rat's model of energy metabolism dysfunction with the changes of behavior and P3-like potential indicating dementia to some extent.
Objective: To study the effect of Xinnao Shutong capsule(XNST) on energy metabolism dysfunction,free radical injury and inflammatic factors in the course of acute cerebral ischemic damage,and try to reveal the mechanism of the protection against ischemia.
OFR-triggered lipid peroxidation, cellular energy metabolism disturbance and apoptosis may be principal manifestation of renal tubule epithelium cells injury in post-resuscitation rats. The results of this study demonstrate that Fas, Bcl-2 and NF- κB expression- induced by CPR seem to be responsible for the kidney apoptosis.
CONCLUSION:There are differences in the metabolic changes and ischemia reperfusion injury in different tissues after hemorrhagic shock and resuscitation. Moreover,the energy metabolism impairment and ischemia reperfusion injury of intestine are more severe than those of myocardium and skeleton muscle.
Method: The microdialysis and high performance liquid chromatography(HPLC)-post column Immobilized enzyme reactor(IMER)-electrochemical detection(ED) were used to establish a model of mitochondrial energy metabolism impairment which induced by perfusion with sodium azide(NaN_3), and measure continuously the effects of TZ on extracellular ACh, choline(Ch) and catecholamine of model rats.
CONCLUSION: CLA ameliorates the energy metabolism impairment of DM liver by suppressing the oxidative stress and improving the activity of enzymes in mitochondrial respiratory chain,and CLA has effective protection from the oxidative injury induced by DM.