Article(id=1292126382419636426, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126355785802497, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.04.011, 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=1785996536115, onlineDateStr=2026-08-06, pubDate=1772208000000, pubDateStr=2026-02-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996536115, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996536115, creator=13701087609, updateTime=1785996536115, updator=13701087609, issue=Issue{id=1292126355785802497, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='4', pageStart='451', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1772208000000', pubDateStr='2026-02-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996529766, creator='13701087609', updateTime=1786014519902, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201811952292026, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126355785802497, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201811952292027, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126355785802497, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=523, endPage=529, ext={EN=ArticleExt(id=1292126382604185803, articleId=1292126382419636426, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Study on the mechanism by which gastrodin regulates SYNPO2 to influence the PI3K/Akt/mTOR signaling pathway and improve hypoxic-ischemic brain damage in neonatal rats, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effect and mechanism of gastrodin regulating synaptopodin 2 (SYNPO2) on hypoxic-ischemic brain damage (HIBD) in neonatal rats.
Methods The left common carotid artery of neonatal rats was ligated, and the rats were placed in a hypoxic chamber for 40 minutes to establish the HIBD model. Rats were randomly divided into sham operation group (no common carotid artery ligation or hypoxia treatment), model group (HIBD model established), gastrodin group (intraperitoneal injection of gastrodin 100 mg·kg-1 1 hour before common carotid artery ligation, 1 hour after hypoxia, and 12 hours after hypoxia), gastrodin+oe-NC group (3 days before modeling, 3 microliters oe-NC was transplanted intracerebroventricularly in rats, subsequent treatment same as the gastrodin group) and gastrodin+oe-SYNPO2 group (3 days before modeling, 3 microliters oe-SYNPO2 was transplanted intracerebroventricularly in rats, subsequent treatment same as the gastrodin group), with 10 rats in each group. Western blot was used to detect the levels of SYNPO2 and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway-related proteins; short-term behavioral tests were used to detect neurological function in each group; the dry-wet weight method was used to detect brain water content; TdT-mediated dUTP nick end labeling was used to detect the apoptosis rate of brain tissue cells in each group; immunofluorescence was used to detect the levels of lysosomal associated membrane protein 1 (LAMP1) and microtubule associated protein 1 light chain 3 beta (LC3B) proteins in brain tissue of each group.
Results The relative expression levels of SYNPO2 protein in the sham operation group, model group, gastrodin group, gastrodin+oe-NC group and gastrodin+oe-SYNPO2 group were 1.00±0.16, 2.05±0.34, 1.38±0.18, 1.35±0.17 and 1.68±0.22, respectively; the relative expression levels of phosphorylated PI3K (p-PI3K)/PI3K protein were 1.00±0.19, 0.25±0.04, 0.65±0.08, 0.68±0.07 and 0.35±0.05, respectively; the relative expression levels of phosphorylated Akt (p-Akt)/Akt protein were 1.00±0.13, 0.28±0.04, 0.49±0.06, 0.51±0.07 and 0.31±0.04, respectively; the relative levels of phosphorylated mTOR (p-mTOR)/mTOR protein were 1.00±0.16, 0.22±0.04, 0.52±0.06, 0.54±0.07 and 0.29±0.05, respectively; the righting reflex latency periods were (2.56±0.33), (14.86±2.12), (5.66±0.75), (5.23±0.79) and (10.33±1.56) s, respectively; the negative geotaxis latency periods were (17.86±2.44), (56.33±8.22), (22.12±3.56), (23.05±3.22) and (40.22±5.66) s, respectively; the cliff avoidance reflex latency periods were (7.11±0.85), (16.55±2.32), (7.22±0.85), (7.83±0.96) and (13.55±2.45) s, respectively; the water contents were (51.56±6.47)%, (62.16±6.22)%, (55.02±6.25)%, (54.63±7.22)% and (61.98±5.17)%, respectively; the apoptosis rates were (5.17±0.65)%, (75.32±9.65)%, (25.65±3.89)%, (23.85±2.98)% and (50.56±6.89)%, respectively; the relative fluorescence intensity of LAMP1 were 1.00±0.15, 3.85±0.44, 1.14±0.15, 1.18±0.19 and 3.22±0.39, respectively; the relative fluorescence intensity of LC3B were 1.00±0.18, 3.45±0.52, 1.25±0.16, 1.21±0.15 and 1.68±0.19, respectively; the above indicators of the model group were statistically significant compared with the sham operation group, the above indicators of the gastrodin group were statistically significant compared with the model group, and the above indicators of the gastrodin+oe-SYNPO2 group were statistically significant compared with the gastrodin+oe-NC group (P<0.05, P<0.01, P<0.001).
