Protection Of Astragalus Polysaccharide And Its Mechanism In Cardiac Myocyte Of Neonatal Rats Injured By Radiation

Objective: To investigate the effect of APS on antiradiation damage in cardiacmyocytesand its mechanism.Methods: Primary extraction techniques successfully cultured myocardial cells in vitro,X–ray establishment of cardiacmyocyte damage model and the intervention by differentconcentration of APS. The experiment was divided into the following five groups: Normalcontrol group; Radiation damage model group(6Gy); Low-dose APS intervenetion group(0.025mg/mL); Medium-dose APS intervention group(0.05mg/mL); High–dose APSintervenetion group(0.1mg/mL). The growth inhibition rate of myocardial cells of everygroups was assessed using MTT assay; The cell cycle and apoptosis of every groups wasdetected by flow cytometry; The mitochondrial function of every groups was evaluated bylaser confocal microscope; The levels of ROS of every groups was measured by fluorescentprobe DCFH-DA; The protein expression of CytC, caspases-3, caspases-9in the myocardialcells of every groups were determined with western blot method.Result: The cardiacmyocyte of normally cultured were round shape,but after radiationdamage, they are turned round and floated at different levels the cell apoptosis had began.Compared with the normal group, the model group showed that the growth inhibition rate ofcardiacmyocyte was increased, the X-ray can prolong the period and increases the apoptosisratio of cardiacmyocyte, the mitochondrial disorder in model group and the ΔΨm decreased,the levels of ROS, CytC, caspases-3, caspases-9expression increased（p＜0.05）. Comparedwith the model group, the APS intervention groups showed that the growth inhibition rate ofcardiacmyocyte was decreased, the cell cycle shortened and the apoptosis ratio ofcardiacmyocyte decreased, the mitochondrial function improved and the ΔΨm increased, thelevels of ROS CytC, caspases-3, caspases-9expression decreased（p＜0.05）.Conclusions:1. APS can protect against mitochondria function of cardiacmyocyte injured byRadiation in neonatal rats through chucking away ROS, shortening cell cycle, stabilizing theΔΨm, decreasing the expression of CytC, caspases-3, caspases-9.2. APS can protect against mitochondria function of cardiacmyocyte injured by Radiation in neonatal rats through Supporting the Healthy Energy, supplementing Qi andnourishing Yin, activating blood and resolving stasis.