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目的探讨助阳宁神方(ZNF)拮抗皮质酮诱导海马功能重塑性损伤的作用。方法 5羟-色氨酸(5-HTP)诱导的甩头行为模型实验中,50只ICR小鼠,随机均分为正常组、氟西汀组和高、中、低三个剂量ZNF胃饲组,在连续给药第3、7天的给药15min后,记录各组甩头率。取40只C57BL/6N小鼠,皮下皮质酮注射建立应激抑郁动物模型,随机均分成模型对照组、氟西汀组和高、中、低三个剂量ZNF组;另取8只作为正常对照组;实验4周后处死动物,取脑剥离海马,Western blot检测胶质纤维酸性蛋白(GFAP)、神经微丝轻链蛋白(NF-L)和突触囊泡蛋白(SYP)的表达。结果在连续给药第3、7天的给药15min后,氟西汀组甩头率明显高于正常组(80%和90%vs.40%)(P<0.01)。在应激抑郁实验中,与正常对照组比较,模型对照组GFAP、NF-L和SYP的表达显著下调(P<0.01或P<0.05),而氟西汀组和高、中、低三个剂量ZNF组GFAP、NF-L及SYP的表达水平明显上调(P<0.05)。结论 ZNF可通过上调GFAP、NF-L及SYP的表达,保护星形胶质细胞和神经元,拮抗皮质酮诱导的海马功能重塑性损伤的作用。
Objective To investigate the effects of nourishing yangshen recipe (ZNF) on antagonizing corticosterone-induced impairment of hippocampal function remodeling. Method 5 In the experimental model of head-shaved behavior induced by hydroxy-tryptophan (5-HTP), 50 ICR mice were randomly divided into normal group, fluoxetine group and high, medium and low doses of ZNF gastric feeding Group, in the continuous administration of the first 3,7 days after administration 15min, record the rate of each group tampering. Forty C57BL / 6N mice were randomly divided into model control group, fluoxetine group and high, medium and low dose ZNF groups. Eight mice were used as normal control The rats were sacrificed 4 weeks after the experiment. The hippocampus was dissected and the expression of glial fibrillary acidic protein (GFAP), neural microfilament light chain protein (NF-L) and synaptophysin (SYP) were detected by Western blot. Results The shampooing rate of fluoxetine group was significantly higher than that of the normal group (80% and 90% vs. 40%) (P <0.01) 15min after administration on the 3rd and 7th day. In the stress depression test, the expression of GFAP, NF-L and SYP were significantly down-regulated in the model control group compared with the normal control group (P <0.01 or P <0.05), while the fluoxetine group and high, middle and low The levels of GFAP, NF-L and SYP in ZNF group were significantly increased (P <0.05). Conclusion ZNF can protect the astrocytes and neurons by up-regulating the expression of GFAP, NF-L and SYP and antagonize the corticosterone-induced impairment of hippocampal function remodeling.