Protective Effect Of Black Chokeberry Juice On Oxidative Damage To Neurons

Aging is an inevitable life process that every living organism must experience.Brain nerve injury caused by aging affects the quality of life of the elderly and brings serious medical and social problems.So,the mitigation of brain nerve injury in the elderly has become one of the important research topics of geriatrics.The fruit of black chokeberry contains various polyphenolic compounds with a certain antioxidant capacity.Therefore,the aim of this study was to investigate the neuroprotective effect of the black chokeberry juice(BCJ).The aim of this study was to investigate the protective effect of BCJ on oxidative damage to nerve cells.The experimental study and results were as follows.Firstly,a model of aging was established in mice induced by D-galactose.The Morris water maze test was used to examine the effects of BCJ on spatial memory and exploration skills in mice.The results showed that mice had learning disabilities that induced by D-galactose.But the escape latency and escape distance were significantly lower in the BCJ treated group compared with the model group within five days.This indicated that BCJ could improve the learning ability of mice.In addition,the number of times the mice reached the target quadrant and the time spent in the target quadrant increased significantly in the experimental group,indicating that BCJ has the effect of improving the spatial exploration ability of mice.Secondly,the antioxidant and anti-apoptotic capacity of mouse hippocampal tissue was examined at the end of the behavioural test.The results showed that BCJ significantly increased GSH content,SOD activity and T-AOC and inhibit the elevation of MDA in the hippocampus of aging mice.In addition,HE staining showed that D-galactose significantly reduced the number of neurons in the hippocampal region,while BCJ significantly inhibited the reduction in the number of neurons induced by neuronal injury in mice.Protein and gene expression in the hippocampus of mice were examined by Western blot and q PCR techniques.The results showed that BCJ could inhibit the upregulation of Keap-1 and downregulation of Nrf-2 induced by D-galactose.It also regulated the expression levels of Bcl-2 and PARP.It improved cognitive impairment in mice by enhancing their antioxidant and anti-apoptotic capacity.In addition,a peroxide-induced oxidative stress cell model was established using PC12 cells to preliminary investigate the mechanism of the neuroprotective effect of BCJ.The results showed that 0.5 m M hydrogen peroxide decreased the cell viability to 60.67±4.64%,and the cell apposition became poor,which is used as a model for oxidative damage to nerve cells.Compared with the model group,BCJ was able to significantly increase PC12 cell survival.BCJ was also able to increase the activity of antioxidant enzymes(i.e.,SOD and CAT)in PC12 cells.Akt and p-Akt protein expression were detected by flow cytometry and Western blot.It was demonstrated that BCJ could reverse the blocking effect of PI3 K inhibitor LY294002,activate PI3K/Akt signaling pathway and increase Akt phosphorylation.BCJ also reversed the cell cycle blocking effect of hydrogen peroxide,thereby promoting proliferation of PC12 cells.In conclusion,through in vivo and in vitro experiments,it was confirmed that BCJ had protective effects on oxidative damage of neural cells.BCJ could improve spatial learning ability and exploration of aging mice,and enhance hippocampal antioxidant and anti-apoptotic ability.Its mechanism of action might be related to PI3K/Akt pathway and cell cycle.