Article(id=1291404893600866731, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404875351449891, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.09.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1736265600000, receivedDateStr=2025-01-08, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824519777, onlineDateStr=2026-08-04, pubDate=1747411200000, pubDateStr=2025-05-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824519777, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824519777, creator=13701087609, updateTime=1785824519777, updator=13701087609, issue=Issue{id=1291404875351449891, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='9', pageStart='1201', pageEnd='1350', issueExtLink='null', onlineDate='null', pubDate='1747411200000', pubDateStr='2025-05-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824515426, creator='13701087609', updateTime=1785824515426, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=1254, endPage=1260, ext={EN=ArticleExt(id=1291404895274394028, articleId=1291404893600866731, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Protective effects of 6-gingerol on acute respiratory distress syndrome in juvenile mice by regulating the PI3K/Akt signaling pathway through Nur77, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the protective effects and potential mechanisms of 6-gingerol against acute respiratory distress syndrome (ARDS) in juvenile mice through nerve growth factor-induced clone B (Nur77).
Methods The juvenile mouse model of ARDS was established by tracheal instillation of lipopolysaccharide. After modeling, 48 juvenile mice were randomly divided into the model group, the 6-gingerol group (intraperitoneal injection of 30 mg·kg-1 6-gingerol), the 6-gingerol+sh-NC group (intranasal instillation of sh-NC negative control adenovirus+intraperitoneal injection of 30 mg·kg-1 6-gingerol), and the 6-gingerol+sh-Nur77 group (intranasal instillation of sh-Nur77 adenovirus+intraperitoneal injection of 30 mg·kg-1 6-gingerol). Another 12 normal juvenile mice were given an equal volume of sterile 0.9% NaCl by tracheal instillation as the sham operation group. Detected the lung wet/dry (W/D) ratio of young mice in each group. The immunohistochemistry method was used to detect the positive expression of collagen Ⅲ in lung tissues. The kit was used to detect apoptosis in the lung tissues of young mice. The expressions of pathway-related proteins were detected by Western blotting.
Results The W/D ratios of the sham operation group, the model group, the 6-gingerol group, the 6-gingerol+sh-NC group and the 6-gingerol+sh-Nur77 group were 2.20±0.26, 6.65±0.92, 3.89±0.52, 3.72±0.44 and 5.55±0.78, respectively; the positive levels of collagen Ⅲ were 1.00±0.22, 3.99±0.54, 1.85±0.28, 1.76±0.29 and 2.79±0.34, respectively; the apoptosis rates were (4.65±0.66)%, (39.62±5.03)%, (18.63±2.33)%, (17.82±2.12)% and (33.65±5.03)%, respectively; the levels of phosphorylated phosphatidylinositol 3-kinase/phosphatidylinositol 3-kinase (p-PI3K/PI3K) were 1.00±0.13, 1.66±0.22, 1.23±0.17, 1.21±0.14 and 1.58±0.24, respectively; the levels of phosphorylated protein kinase B/protein kinase B (p-Akt/Akt) were 1.00±0.16, 1.78±0.26, 1.33±0.21, 1.38±0.19 and 1.60±0.22, respectively. Compared with the sham operation group, the differences in the above indicators of the model group were statistically significant (all P<0.05); compared with the model group, the differences in the 6-gingerol group were statistically significant (all P<0.05); compared with the 6-gingerol+sh-NC group, the differences in the 6-gingerol+sh-Nur77 group were also statistically significant (all P<0.05).
Conclusion 6-gingerol intervention can improve lung injury in young ARDS mice, up-regulate the expression of Nur77, inhibit lung tissue inflammatory response, reduce lung tissue apoptosis, and promote coagulation/fibrinolytic balance, and its mechanism of action may be related to the inhibition of PI3K/Akt pathway.
, authors=Shi-yong HUANG, Jing ZHENG, authorsList=Shi-yong HUANG, Jing ZHENG, authorCompany=null, correspAuthors=Jing ZHENG, 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=1291404895580578221, articleId=1291404893600866731, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=6-姜酚通过Nur77调控PI3K/Akt信号通路对幼年鼠急性呼吸窘迫综合征的保护作用, 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 研究6-姜酚通过神经生长因子诱导基因B（Nur77）对急性呼吸窘迫综合征（ARDS）幼鼠的保护作用及其可能的机制。
方法 用气管滴注脂多糖法建立ARDS幼鼠模型，将建模后的48只幼鼠随机分为模型组、6-姜酚组（腹腔注射30 mg·kg-1 6-姜酚）、6-姜酚+sh-NC组（鼻滴sh-NC阴性对照腺病毒+腹腔注射30 mg·kg-1 6-姜酚）和6-姜酚+sh-Nur77组（鼻滴sh-Nur77腺病毒+腹腔注射30 mg·kg-1 6-姜酚），另取12只正常幼鼠气管滴注等量无菌0.9% NaCl为假手术组。检测各组幼鼠肺湿/干（W/D）比值，以免疫组化法检测肺组织Ⅲ型胶原蛋白（collagen Ⅲ）阳性表达情况，以试剂盒法检测幼鼠肺部组织细胞凋亡情况，以蛋白质印迹法检测通路相关蛋白表达情况。
结果 假手术组、模型组、6-姜酚组、6-姜酚+sh-NC组和6-姜酚+sh-Nur77组的W/D比值分别为2.20±0.26、6.65±0.92、3.89±0.52、3.72±0.44和5.55±0.78，collagen Ⅲ阳性水平分别为1.00±0.22、3.99±0.54、1.85±0.28、1.76±0.29和2.79±0.34，细胞凋亡率分别为（4.65±0.66）%、（39.62±5.03）%、（18.63±2.33）%、（17.82±2.12）%和（33.65±5.03）%，磷酸化磷脂酰肌醇3-激酶/磷脂酰肌醇3-激酶（p-PI3K/PI3K）水平分别为1.00±0.13、1.66±0.22、1.23±0.17、1.21±0.14和1.58±0.24，磷酸化蛋白激酶B/蛋白激酶B（p-Akt/Akt）水平分别为1.00±0.16、1.78±0.26、1.33±0.21、1.38±0.19和1.60±0.22。模型组的上述指标与假手术组相比，6-姜酚组的上述指标与模型组相比，6-姜酚+sh-Nur77组的上述指标与6-姜酚+sh-NC组相比，在统计学上差异均有统计学意义（均P<0.05）。
结论 6-姜酚干预能够改善ARDS幼鼠肺损伤，通过上调Nur77表达，抑制肺组织炎症反应，减少肺组织细胞凋亡，并促进凝血/纤溶平衡，其作用机制可能与抑制PI3K/Akt通路有关。
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黄世勇（1975-），男，副主任医师，主要从事儿童呼吸重症方面的工作
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