Ruan Bo, Wang Rui, Yang Yuan-Jian, Wang Dong-Fan, Wang Jia-Wen, Zhang Chang-Cheng, Yuan Ding, Zhou Zhi-Yong, Wang Ting
Medical College,Three Gorges University Yichang 443002,China.
Department of Medical Experimental Center,Jiangxi Mental Hospital Nanchang 330029,China.
Zhongguo Zhong Yao Za Zhi. 2019 Jan;44(2):344-349. doi: 10.19540/j.cnki.cjcmm.20180921.001.
The aim of this paper was to investigate the effect of total saponins from Panax japonicus( SPJ) on cognitive decline of natural aging rats and its mechanism. Thirty male SD rats of eighteen month old were randomly divided into three groups: aged group,10 mg·kg(-1) SPJ-treated group and 30 mg·kg(-1) SPJ-treated group. The SPJ-treated groups were given SPJ at the dosages of 10 mg·kg(-1) and 30 mg·kg(-1),respectively,from the age of 18 to 24 months. Aged group were lavaged the same amount of saline,10 six-month-old rats were used as control group,with 10 rats in each group. The open field test,novel object recognition and Morris water maze were performed to detect the changes of cognitive function in each group. The changes of synaptic transmission of long-term potentiation( LTP) in hippocampal CA1 region were detected by field potential recording. Western blot was used to detect the protein levels of NLRP3,ASC,caspase-1 and the changes of Glu A1,Glu A2,CAMKⅡ,CREB and phosphorylation of CAMKⅡ,CREB in each group.The results showed that SPJ could improve the decline of cognitive function in aging rats,reduce the damage of LTP in the hippocampal CA1 region of aged rats,and decrease the expression of NLRP3,ASC,caspase-1 in aging rats. At the same time,SPJ could enhance the membrane expression of AMPA receptor( Glu A1 and Glu A2),and increase the expression of p-CAMKⅡand p-CREB in aging rats.SPJ could improve cognitive decline of natural aging rats,and its mechanism may be related to regulating NLRP3 inflammasome,thus regulating the membrane expression of AMPA receptor,and enhancing the expression phosphorylation of CAMKⅡ and CREB.
本文旨在研究竹节参总皂苷（SPJ）对自然衰老大鼠认知功能衰退的影响及其机制。将30只18月龄雄性SD大鼠随机分为三组：老龄组、10 mg·kg⁻¹ SPJ处理组和30 mg·kg⁻¹ SPJ处理组。SPJ处理组分别从18月龄至24月龄给予10 mg·kg⁻¹和30 mg·kg⁻¹剂量的SPJ。老龄组灌胃等量生理盐水，选取10只6月龄大鼠作为对照组，每组10只。通过旷场试验、新物体识别试验和莫里斯水迷宫试验检测各组认知功能的变化。采用场电位记录法检测海马CA1区长期增强（LTP）突触传递的变化。用蛋白质免疫印迹法检测各组NLRP3、ASC、caspase-1蛋白水平以及Glu A1、Glu A2、CAMKⅡ、CREB蛋白水平及CAMKⅡ、CREB磷酸化水平的变化。结果表明，SPJ可改善衰老大鼠认知功能衰退，减轻衰老大鼠海马CA1区LTP损伤，降低衰老大鼠NLRP3、ASC、caspase-1表达。同时，SPJ可增强衰老大鼠AMPA受体（Glu A1和Glu A2）的膜表达，增加衰老大鼠p-CAMKⅡ和p-CREB的表达。SPJ可改善自然衰老大鼠的认知功能衰退，其机制可能与调节NLRP3炎性小体有关，从而调节AMPA受体的膜表达，增强CAMKⅡ和CREB的表达及磷酸化。
