Article(id=1292126400178312119, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.01.016, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1758470400000, receivedDateStr=2025-09-22, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996540350, onlineDateStr=2026-08-06, pubDate=1768579200000, pubDateStr=2026-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996540350, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996540350, creator=13701087609, updateTime=1785996540350, updator=13701087609, issue=Issue{id=1292126377440989952, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='1', pageStart='1', pageEnd='147', issueExtLink='null', onlineDate='null', pubDate='1768579200000', pubDateStr='2026-01-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996534929, creator='13701087609', updateTime=1786014708731, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292202603945947673, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292202603950141978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=100, endPage=106, ext={EN=ArticleExt(id=1292126400375444408, articleId=1292126400178312119, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of propofol alleviating intestinal ischemia-reperfusion injury in rats, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective

To investigate the potential mechanism of propofol in improving intestinal ischemia-reperfusion injury (IIRI).

Methods

SD rats were randomly divided into sham group, model group (the superior mesenteric artery was clamped for 45 min and reperfusion for 2 h), experimental-L group (injection of 30 mg·kg-1 propofol before ischemia), experimental-M group (injection of 45 mg·kg-1 propofol before ischemia), experimental-H group (injection of 60 mg·kg-1 propofol before ischemia); after reperfusion, the rats were killed and intestinal tissues were taken for use. Hematoxylin-eosin (HE) staining was used to observe the intestinal histopathological changes, Western blot assay was used to detect the expression of Bcl-2 antagonist killer(BAK), Bcl-2 associated X(BAX) and other proteins, and real-time quantitative polymerase chain reaction (RT-qPCR) assay was used to detect the expression of cytoplasmic mitochondrial DNA (mtDNA). The enzyme activity and enzyme-linked immunosorbent assay was used to detect the expression of adenosine triphosphate (ATP) and interleukin (IL)-1β in intestinal tissue.

Results

The pathological injury scores (Chiu’s methods) in sham group, model group, experimental-L group, experimental-M group and experimental-H group were (0±0), (4.20±0.60), (3.00±0.45), (2.20±0.40) and (1.00±0.77) points, respectively; the relative expression levels of BAK protein were 0.24±0.03, 0.66±0.08, 0.56±0.08, 0.40±0.05 and 0.34±0.03, respectively; the relative expression levels of BAX protein were 0.35±0.03, 0.79±0.11, 0.62±0.03, 0.51±0.05 and 0.40±0.04, respectively; the relative expression levels of NOD-like receptor pyrin domain-containing protein 3 (NLRP3) protein were 0.32±0.03, 1.05±0.12, 0.81±0.11, 0.64±0.08 and 0.49±0.08, respectively; the relative expression levels of Cyclic guanosine monophosphate adenosine synthase (cGAS) protein were 0.23±0.02, 0.97±0.10, 0.78±0.08, 0.63±0.07 and 0.45±0.07, respectively; the relative expression levels of the NADH dehydrogenase subunit (ND)1 mRNA were 1.00±0.08, 2.23±0.29, 1.79±0.13, 1.59±0.11 and 1.34±0.09, respectively; the levels of ATP production were 1.00±0.14, 0.47±0.03, 0.65±0.07, 0.80±0.06 and 0.81±0.12, respectively. Compared model group with the sham group and compared experimental-L, M, H group with model group, the differences of above indicators were all statistically significant (all P<0.05).

Conclusion

Propofol can dose-dependently improve intestinal injury in IIRI rats and this protective effect was accompanied by downregulation of BAK/BAX protein expression, reduction of mtDNA release, and decreased activity of the downstream cGAS/NLRP3 inflammatory pathway.

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目的

探讨丙泊酚改善肠缺血再灌注损伤(IIRI)的潜在作用机制。

方法

将SD大鼠随机分为假手术组、模型组(夹闭肠系膜上动脉45 min后再灌注2 h)、低剂量实验组(缺血前注射30 mg·kg-1丙泊酚)、中剂量实验组(缺血前注射45 mg·kg-1丙泊酚)和高剂量实验组(缺血前注射60 mg·kg-1丙泊酚),再灌注结束后处死大鼠,取肠组织备用。用苏木精-伊红(HE)染色法观察肠组织病理学改变,用蛋白质印迹法检测Bcl-2拮抗杀伤蛋白(BAK)、Bcl-2相关X蛋白(BAX)等蛋白表达,用实时定量聚合酶链反应(RT-qPCR)实验法检测胞质线粒体DNA(mtDNA)表达,用酶活性及酶联免疫吸附测定试剂盒法检测肠组织腺苷三磷酸(ATP)和白细胞介素(IL)-1β表达。

