| 蒋志平,张蕾,丁煌,等.环泊酚上调核因子 E2相关因子 2表达减轻失血性休克大鼠肺损伤机制研究[J].安徽医药,2025,29(6):1101-1105. |
| 环泊酚上调核因子 E2相关因子 2表达减轻失血性休克大鼠肺损伤机制研究 |
| Protective effect of ciprofol pretreatment on lung injury via upregulating Nrf2 protein expression in rats with hemorrhagic shock |
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| DOI：10.3969/j.issn.1009-6469.2025.06.008 |
| 中文关键词: 环泊酚 丙泊酚 再灌注损伤 预处理 核因子 E2相关因子 2 肺损伤 |
| 英文关键词: Ciprofol Propofol Reperfusion injury Pretreatment Nrf2 Lung injury |
| 基金项目:湖北省自然科学基金面上项目( 2020CFB705) |
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| 中文摘要: |
| 目的研究环泊酚预处理是否通过上调核因子 E2相关因子 2(Nrf2)表达减轻失血性休克导致的大鼠急性肺组织损伤。方法将 2022年 1月至 2023年 6月雄性 SD大鼠 32只按随机数字表法分为四组( n=8)对照组、失血性休克组、丙泊酚组和环泊酚组。丙泊酚组按 10 mg·kg.1·h.1泵注丙泊酚 20 min；环泊酚组按 2 mg·kg.1·h.1泵注环泊:酚 20 min；而对照组和失血性休克组在 20 min内通过尾静脉灌注相应剂量的生理盐水。 30 min后，丙泊酚组和环泊酚组均在 10 min内经股动脉导管均匀抽取 35 mL/kg血液诱发失血性休克。缺血状态 60 min后，通过在 30 min内以恒定速率输注失血和乳酸林格氏液( 35 mL/kg)使大鼠复苏。复苏后 4h，测定大鼠肺组织中超氧化物歧化酶( SOD)活性、丙二醛、 Nrf2、B细胞淋巴瘤 -2(Bcl-2)、 Bcl-2相关 X蛋白( Bax)和胱天蛋白酶 3(caspase-3)的含量，并测量支气管肺泡灌洗液( BALF)中的蛋白质含量和细胞数量以及观察肺组织病理改变。结果与对照组比较，失血性休克组大鼠肺组织中丙二醛、 Bax和 caspase-3水平升高(均 P<0.05)SOD活性、 Nrf2(0.28±0.12比 0.75±0.13)和 Bcl-2蛋白水平降低(均 P<0.05)，BALF中蛋白质和细胞计数、肺组织细胞凋亡率及 病理学评分升高(均 P<0.05)；与失血性休克组比较，丙泊酚组和环泊酚组大鼠肺组织中丙二醛、 Bax和 caspase-3水平降低(均 P<0.05)，SOD活性、 Nrf2(0.52±0.12和 0.55±0.13)和 Bcl-2蛋白水平升高(均 P<0.05)，而 BALF中蛋白质和细胞计数、肺组织细胞凋亡率及病理学评分显著降低(均 P<0.05)。结论环泊酚及丙泊酚预处理均对缺血再灌注大鼠的肺损伤具有保护作用，两者肺保护效应相近，这可能与上调肺组织 Nrf2蛋白表达从而增强肺组织抗氧化作用有关。 |
| 英文摘要: |
| Objective To investigate whether ciprofol pretreatment can protect against lung injury in rats with hemorrhagic shock byupregulating the expression of nuclear factor E2-related factor 2 (Nrf2).Methods Thirty-two male SD rats from January 2022 to June 2023 were randomly divided into 4 groups (n=8) according to the random number table: control group, hemorrhagic shock (HS) group,propofol group and ciprofol group. In the propofol group, propofol was administered at 10 mg·kg.1·h.1 for 20 min, In the ciprofol group, ciprofol was administered at 2 mg·kg.1·h.1 for 20 min. the control and HS groups received an equivalent volume of normal saline viatail vein infusion over 20 minutes. After 30 minutes, except for the control group, the other groups had 35 mL/kg of blood withdrawnthrough a femoral artery catheter over 10 minutes to induce hemorrhagic shock. After 60 minutes of ischemia, the rats were resuscitatedby infusing shed blood and lactated Ringer's solution (35 mL/kg) at a constant rate over 30 minutes. Four hours after resuscitation, thelevels of superoxide dismutase (SOD), malondialdehyde (MDA), Nrf2, Bcl-2, Bax, and caspase-3 were measured in lung tissue. The pro-tein and cell contents in bronchoalveolar lavage fluid (BALF) were also measured, and the percentage of apoptotic cells in lung tissueand pathological changes were observed.Results Compared to the control group, the HS group showed increased levels of MDA, Bax, and caspase-3 (all P<0.05), decreased SOD activity, Nrf2 (0.28±0.12 vs. 0.75±0.13), and Bcl-2 protein levels (all P<0.05), and in-creased protein and cell counts in BALF, lung tissue cell apoptosis rate, and pathological score (all P<0.05). Compared to the HS group, the propofol and ciprofol groups showed decreased MDA, Bax, and caspase-3 levels (all P<0.05), increased SOD activity, Nrf2 (0.52±0.12 and 0.55±0.13), and Bcl-2 protein levels (all P<0.05), and significantly decreased protein and cell counts in BALF, lung tis-sue cell apoptosis rate, and pathological score (all P<0.05).Conclusion Both ciprofol and propofol pretreatment offer protective ef-fects against ischemia-reperfusion-induced lung injury in rats, with similar protective effects, likely due to up-regulating Nrf2 protein expression in lung tissue to enhance its antioxidant capacity. |
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