Article(id=1291704991165731636, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704892859638107, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.19.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1742227200000, receivedDateStr=2025-03-18, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896068612, onlineDateStr=2026-08-05, pubDate=1760630400000, pubDateStr=2025-10-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896068612, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896068612, creator=13701087609, updateTime=1785896068612, updator=13701087609, issue=Issue{id=1291704892859638107, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='19', pageStart='2701', pageEnd='2850', issueExtLink='null', onlineDate='null', pubDate='1760630400000', pubDateStr='2025-10-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896045171, creator='13701087609', updateTime=1785896787712, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291708007352656266, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704892859638107, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291708007352656267, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704892859638107, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2749, endPage=2753, ext={EN=ArticleExt(id=1291704991383835445, articleId=1291704991165731636, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of L-carnitine on hypoxic-ischemic brain damage in neonatal mice by regulating PI3K/AKT pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effect of L-carnitine on hypoxic-ischemic brain damage in neonatal mice by regulating PI3K/AKT pathway.
Methods Eighty mice with successful hypoxic-ischemic brain damage models were randomly divided into model group, L-carnitine low-dose group, L-carnitine medium-dose group and L-carnitine high-dose group, with 20 mice in each group, and 20 mice without modeling were used as sham operation group. The mice in the L-carnitine low-dose group, L-carnitine medium-dose group and L-carnitine high-dose group were intraperitoneally injected with L-carnitine at 100, 250 and 500 mg·kg-1, respectively. The mice in the sham-operation group and the model group were intraperitoneally injected with the same amount of normal saline, the administration lasted for one week. The pathological changes of brain tissue were analyzed by hematoxylin-eosin staining. TCC staining was used to analyze the cerebral infarction area. The apoptosis of neurons in mouse brain tissue was analyzed by in situ terminal assay. The levels of inflammatory factors in brain tissue of mice were detected by enzyme-linked immunosorbent assay. The expression levels of PI3K/AKT pathway-related proteins were detected by Western blotting.
Results The brain tissue cells of the sham operation group were closely arranged and the structure was intact. In the model group, the brain tissue structure was disordered, a large number of cells were shed, the intercellular space was enlarged, and the morphology was swollen. The brain tissue loss of mice in different L-carnitine dose groups was gradually improved. The cerebral infarction rates in the sham-operated group, the model group, the low-dose L-carnitine group, the middle-dose L-carnitine group, and the high-dose L-carnitine group were (0.83±0.08)%, (59.32±3.12)%, (33.72±1.55)%, (25.58±1.21)%, and (9.81±1.07)%, respectively; the apoptosis rates of neurons were (1.85±0.18)%, (37.31±1.25)%, (21.67±1.02)%, (15.62±2.31)% and (6.63±0.88)%, respectively; the levels of interleukin-6 were (1.32±0.08), (13.21±1.16), (9.33±0.19), (6.03±0.18) and (3.73±0.15) pg·mL-1, respectively; the levels of tumor necrosis factor α were (2.02±0.15), (15.07±1.26), (10.08±2.06), (7.13±1.16) and (4.06±0.08) pg·mL-1, respectively; the relative expression levels of PI3K protein were 0.65±0.09, 0.10±0.01, 0.19±0.03, 0.35±0.03 and 0.55±0.06, respectively; the relative AKT protein expression levels were 0.69±0.05, 0.11±0.02, 0.21±0.02, 0.39±0.03 and 0.63±0.06, respectively. Compared with the model group, the above indicators in the L-carnitine low-dose group, the L-carnitine medium-dose group and the L-carnitine high-dose group had statistically significant differences (all P<0.05).
Conclusion L-carnitine can alleviate hypoxic-ischemic brain damage in neonatal mice, and its mechanism may be related to the regulation of PI3K/AKT signaling pathway.
, authors=Xian WANG, Wei-ling HUANG, Tian-jiao ZHU, Xing ZHENG, Zhong WANG, authorsList=Xian WANG, Wei-ling HUANG, Tian-jiao ZHU, Xing ZHENG, Zhong WANG, authorCompany=null, correspAuthors=Zhong WANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291704991660659510, articleId=1291704991165731636, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=左卡尼汀调控PI3K/AKT通路对新生小鼠缺氧缺血性脑损伤的研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探究左卡尼汀调控（PI3K/AKT）通路对新生小鼠缺氧缺血性脑损伤的影响。
方法 缺氧缺血性脑损伤模型建立成功的80只小鼠被随机分为模型组、左卡尼汀低剂量组、左卡尼汀中剂量组和左卡尼汀高剂量组，每组20只，未建模的20只小鼠作为假手术组。左卡尼汀低剂量组、左卡尼汀中剂量组、左卡尼汀高剂量组的小鼠分别每日通过腹部注射左卡尼汀100、250、500 mg·kg-1，假手术组与模型组的小鼠通过腹部注射等量生理盐水，给药1周。通过苏木素伊红染色分析小鼠脑组织病理变化；通过TCC染色分析各组小鼠脑梗死面积；通过原位末端法分析小鼠脑组织神经元的凋亡；通过酶联免疫吸附实验检测小鼠脑组织炎症因子水平；通过蛋白质印迹实验检测PI3K/AKT通路相关蛋白的表达水平。
结果 假手术组小鼠脑组织细胞排列紧密，结构完整。模型组小鼠脑组织结构紊乱，大量细胞脱落，细胞间隙增大，形态肿胀。不同左卡尼汀剂量组小鼠的脑组织损失逐渐改善。假手术组、模型组、左卡尼汀低剂量组、左卡尼汀中剂量组和左卡尼汀高剂量组的小鼠脑梗死率分别为（0.83±0.08）%、（59.32±3.12）%、（33.72±1.55）%、（25.58±1.21）%和（9.81±1.07）%，神经元凋亡率分别为（1.85±0.18）%、（37.31±1.25）%、（21.67±1.02）%、（15.62±2.31）%和（6.63±0.88）%，白细胞介素-6的水平分别为（1.32±0.08）、（13.21±1.16）、（9.33±0.19）、（6.03±0.18）和（3.73±0.15）pg·mL-1，肿瘤坏死因子α的水平分别为（2.02±0.15）、（15.07±1.26）、（10.08±2.06）、（7.13±1.16）和（4.06±0.08）pg·mL-1，PI3K蛋白相对表达水平分别为0.65±0.09、0.10±0.01、0.19±0.03、0.35±0.03和0.55±0.06，AKT蛋白相对表达水平分别为0.69±0.05、0.11±0.02、0.21±0.02、0.39±0.03和0.63±0.06。左卡尼汀低剂量组、左卡尼汀中剂量组和左卡尼汀高剂量组的上述指标分别与模型组相比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 左卡尼汀能够减轻新生小鼠缺氧缺血性脑损伤的损伤程度，其作用机制可能与调控PI3K/AKT信号通路相关。
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王娴（1978-），女，副主任医师，主要从事新生儿方面研究
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