结果

假手术组、模型组、低剂量实验组、中剂量实验组和高剂量实验组大鼠病理损伤评分(Chiu’s法)分别为(0±0)、(4.20±0.60)、(3.00±0.45)、(2.20±0.40)和(1.00±0.77)分;BAK蛋白相对表达水平分别为0.24±0.03、0.66±0.08、0.56±0.08、0.40±0.05和0.34±0.03;BAX蛋白相对表达水平分别为0.35±0.03、0.79±0.11、0.62±0.03、0.51±0.05和0.40±0.04;NOD样受体热蛋白结构域相关蛋白3(NLRP3)蛋白相对表达水平分别为0.32±0.03、1.05±0.12、0.81±0.11、0.64±0.08和0.49±0.08;环鸟苷单磷酸腺苷合成酶(cGAS)蛋白相对表达水平分别为0.23±0.02、0.97±0.10、0.78±0.08、0.63±0.07和0.45±0.07;NADH脱氢酶亚基(ND)1 mRNA相对表达水平分别为1.00±0.08、2.23±0.29、1.79±0.13、1.59±0.11和1.34±0.09;ATP生成相对水平分别为1.00±0.14、0.47±0.03、0.65±0.07、0.80±0.06和0.81±0.12;上述指标模型组与假手术组比较,低、高剂量实验组分别与模型组比较,在统计学上差异均有统计学意义(均P<0.05)。

结论

丙泊酚可以剂量依赖性地减轻肠缺血再灌注损伤。该保护作用伴随着BAK/BAX蛋白表达下调、胞质mtDNA释放减少以及下游cGAS/NLRP3炎症通路活性的降低。

, authors=高誉华, 毛轲, 刘鹏森, 杜思龙, authorsList=高誉华, 毛轲, 刘鹏森, 杜思龙, authorCompany=null, correspAuthors=高誉华, authorNote=

高誉华(1987-),女,主治医师,主要从事麻醉与疼痛方面的工作和研究

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高誉华,主治医师 MP: 18736037837 E-mail:
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丙泊酚减轻大鼠肠缺血再灌注损伤的研究
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高誉华 , 毛轲 , 刘鹏森 , 杜思龙
中国临床药理学杂志 | 临床与基础桥接研究 2026,42(1): 100-106
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中国临床药理学杂志 |临床与基础桥接研究 2026 , 42 (1) : 100 -106
丙泊酚减轻大鼠肠缺血再灌注损伤的研究
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高誉华 , 毛轲, 刘鹏森, 杜思龙
作者信息
  • 河南省中医院/河南中医药大学 第二附属医院 麻醉科,河南 郑州 450002
通讯作者:
高誉华,主治医师 MP: 18736037837 E-mail:
作者简介:

高誉华(1987-),女,主治医师,主要从事麻醉与疼痛方面的工作和研究

Research of propofol alleviating intestinal ischemia-reperfusion injury in rats
Yu-hua GAO , Ke MAO, Peng-sen LIU, Si-long DU
Affiliations
  • Department of Anesthesiology, Henan Hospital of Traditional Chinese Medicine/Second Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou 450002, Henan Province, China
出版时间: 2026-01-17 doi: 10.13699/j.cnki.1001-6821.2026.01.016
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目的

探讨丙泊酚改善肠缺血再灌注损伤(IIRI)的潜在作用机制。

方法

将SD大鼠随机分为假手术组、模型组(夹闭肠系膜上动脉45 min后再灌注2 h)、低剂量实验组(缺血前注射30 mg·kg-1丙泊酚)、中剂量实验组(缺血前注射45 mg·kg-1丙泊酚)和高剂量实验组(缺血前注射60 mg·kg-1丙泊酚),再灌注结束后处死大鼠,取肠组织备用。用苏木精-伊红(HE)染色法观察肠组织病理学改变,用蛋白质印迹法检测Bcl-2拮抗杀伤蛋白(BAK)、Bcl-2相关X蛋白(BAX)等蛋白表达,用实时定量聚合酶链反应(RT-qPCR)实验法检测胞质线粒体DNA(mtDNA)表达,用酶活性及酶联免疫吸附测定试剂盒法检测肠组织腺苷三磷酸(ATP)和白细胞介素(IL)-1β表达。

结果

假手术组、模型组、低剂量实验组、中剂量实验组和高剂量实验组大鼠病理损伤评分(Chiu’s法)分别为(0±0)、(4.20±0.60)、(3.00±0.45)、(2.20±0.40)和(1.00±0.77)分;BAK蛋白相对表达水平分别为0.24±0.03、0.66±0.08、0.56±0.08、0.40±0.05和0.34±0.03;BAX蛋白相对表达水平分别为0.35±0.03、0.79±0.11、0.62±0.03、0.51±0.05和0.40±0.04;NOD样受体热蛋白结构域相关蛋白3(NLRP3)蛋白相对表达水平分别为0.32±0.03、1.05±0.12、0.81±0.11、0.64±0.08和0.49±0.08;环鸟苷单磷酸腺苷合成酶(cGAS)蛋白相对表达水平分别为0.23±0.02、0.97±0.10、0.78±0.08、0.63±0.07和0.45±0.07;NADH脱氢酶亚基(ND)1 mRNA相对表达水平分别为1.00±0.08、2.23±0.29、1.79±0.13、1.59±0.11和1.34±0.09;ATP生成相对水平分别为1.00±0.14、0.47±0.03、0.65±0.07、0.80±0.06和0.81±0.12;上述指标模型组与假手术组比较,低、高剂量实验组分别与模型组比较,在统计学上差异均有统计学意义(均P<0.05)。

