甜叶菊浸膏对抑郁小鼠脾脏组织中DBP和SP蛋白表达的影响

目的 探讨甜叶菊浸膏的抗抑郁活性及其对脾脏和大脑皮层组织中白蛋白启动子D位点结合蛋白(DBP)与P物质(SP)蛋白表达的影响.方法 将60只BALB/c ♂小鼠随机均分为对照组、模型组、阳性对照组、甜叶菊浸膏低剂量组(SEL,1.5 g·kg-1)和高剂量组(SEH,3 g·kg-1).用皮质酮悬液按20 mg· kg-剂量连续于腹腔注射21 d,复制小鼠抑郁模型,每天给药1次.待造模成功后,通过ig途径给予药物治疗.正常对照组和模型组继续给予生理盐水,阳性对照组给予氟西汀(30 mg·kg-1),甜叶菊浸膏各组给予相应剂量的药物,连续给药7d,每天给药1次.用旷场法测定各组小鼠的平行移动格数和直立次数等行为学指标;用Western Blot技术测定小鼠脾脏与大脑皮质中DBP和SP蛋白的表达.结果 模型组小鼠的平行移动格数和直立次数明显减少,与对照组的比较有显著性差异(P＜0.01),提示模型建立成功.给予甜叶菊浸膏后,可剂量依赖性地增加抑郁小鼠的平行移动格数(SEL:54.17±13.33,SEH:73.17±13.90)和直立次数(SEL:35.42 ±5.12,SEH:54.83±11.60),与模型组的比较有显著性差异(移动格数:20.08±3.53,直立次数:9.33 ±1.83);甜叶菊浸膏显著地增加了脾脏和脑组织中SP蛋白的表达水平,与模型组的比较有显著性差异(P ＜0.05,P＜0.01);甜叶菊浸膏减少了脾脏组织中DBP蛋白的表达,却增加了脑组织中DBP蛋白的水平,与模型组的比较有显著性差异(P＜0.01).结论甜叶菊浸膏可有效改善小鼠的抑郁症状,其抗抑郁机制可能与调控大脑皮层和脾脏组织中DBP及SP蛋白的表达水平有关.

Effects of stevia extracts on expressions of DBP and SP proteins in the spleen of mice

OBJECTIVE To investigate the antidepressant activity of stevia extracts (SE) and its effects on expression of D site of albumin promoter binding protein(DBP) and SP proteins in spleen and cerebral cortex of mice.METHODS 60 BALB/c female mice were randomly divided into control group,model group,positive control group,SE 1.5 g· kg-1 group and 3 g· kg-1 group.The depression models were established by intra peritoneal injection of corticosterone suspension at 20 mg· kg-1,and all mice were injected once a day for 21 days.All the animals received intragastric administration from the same day after the modeling.The mice of the control and model group were given normal saline.The mice of positive control group were given fluoxetine at 30 mg· kg-1.The animals in other two groups were given SE at the corresponding dose respectively.All mice were administrated once a day for 7 days.Open field method was used to determine the mobile number and the number of rearing,and the levels of DBP and SP protein expression in the spleen and cerebral cortex were measured by western blot technology.RESULTS The mobile numbers and the number of rearing(standing on hind limbs) of mice in depressed model group were significantly decreased compared the with control group(P ＜ 0.01).It suggested that the depression model was set up successfully.SE could obviously increase the mobile number (SEL:54.17 ± 13.33,SHE:73.17 ± 13.90) and the number of rearing(SEL:35.42-± 5.12,SEH:54.83 ± 11.60) with the dosage increasing in mice,compared with the mice in model group(the mobile number:20.08-± 3.53,the number of rearing:9.33 ± 1.83),there was a significantly difference (P ＜ 0.05,P ＜ 0.01).Compared with the SP protein levels in model group,SE groups showed significant increased in spleen and cerebral cortex (P ＜ 0.05,P ＜ 0.01).Moreover,SE decreased the expression of DBP protein in the spleen,but increased the level of DBP in the cerebral cortex(P ＜ 0.01).CONCLUSION SE can effectively improve depressive symptoms in mice,and the mechanism of anti-depression might be related to the regulation of DBP and SP protein expression levels in the cerebral cortex and spleen.