Preliminary Study On The Anti-aging Mechanism Of Astragaloside-? On Radiation-induced Brain Cells

According to the research,a variety of natural drugs have significant effects in radiation therapy.Compared with chemical drugs,natural drugs have gradually attracted attention,because it has many advantages such as multi-channel,multi-target,and small side effects.In this experiment,the monomeric component of natural medicine,astragaloside-IV,was used as experimental materials.In vivo experiments were performed using ⁶⁰Co?rays to stimulate the mice.In vitro experiments were performed using UV lamps to stimulate PC12 cells.We established a radiation-induced neuronal senescence injury model and the experiment was divided into Control group,DMSO group,DMSO+R group and AS-IV+R group.In vitro and in vivo experiments were used to investigate the repairing effect of astragaloside-IV on radiation-induced neuronal senescence and its intrinsic mechanism.In order to study the protective mechanism of astragaloside-IV on radiation-induced neuronal senescence,this paper uses radiation-induced cell senescence as a model,using biochemical indicators,SA-?-gal senescence staining,flow cytometry,Western blotting and other techniques to analyze the protective mechanism of astragaloside-IV on radiation-induced neuronal senescence.Result1.Enzyme-labeled colorimetric assay showed that SOD activity was decreased?P<0.001?and MDA content was increased?P<0.001?in brain tissue of irradiated mice,while AS-IV+R group SOD activity was increased and MDA content was decreased in brain tissue of irradiated mice.2.Western blotting showed that the expression of p21?P<0.01?,p16?P<0.01?,CyclinD and RB?P<0.05?protein in the brain of DMSO+R group increased,while the expression of CDK2,CDK4,CyclinE and E2F1 decreased.The brain tissue of mouse in AS-IV-H+R group p21?P<0.05?,p16?P<0.05?,RB?P<0.05?,CyclinD protein expression showed a downward trend,while CDK2,CDK4,CyclinE,E2F1protein expression showed an upward trend.3.SA-?-Gal staining showed that the number of SA-?-Gal positive cells in PC12cells in the DMSO+R group increased?P<0.001?,while the number of SA-?-Gal positive cells in the AS-IV+R group decreased?P<0.05?.4.The results of flow cytometry showed that the proportion of cells in the DMSO+R group was up-regulated in the G₁ phase?P<0.05?,while the proportion of cells in the AS-IV+R group was decreased in the G₁ phase.5.Western blotting showed that the expression of p21?P<0.001?,p16?P<0.001?,RB?P<0.05?and CyclinD protein in PC12 cells of DMSO+R group was increased,while the expression of CDK2?P<0.01?,CDK4?P<0.05?,CyclinE and E2F1 protein was decreased.The expression of p21?P<0.001?,p16?P<0.05?,RB?P<0.05?and CyclinD proteins in PC12 cells of AS-IV+R group was decreased,while the expression of CDK2?P<0.05?,CDK4?P<0.01?,CyclinE and E2F1 proteins was upward.In conclusion1.AS-IV can antagonize radiation-induced brain cell senescence.2.The mechanism of AS-IV antagonistic radiation-induced brain cell senescence may be related to the regulation of senescence signaling pathways p53-p21 and p16-RB.