结论

丙泊酚可以剂量依赖性地减轻肠缺血再灌注损伤。该保护作用伴随着BAK/BAX蛋白表达下调、胞质mtDNA释放减少以及下游cGAS/NLRP3炎症通路活性的降低。

丙泊酚  /  肠缺血再灌注损伤  /  Bcl-2拮抗杀伤蛋白/Bcl-2相关X蛋白  /  线粒体DNA  /  氧化应激  /  炎症反应
Objective

To investigate the potential mechanism of propofol in improving intestinal ischemia-reperfusion injury (IIRI).

Methods

SD rats were randomly divided into sham group, model group (the superior mesenteric artery was clamped for 45 min and reperfusion for 2 h), experimental-L group (injection of 30 mg·kg-1 propofol before ischemia), experimental-M group (injection of 45 mg·kg-1 propofol before ischemia), experimental-H group (injection of 60 mg·kg-1 propofol before ischemia); after reperfusion, the rats were killed and intestinal tissues were taken for use. Hematoxylin-eosin (HE) staining was used to observe the intestinal histopathological changes, Western blot assay was used to detect the expression of Bcl-2 antagonist killer(BAK), Bcl-2 associated X(BAX) and other proteins, and real-time quantitative polymerase chain reaction (RT-qPCR) assay was used to detect the expression of cytoplasmic mitochondrial DNA (mtDNA). The enzyme activity and enzyme-linked immunosorbent assay was used to detect the expression of adenosine triphosphate (ATP) and interleukin (IL)-1β in intestinal tissue.

Results

The pathological injury scores (Chiu’s methods) in sham group, model group, experimental-L group, experimental-M group and experimental-H group were (0±0), (4.20±0.60), (3.00±0.45), (2.20±0.40) and (1.00±0.77) points, respectively; the relative expression levels of BAK protein were 0.24±0.03, 0.66±0.08, 0.56±0.08, 0.40±0.05 and 0.34±0.03, respectively; the relative expression levels of BAX protein were 0.35±0.03, 0.79±0.11, 0.62±0.03, 0.51±0.05 and 0.40±0.04, respectively; the relative expression levels of NOD-like receptor pyrin domain-containing protein 3 (NLRP3) protein were 0.32±0.03, 1.05±0.12, 0.81±0.11, 0.64±0.08 and 0.49±0.08, respectively; the relative expression levels of Cyclic guanosine monophosphate adenosine synthase (cGAS) protein were 0.23±0.02, 0.97±0.10, 0.78±0.08, 0.63±0.07 and 0.45±0.07, respectively; the relative expression levels of the NADH dehydrogenase subunit (ND)1 mRNA were 1.00±0.08, 2.23±0.29, 1.79±0.13, 1.59±0.11 and 1.34±0.09, respectively; the levels of ATP production were 1.00±0.14, 0.47±0.03, 0.65±0.07, 0.80±0.06 and 0.81±0.12, respectively. Compared model group with the sham group and compared experimental-L, M, H group with model group, the differences of above indicators were all statistically significant (all P<0.05).

Conclusion

Propofol can dose-dependently improve intestinal injury in IIRI rats and this protective effect was accompanied by downregulation of BAK/BAX protein expression, reduction of mtDNA release, and decreased activity of the downstream cGAS/NLRP3 inflammatory pathway.

propofol  /  intestinal ischemia-reperfusion injury  /  Bcl-2 antagonist killer/Bcl-2 associated X protein  /  mitochondrial DNA  /  oxidative stress
高誉华, 毛轲, 刘鹏森, 杜思龙. 丙泊酚减轻大鼠肠缺血再灌注损伤的研究. 中国临床药理学杂志, 2026 , 42 (1) : 100 -106 . DOI: 10.13699/j.cnki.1001-6821.2026.01.016
Yu-hua GAO, Ke MAO, Peng-sen LIU, Si-long DU. Research of propofol alleviating intestinal ischemia-reperfusion injury in rats[J]. Chinese Journal of Clinical Pharmacology, 2026 , 42 (1) : 100 -106 . DOI: 10.13699/j.cnki.1001-6821.2026.01.016

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doi: 10.13699/j.cnki.1001-6821.2026.01.016
  • 接收时间:2025-09-22
  • 首发时间:2026-08-06
  • 出版时间:2026-01-17
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  • 收稿日期:2025-09-22
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    河南省中医院/河南中医药大学 第二附属医院 麻醉科,河南 郑州 450002

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高誉华,主治医师 MP: 18736037837 E-mail:
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
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