Abstract

The repair effect of baicalin on rat hippocampal neuronal cells after injury was explored in this study. According to the concentration gradient, glutamate which induced hippocampal neuronal cells damage was categorized into four groups; control, 62.5 μM, 125 μM and 250 μM. Baicalin was pretreated with 0, 1, 10, 20 and 40 μM concentrations for 1 h. The morphological changes of neuronal cells were detected by reactive oxygen species, and cell proliferation was detected by cell counting kit-8. The apoptosis of hippocampal neuronal cells was detected by flow cytometry. The degree of cell damage was determined by the amount of lactate dehydrogenase released in the extracellular system. The expression of related proteins was detected by Western blot. Real-time fluorescence-based quantitative polymerase chain reaction was used to detect messenger ribonucleic acid levels of related genes. With an increase of glutamate concentration, the survival rate of neuronal cells decreased gradually, and the apoptosis rate and cytotoxicity increased with the increase of glutamate concentration. Compared with the control group, the reactive oxygen species level of neuronal cells in baicalin-treated group was reduced, which was inversely proportional to the concentration of baicalin. As the concentration of baicalin increases, the survival rate of neuronal cells increases. Compared with the control group, the apoptosis rate of neuronal cells was reduced, and the levels of inflammation-related factors like interleukin-6, interleukin-1 beta and tumor necrosis factor alpha significantly decreased. The protein expressions of N-methyl D-aspartate receptor subtype 2B, phosphorylated-extracellular signal-regulated kinase and phosphorylated-cyclic adenosine 3’,5’-monophosphate response element-binding protein significantly increased after treatment with high concentration of baicalin. Baicalin can increase glutamate-induced neuronal cell injury, reduce the cytotoxicity, reduce the expression of inflammatory factors, and promote the reduction of apoptosis.