Conclusion Gastrodin inhibits SYNPO2, alleviates brain edema and neurological dysfunction in HIBD rats, protects neuronal structural integrity, reduces neuronal apoptosis, and alleviates excessive autophagy, which may be achieved by activating the PI3K/Akt/mTOR pathway.
, authors=Qing-yu HU
1, Wen-juan LIU
1, Zong-li LÜ
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目的 探讨天麻素调控突触相关蛋白2（SYNPO2）对新生大鼠缺氧缺血性脑损伤（HIBD）的作用及其机制。
方法 结扎新生大鼠左侧颈总动脉，置于缺氧箱中持续缺氧40 min，建立HIBD模型。将大鼠随机分为假手术组（不进行结扎颈总动脉和缺氧处理）、模型组（建立HIBD模型）、天麻素组（分别于颈总动脉结扎前1 h、缺氧后1 h、缺氧后12 h腹腔注射天麻素100 mg·kg-1）、天麻素+oe-NC组（造模前第3 d，大鼠侧脑室内移植3 μL oe-NC，随后处理同天麻素组）和天麻素+oe-SYNPO2组（造模前第3d，大鼠侧脑室内移植3 μL oe-SYNPO2，随后处理同天麻素组），每组10只。蛋白免疫印迹法检测SYNPO2、磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/雷帕霉素靶蛋白（mTOR）信号通路相关蛋白水平；短期行为学测试检测各组大鼠神经功能；干湿重法检测大鼠脑含水量；原位末端标记染色法检测各组大鼠脑组织细胞凋亡率；免疫荧光法检测各组大鼠脑组织中溶酶体相关膜蛋白1（LAMP1）和微管相关蛋白1轻链3β（LC3B）蛋白水平。
结果 假手术组、模型组、天麻素组、天麻素+oe-NC组和天麻素+oe-SYNPO2组SYNPO2蛋白相对表达水平分别为1.00±0.16、2.05±0.34、1.38±0.18、1.35±0.17和1.68±0.22，磷酸化PI3K（p-PI3K）/PI3K蛋白相对水平分别为1.00±0.19、0.25±0.04、0.65±0.08、0.68±0.07和0.35±0.05，磷酸化Akt（p-Akt）/Akt蛋白相对水平分别为1.00±0.13、0.28±0.04、0.49±0.06、0.51±0.07和0.31±0.04，磷酸化mTOR（p-mTOR）/mTOR蛋白相对水平分别为1.00±0.16、0.22±0.04、0.52±0.06、0.54±0.07和0.29±0.05，翻正反射潜伏期分别为（2.56±0.33）、（14.86±2.12）、（5.66±0.75）、（5.23±0.79）和（10.33±1.56）s，负趋地性潜伏期分别为（17.86±2.44）、（56.33±8.22）、（22.12±3.56）、（23.05±3.22）和（40.22±5.66）s，避崖反射潜伏期分别为（7.11±0.85）、（16.55±2.32）、（7.22±0.85）、（7.83±0.96）和（13.55±2.45）s，含水量分别为（51.56±6.47）%、（62.16±6.22）%、（55.02±6.25）%、（54.63±7.22）%、（61.98±5.17）%，凋亡率分别为（5.17±0.65）%、（75.32±9.65）%、（25.65±3.89）%、（23.85±2.98）%和（50.56±6.89）%，LAMP1相对荧光强度分别为1.00±0.15、3.85±0.44、1.14±0.15、1.18±0.19和3.22±0.39，LC3B相对荧光强度分别为1.00±0.18、3.45±0.52、1.25±0.16、1.21±0.15和1.68±0.19。模型组的上述指标与假手术组相比，天麻素组的上述指标与模型组相比，天麻素+oe-SYNPO2组的上述指标与天麻素+oe-NC组相比，在统计学上差异均有统计学意义（P<0.05，P<0.01，P<0.001）。
结论 天麻素通过抑制SYNPO2，减轻HIBD大鼠脑水肿和神经功能障碍，保护神经元结构完整性，减少神经元凋亡，减轻过度自噬，可能是通过激活PI3K/Akt/mTOR通路实现的。
, authors=胡清宇
1, 刘文娟
1, 吕宗立
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