Article(id=1292126463029965571, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.01.011, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1746374400000, receivedDateStr=2025-05-05, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996555334, onlineDateStr=2026-08-06, pubDate=1768579200000, pubDateStr=2026-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996555334, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996555334, creator=13701087609, updateTime=1785996555334, 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=66, endPage=71, ext={EN=ArticleExt(id=1292126465060008708, articleId=1292126463029965571, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of artesunate on hippocampal neuronal damage in schizophrenia rats by adjusting JAK1/STAT3 signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effects and mechanism of artesunate on hippocampal neuronal damage in schizophrenia rats by adjusting Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.
Methods This study induced a rat model of schizophrenia using ketamine and divided them into model group, low-dose experimental group (5 mg·kg-1 artesunate), medium-dose experimental group (10 mg·kg-1 artesunate), and high-dose experimental group (20 mg·kg-1 artesunate), each with 12 rats. Another 12 rats were considered as normal group. After 21 days of administration, the open field test and three box social behavior experiment were used to detect schizophrenia symptoms in rats; hematoxylin-eosin (HE) staining was used to observe hippocampal neural tissue; Nissl staining was used to observe neuronal damage; terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) staining was used to detect neuronal apoptosis in the hippocampus; enzyme-linked immunosorbent assay (ELISA) was used to detect brain-derived neurotrophic factor (BDNF) in the hippocampus; Western blotting was used to detect JAK1 and STAT3-related protein expression in the hippocampus.
Results The intersection distances of the central areas of blank group, model group and low, medium and high dose experimental groups were (0.65±0.08), (1.48±0.18), (1.27±0.15), (1.08±0.13) and (0.77±0.09) m, respectively; social interaction times are (63.53±7.39), (31.73±4.09), (38.38±5.32), (44.97±5.13) and (54.78±6.27) s, respectively ; the number of Nissl-positive cells in the hippocampus were (121.38±13.54), (62.63±6.87), (80.85±8.93) , (98.24±9.49) and (118.23±12.63) cells, respectively ; the apoptosis rates were (2.94±0.46)%, (34.73±3.83)%, (25.75±2.92)%, (16.49±2.21)% and (6.83±1.02)%, respectively; the levels of BDNF were (172.58±19.48), (68.49±8.31), (92.26±10.22), (115.08±13.34) and (142.82±16.37) pg·mg-1, respectively; p-JAK1 protein relative expression levels were 0.38±0.05, 0.87±0.09, 0.73±0.09, 0.60±0.08 and 0.44±0.06, respectively ; p-STAT3 protein relative expression levels were 0.31±0.04, 0.79±0.09, 0.66±0.08, 0.53±0.06 and 0.38±0.05, respectively, when comparing the above indicators between model group and blank group, comparing the above indicators between low, medium, high dose experimental groups and model group, there were statistically significant differences (all P<0.05).
Conclusion Artesunate may improve hippocampal neuronal damage in schizophrenia rats by inhibiting JAK1/STAT3 signaling pathway.
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目的 探讨青蒿琥酯调节Janus激酶1（JAK1）/信号转导转录激活因子3（STAT3）信号通路对精神分裂症大鼠海马神经元损伤的影响及其机制。
方法 通过氯胺酮诱导大鼠精神分裂症模型，并分为模型组、低剂量实验组（5 mg·kg-1青蒿琥酯）、中剂量实验组（10 mg·kg-1青蒿琥酯）和高剂量实验组（20 mg·kg-1青蒿琥酯），每组12只，另取12只大鼠为空白组（正常喂养）。给药21天后，用旷场测试和三箱社交行为实验检测大鼠的精神分裂症状；用苏木精伊红（HE）染色法观察海马体神经组织；用Nissl染色法观察神经元损伤；用末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色法检测海马体神经元凋亡；用酶联免疫吸附实验（ELISA）法检测海马体脑源性神经营养因子（BDNF）；用蛋白质印迹法检测海马体JAK1和STAT3相关蛋白表达。
结果 空白组、模型组和低、中、高剂量实验组的中心区域交叉距离分别为（0.65±0.08）、（1.48±0.18）、（1.27±0.15）、（1.08±0.13）和（0.77±0.09）m；社交互动时间分别为（63.53±7.39）、（31.73±4.09）、（38.38±5.32）、（44.97±5.13）和（54.78±6.27）s；海马体Nissl阳性细胞数分别为（121.38±13.54）、（62.63±6.87）、（80.85±8.93）、（98.24±9.49）和（118.23±12.63）个；凋亡率分别为（2.94±0.46）%、（34.73±3.83）%、（25.75±2.92）%、（16.49±2.21）%和（6.83±1.02）%；BDNF分别为（172.58±19.48）、（68.49±8.31）、（92.26±10.22）、（115.08±13.34）和（142.82±16.37）pg·mg-1；p-JAK1蛋白相对表达水平分别为0.38±0.05、0.87±0.09、0.73±0.09、0.60±0.08和0.44±0.06；p-STAT3蛋白相对表达水平分别为0.31±0.04、0.79±0.09、0.66±0.08、0.53±0.06和0.38±0.05，模型组的上述指标与空白组比较，低、中、高剂量实验组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 青蒿琥酯可能通过抑制JAK1/STAT3信号通路改善精神分裂症大鼠海马神经元损伤。
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雷雨（1981-），女，主治医师，主要从事精神疾病诊疗方面的研究
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