基于抗炎及抗氧化研究人参皂苷对衰老模型大鼠七氟烷麻醉后认知功能障碍的改善作用  

Improvement effect of ginsenoside on cognitive impairment of aging rats after sevoflurane anesthesia based in anti inflammatory and antioxidant effect

作　　者：樊荣[1] Fan Rong(Department of Anesthesiology,The First People’s Hospital of Xi’an,Xi’an 710002,Shanxi,China)

机构地区：[1]西安市第一医院麻醉科,陕西西安710002

出　　处：《贵州医药》2021年第4期507-509,521,共4页Guizhou Medical Journal

摘　　要：目的研究人参皂苷对衰老模型大鼠七氟烷麻醉后认知功能障碍及炎症反应、氧化应激反应的改善作用及机制。方法成年雄性SD大鼠随机分为对照组、衰老组、衰老+七氟烷组、衰老+七氟烷+人参皂苷组,采用皮下注射D-半乳糖的方式建立衰老模型,在麻醉箱内给予体积分数3.2%七氟醚,七氟醚麻醉后给予50 mg/kg人参皂苷Re灌胃、持续4周。采用Morris水迷宫检测逃避潜伏期、穿越平台次数,采用试剂盒检测血清及海马中炎症因子IL-1β、IL-6、TNF-α及氧化应激指标SOD、GPX、MDA的含量,采用Western blot检测海马中p-p38MAPK、p-ERK1/2、p-JNK的表达水平。结果与对照组比较,衰老组的逃避潜伏期延长,穿越平台次数、SOD、GPX的含量、p-ERK1/2的表达减少,IL-1β、IL-6、TNF-α、MDA的含量及p-p38MAPK、p-JNK的表达增加;与衰老组比较,衰老+七氟烷组的逃避潜伏期延长,穿越平台次数、SOD、GPX的含量、p-ERK1/2的表达减少,IL-1β、IL-6、TNF-α、MDA的含量及p-p38MAPK、p-JNK的表达增加;与衰老+七氟烷组比较,衰老+七氟烷+人参皂苷组的逃避潜伏期缩短,穿越平台次数、SOD、GPX的含量、p-ERK1/2的表达增加,IL-1β、IL-6、TNF-α、MDA的含量及p-JNK的表达减少,p-p38MAPK的表达无明显变化。结论人参皂苷Re能够改善衰老模型大鼠七氟烷麻醉后的认知功能障碍并减轻炎症反应、氧化应激反应,调控ERK1/2及JNK通路是可能的分子机制。Objective To study the effect and mechanism of ginsenoside on cognitive dysfunction,inflammatory response and oxidative stress after sevoflurane anesthesia in aging rats.Methods Adult male SD rats were randomly divided into control group,aging group,aging+sevoflurane group,aging+sevoflurane+ginsenoside group.The aging model was established by subcutaneous injection of D-galactose,the volume fraction 3.2%of sevoflurane was given in the anesthesia box,50 mg/kg ginsenoside Re was given by gavage for 4 weeks after sevoflurane anesthesia.Morris water maze was used to detect the escape latency and crossing platform times.Serum and hippocampus inflammatory factors IL-1β,IL-6,TNF-αand oxidative stress indexes SOD,GPX and MDA were detected by kit.Western blot(WB)was used to detect the expression levels of p-p38MAPK,p-ERK1/2 and p-JNK in hippocampus.Result Compared with the control group,the escape latency prolonged,the crossing platform times,the contents of SOD,GPX,the expression of p-ERK1/2 decreased,and the contents of IL-1β,IL-6,TNF-α,MDA and the expression of p-p38MAPK,p-JNK increased in the aging group.Compared with the aging group,the escape latency prolonged,the crossing platform times,the contents of SOD,GPX,the expression of p-ERK1/2 decreased,and the contents of IL-1β,IL-6,TNF-α,MDA and the expression of p-p38MAPK,p-JNK increased in the aging+sevoflurane group.Compared with the aging+sevoflurane group,the escape latency shortened,the crossing platform times,the contents of SOD,GPX,the expression of p-ERK1/2 increased,and the contents of IL-1β,IL-6,TNF-α,MDA and the expression of p-JNK decreased,the expression of p-p38MAPK there were no significant change in aging+sevoflurane+ginsenoside group.Conclusion Ginsenoside Re can improve the cognitive function of aging rats after sevoflurane anesthesia,reduce the inflammatory response and oxidative stress response,and regulate ERK1/2 and JNK pathway was the possible molecular mechanism.

关 键 词：衰老 七氟烷 人参皂苷 炎症反应 氧化应激反应 信号通路 

分 类 号：R614[医药卫生—麻醉学] R-332[医药卫生—外科学]