Protective effects of citicoline sodium on developmental convulsive cerebral injury in rats
Objective To explore the protective effect and mechanism of citicoline sodium on developmental convulsive cerebral injury in rats.Method SD rats were randomly divided into control group,model group and experimental group with 10 in each group.The rat developmental convulsive model was established by intraperitoneal injection of lithium chloride,scopolamine hydrobromide and pilocarpine.After successful modeling,the rats in experimental group were intraperitoneally injected with cytidine sodium(500 mg·kg-1)once a day for one week.The control group and the model group were intraperitoneally injected with the same amount of 0.9％NaCl at the same time point.Griess detection of nitric oxide(NO)concentration in serum;enzyme-linked immunosorbent assay(ELISA)detection of interleukin-6(IL-6)and interleukin-1 β(IL-1β)content in cerebrum;biochemical detection detection of superoxide dismutase(SOD)activity and malondialdehyde(MDA)content in cerebrum;real-time quantitative polymerase chain reaction(qRT-PCR)detection of mRNA levels of inducible nitric oxide synthase(iNOS)in cerebrum;Western blot detection of protein levels of G protein-coupled receptors 39 antibody(GPR39),protein kinase B(AKT),and extracellular regulated protein kinases(ERK)in cerebrum.Results In control group,model group and experimental group,the level of IL-6 in rats cerebrum were(37.16±6.34),(119.31±19.26)and(74.52±12.37)pg·mL-1,respectively;the contents of IL-1 β were(7.46±1.25),(42.73±8.41)and(24.18±4.62)pg·mL-1,respectively;SOD activity were(384.51±34.72),(229.16±27.42)and(218.47±33.59)U·gp-1,respectively;MDA content were(1.06±0.15),(1.82±0.21)and(1.24±0.17)U·gp-1,respectively;serum NO levels were(13.62±2.06),(29.34±5.37)and(16.55±3.15)μmol·L-1,respectively;mRNA levels of iNOS were 1.00±0.15,2.19±0.24 and 1.62±0.18,respectively;protein levels of GPR39 were 0.41±0.05,1.03±0.19 and 0.74±0.08,respectively;p-AKT/AKT values were 0.46±0.07,0.13±0.04 and 0.36±0.05,respectively;p-ERK/ERK values were 0.37±0.11,0.11±0.03 and 0.42±0.05,respectively.The above indicators showed statistically significant differences between the control group and the model group(P＜0.01,P＜0.001);the difference between the model group and the experimental group was statistically significant(P＜0.05,P＜0.01,P＜0.001).Conclusion Cytidine sodium can effectively alleviate the degree of developmental convulsive cerebral injury rats,inhibit inflammatory reactions,and improve oxidative stress.Its mechanism may be related to the activation of GPR39/AKT/ERK signaling pathway.
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