三七总皂苷对创伤性脑损伤大鼠神经元凋亡的保护作用  

Protective effects of Panax notoginseng saponins on P13K/Akt/mTOR signalling pathway and neuronal apoptosis in hippocampus of rats with traumatic brain injury

作　　者：林晨[1] 陈闯[1] LIN Chen;CHEN Chuang(Department of Emergency,Zhejiang Hospital,Hangzhou,Zhejiang 310013,China)

机构地区：[1]浙江医院急诊科,浙江杭州310013

出　　处：《中华全科医学》2021年第6期932-935,共4页Chinese Journal of General Practice

基　　金：浙江省医药卫生科技计划项目(2020KY005)。

摘　　要：目的探讨三七总皂苷对创伤性脑损伤(TBI)大鼠海马神经元凋亡的保护作用。方法 SPF级SD大鼠45只,按照随机数字表法随机分为正常组、模型组和三七总皂苷组,每组大鼠15只。正常组和模型组腹腔注射等剂量生理盐水灌胃;三七总皂苷组腹腔注射1%三七总皂苷(50 mg/kg),1次/d,连续14 d。结果三七总皂苷组逃避潜伏期[(21.27±3.29)s]短于模型组[(28.42±3.87)s],而经过原平台位置的次数[(9.73±2.34)次]多于模型组[(5.67±1.20)次,均P<0.05]。三七总皂苷组神经行为学评分[(10.63±2.65)分]和运动功能评分[(7.84±2.12)分]高于模型组[(6.52±1.37)分vs.(4.92±1.35)分,均P<0.05]。三七总皂苷组P13K mRNA(0.87±0.18)、Akt mRNA(0.92±0.17)和mTOR mRNA(1.02±0.18)高于模型组的(0.56±0.13、0.48±0.10、0.67±0.21),均P<0.05。三七总皂苷组Bax表达(1.57±0.38)低于模型组(3.24±0.54),而Bcl-2表达(2.78±0.78)高于模型组(1.26±0.45,均P<0.05)。结论三七总皂苷对TBI大鼠神经元凋亡具有保护作用,其机制可能与上调P13K/Aktm/TOR信号通路及上调Bcl-2和下调Bax表达有关。Objective To investigate the protective effects of Panax notoginseng saponins on the P13 K/Akt/mTOR signalling pathway and neuronal apoptosis in the hippocampus of rats with traumatic brain injury(TBI). Methods Forty-five SPF SD rats were randomly divided into normal, model and Panax notoginseng saponin groups, and each group contained 15 rats. The Normal group and model group were intraperitoneally injected with the same dose of normal saline, whereas the Panax notoginseng saponin group was intraperitoneally injected with 1% Panax notoginseng saponins(50 mg/kg) once a day for 14 days. Results The escape latency of the rats in the Panax notoginseng saponin group [(21.27±3.29)s] was shorter than that in the model group [(28.42±3.87)s], and the number of times they passed the original platform position was(9.73±2.34) times that of the model group [(5.67±1.20) times, all P<0.05]. The neurobehavioural scores(10.63±2.65) and motor function scores(7.84±2.12) of the rats in the Panax notoginseng saponin group were higher than those in the model group(6.52±1.37 and 4.92±1.35;all P<0.05). P13 K mRNA(0.87±0.18), Akt mRNA(0.92±0.17) and mTOR mRNA(1.02±0.18) levels in the Panax notoginseng saponin group were higher than those in the model group(0.56±0.13, 0.48±0.10 and 0.67±0.21,respectively;all P<0.05). The Bax protein expression levels(1.57±0.38) in the Panax notoginseng saponins group were lower than those in the model group(3.24±0.54), whereas the Bcl-2 protein expression levels(2.78±0.78) were higher than those in the model group(1.26±0.45;all P<0.05). Conclusion Panax notoginseng saponins have protective effects against neuronal apoptosis in TBI rats, and the mechanism may be related to the upregulation of the P13 K/Akt/mTOR signalling pathway and Bcl-2 expression and downregulation of Bax expression.

关 键 词：三七总皂苷 创伤性脑损伤 P13K/Aktm/TOR信号通路 神经元凋亡 

分 类 号：R651.15[医药卫生—外科学] R-33[医药卫生—临床医学]