| 张玉龙,杨宇焦,左友波,董碧倩,涂发平.丙泊酚对全肝缺血再灌注大鼠脑损伤的保护作用及机制研究[J].,2021,(1):42-45 |
| 丙泊酚对全肝缺血再灌注大鼠脑损伤的保护作用及机制研究 |
| Study on the Protective Effect and Mechanism of Propofol on Brain Injury after Whole Liver Ischemia Reperfusion in Rats |
| 投稿时间：2020-04-10 |
| DOI：10.13241/j.cnki.pmb.2021.01.007 |
| 中文关键词: 全肝缺血再灌注 脑损伤 丙泊酚 特异性半胱氨酸蛋白酶-3 作用机制 |
| 英文关键词: Whole liver ischemia reperfusion Brain injury Propofol Specific cysteine protease 3 Mechanism of action |
| 基金项目:四川省教育厅科研基金项目（16ZB0240） |
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| 中文摘要: |
| 摘要 目的：探究丙泊酚对全肝缺血再灌注（THIR）大鼠脑损伤的保护作用及机制。方法：选取72只健康成年雄性SD大鼠，将其按照抽签法分成假手术组、对照组以及丙泊酚组。所有大鼠予以12h禁食处理，采用3%戊巴比妥钠行腹腔注射麻醉处理，常规消毒后取上腹部正中切口进入腹腔。假手术组仅暴露肝门，不予以阻断处理。对照组与丙泊酚组则以无创动脉夹阻断肝固有动脉、门静脉和胆总管，在右肾动脉水平处阻断肝下下腔静脉，膈肌水平阻断肝上下腔静脉，进入全肝缺血阶段，阻断30 min后去除动脉夹恢复肝血流。其中丙泊酚组在全肝缺血前10 min予以丙泊酚50 mg/kg腹腔注射干预，假手术组与对照组则予以等量的生理盐水腹腔注射干预。比较三组大鼠再灌注24h后的脑组织细胞凋亡率、特异性半胱氨酸蛋白酶-3（Caspase-3）蛋白表达水平，脑组织超氧化物歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）水平，血清白介素-6（IL-6）以及肿瘤坏死因子-α（TNF-α）水平。结果：对照组与丙泊酚组大鼠的细胞凋亡率及Caspase-3相对表达量均高于假手术组，而丙泊酚组细胞凋亡率及Caspase-3相对表达量均低于对照组（均P＜0.05）。对照组与丙泊酚组大鼠脑组织SOD水平均低于假手术组，而丙泊酚组脑组织SOD水平高于对照组；对照组与丙泊酚组大鼠脑组织MDA、NO水平均高于假手术组，而丙泊酚组脑组织MDA、NO水平低于对照组（均P＜0.05）。对照组与丙泊酚组大鼠血清IL-6、TNF-α水平均高于假手术组，而丙泊酚组血清IL-6、TNF-α水平均低于对照组（均P＜0.05）。结论：丙泊酚可有效抑制THIR大鼠脑损伤引起的细胞凋亡，其主要机制可能与抑制Caspase-3表达、炎症反应以及抗自由基损伤有关。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the protective effect and mechanism of propofol on brain injury in rats after whole liver ischemia reperfusion (THIR). Methods: 72 healthy adult male SD rats were selected, and they were randomly divided into sham operation group, control group and propofol group according to drawing lots method. All the rats were treated with fasting for 12h, and they were given intraperitoneal injection anesthesia with 3% pentobarbital sodium. After routine disinfection, a median incision in the upper abdomen was taken to enter the abdominal cavity. In the sham group, only the hilum of the liver was exposed, and no blocking was performed. In the control group and the propofol group, non-invasive arterial clips were used to block the proper hepatic artery, portal vein and common bile duct, to block the inferior inferior hepatic vena cava at the level of the right renal artery, and to block the superior inferior hepatic vena cava at the level of the diaphragm, to enter the stage of whole liver ischemia, and to remove the arterial clips to restore liver blood flow after blocking for 30 minutes. Propofol group received intraperitoneal injection of propofol 50 mg/kg 10 min before whole liver ischemia, while sham operation group and control group received intraperitoneal injection of normal saline of equal amount. The apoptosis rate, specific cysteinecontaining aspartate-specific proteases-3 (caspase-3) protein expression, superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (no) levels in brain tissue, serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels in brain tissues of the three groups were compared 24h after reperfusion. Results: The apoptosis rate and relative expression of caspase-3 in the control group and the propofol group were higher than that in the sham operation group, while the apoptosis rate and relative expression of caspase-3 in the propofol group were lower than that in the control group (all P<0.05). The level of SOD in brain tissue of both the control group and the propofol group was lower than that of the sham operation group, and the level of SOD in brain tissue of the propofol group was higher than that of the control group. The levels of MDA and NO in the brain tissues of the control group and the propofol group were higher than those of the sham operation group, while the levels of MDA and NO in the brain tissues of the propofol group were lower than those of the control group (all P<0.05). The serum IL-6 and TNF-α levels of the control group and the propofol group were higher than those of the sham operation group, and the serum IL-6 and TNF-α levels of the propofol group were lower than those of the control group (all P<0.05). Conclusion: Propofol can effectively inhibit apoptosis induced by brain injury in THIR rats, the main mechanism may be related to the inhibition of Caspase-3 expression, inflammatory response and anti free radical damage. |
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