Effect of Xinshuai mixture on MAO and COX activity in hypertrophy myocardial cell / 中国生化药物杂志

Objective To study the effects of Xinshuai mixture on mitochondrial function of hypertrophy cardiomyocyte cell in vitro.Methods The primary neonatal rat myocardial cells were cultured to establish hypertrophic myocardial model by AngII.The levels of superoxide dismutase(SOD), methane dicarboxylic aldehyde (MDA), monoamine oxidase(MAO) and cyclooxygenase (COX) were detected by ELISA, as the mitochondrial function and oxidative stress damage.The expression level of caspase-3 mRNA was detected by Real-time PCR.Results Compared with control group, the SOD level in model group reduced markedly, MDA level increased significantly, the activities of MAO increased, the activities of COX decreased, the expression of caspase-3 level increased significantly(P<0.01).Compared with the model group, the SOD level increased and MDA level decreased in Xinshuai mixture group and blank serum group.But the SOD level and activities of MAO, COX in Xinshuai mixture group and blank serum group had significant difference(P<0.05,P<0.01).The expression of caspase-3 mRNA level in Xinshuai mixture was significantly higher than the blank serum group(P<0.01).Conclusion Xinshuai mixture could significantly improve the fuction of mitochondrial in hypertrophy cardiomyocyte cell, reduce the energy metabolism and oxidative stress injury, and protect cardiac myocyte through lower the expression of caspase-3.

A novel way for neurodegenerative diseases within cell and animal model by autophagy induced with rapamycin treatment / 国际生物医学工程杂志

Objective Using rapamycin protecting neurons' mitochondrial within injury model of neurodegenerative disease thus to reduce neuronal damage.Methods Parkinson's disease (PD) injury model of cells and animals were established,then rapamycin was added,and induced autophagy,the polarity changes of mitochondrial membrane potential,intracellular reactive oxygen species (ROS) scavenging and the contents of NF-κB inside the nucleus after dyeing were observed by confocal laser scanning microscopy.Results Rapamycin can induce autophagy and maintain morphology of mitochondria in cells damaged by MPP+.Mitochondrial membrane potential,level of ROS and contents of NF-κB inside the nuclear can be detected obviously reduced in these cells with rapamycin' s function.Furthermore,rapamycin also protects neurons well within PD models of zebrafish and mouse which are damaged by MPTP.Conclusions Rapamycin induces autophagy and protects mitochondria from damage within neurodegenerative disease,and strengthening this kind of protection of mitochondria is a novel way to deal with neurodegenerative diseases.