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远志皂苷对丙泊酚麻醉所致大鼠认知功能障碍的保护作用及机制
引用本文:方昊.远志皂苷对丙泊酚麻醉所致大鼠认知功能障碍的保护作用及机制[J].基因组学与应用生物学,2020,39(3):1401-1407.
作者姓名:方昊
作者单位:华中科技大学同济医学院附属武汉儿童医院,武汉,430000
摘    要:本研究旨在探讨远志皂苷对丙泊酚麻醉所致大鼠认知功能障碍的保护作用及机制。将SD大鼠分别应用远志皂苷(200 mL·kg^-1·d^-1)和/或丙泊酚(60 mL·kg^-1·d^-1)处理3周,通过Morris水迷宫实验来评价认知功能情况,通过苏木精伊红(hematoxylineosin, HE)染色评价组织病理改变。采用原位末端标记技术(TdTmediated dUTP nick and labeling, Tunel)检测大鼠海马神经细胞的凋亡情况。采用酶联免疫吸附法(enzymelinked immunosorbent assay, ELISA)检测氧化损伤指标。采用Western blotting检测Bcl-2和Caspase-3的表达。Morris水迷宫实验显示,远志皂苷显著降低了丙泊酚麻醉大鼠的逃避潜伏期,并提高了穿越平台次数(p<0.05)。苏木精伊红(HE)染色显示,远志皂苷可显著降低丙泊酚引起的大鼠海马组织病变程度。原位末端标记技术(Tunel)实验显示,远志皂苷抑制了丙泊酚引起的大鼠海马神经细胞凋亡(p<0.05)。Western blotting检测显示,远志皂苷抑制了丙泊酚对大鼠脑组织中Bcl-2蛋白的下调及Caspase-3的上调(p<0.05)。酶联免疫吸附检测显示,远志皂苷提高了大鼠脑组织中SOD和GSH的水平,并降低了MDA水平(p<0.05)。远志皂苷可显著改善丙泊酚麻醉大鼠的认知功能并降低海马组织病变程度,其机制与抑制海马神经细胞凋亡和减弱氧化损伤有关。

关 键 词:远志皂苷  丙泊酚  细胞凋亡  海马  氧化应激

Protective Effect and Mechanism of Tenuigenin on Cognitive Dysfunction Induced by Propofol Anesthesia in Rats
Fang Hao.Protective Effect and Mechanism of Tenuigenin on Cognitive Dysfunction Induced by Propofol Anesthesia in Rats[J].Genomics and Applied Biology,2020,39(3):1401-1407.
Authors:Fang Hao
Institution:(Wuhan Children's Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,430000)
Abstract:This study was to investigate the protective effect and mechanism of tenuigenin on cognitive dysfunction induced by propofol anesthesia in rats. SD rats were treated with Polygala saponin(200 mL·kg^-1·d^-1) and/or propofol(60 mL·kg^-1·d^-1) for 3 weeks. Morris water maze experiments were used to evaluate cognitive function.Histopathological changes were evaluated by hematoxylin and eosin(HE) staining. Apoptosis of rat hippocampal nerve cells was detected by in situ end-labeling technology(Tunel). Enzyme-linked immunosorbent assay(ELISA)was used to detect oxidative damage indicators. Western blotting was used to detect the expression of Bcl-2 and Caspase-3. Morris water maze experiments showed that tenuigenin significantly reduced the escape latency of propofol anesthetized rats and increased the number of crossing platforms(p<0.05). Hematoxylin and eosin(HE)staining showed that tenuigenin significantly reduced the degree of hippocampal tissue damage induced by propofol. In situ end labeling(Tunel) experiments showed that tenuigenin inhibited apoptosis of rat hippocampal neurons induced by propofol(p<0.05). Western blotting analysis showed that tenuigenin inhibited the down-regulation of Bcl-2 protein and the up-regulation of Caspase-3 in rat brain tissue induced by propofol(p<0.05). Enzymelinked immunosorbent assay showed that tenuigenin increased the levels of SOD and GSH in rat brain tissue and decreased MDA levels(p<0.05). Tenuigenin can significantly improve the cognitive function of propofol anesthetized rats and reduce the degree of hippocampal tissue lesions. The mechanism is related to the inhibition of hippocampal neuronal apoptosis and the reduction of oxidative damage.
Keywords:Tenuigenin  Propofol  Cell apoptosis  Hippocampus  Oxidative stress
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