[1]康涛,王倩倩.丹参酮ⅡA通过抑制JNK信号通路减轻高糖诱导的周围神经炎性损伤[J].陕西医学杂志,2026,(4):462-466.[doi:DOI:10.3969/j.issn.1000-7377.2026.04.005]
 KANG Tao,WANG Qianqian.Tanshinone ⅡA alleviates high glucoseinduced peripheral neuroinflammatory injury by inhibiting the JNK signaling pathway[J].,2026,(4):462-466.[doi:DOI:10.3969/j.issn.1000-7377.2026.04.005]
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丹参酮ⅡA通过抑制JNK信号通路减轻高糖诱导的周围神经炎性损伤

《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
期数:
2026年4期
页码:
462-466
栏目:
基础研究
出版日期:
2026-04-05

文章信息/Info

Title:
Tanshinone ⅡA alleviates high glucoseinduced peripheral neuroinflammatory injury by inhibiting the JNK signaling pathway
作者:
康涛1王倩倩2
(1.陕西省人民医院神经内2科,陕西 西安 710068;2.西安交通大学第一附属医院中医科,陕西 西安 710061)
Author(s):
KANG Tao1WANG Qianqian2
(1.Department of Neurology Ⅱ,Shaanxi Provincial People’s Hospital,Xi’an 710068,China;2.Departmentof Traditional Chinese Medicine,The First Affiliated Hospital of Xi’an Jiaotong University,Xi’an 710061,China)
关键词:
糖尿病周围神经病变丹参酮ⅡAc-Jun N端激酶磷酸化c-Jun磷酸化转录激活因子2炎性因子
Keywords:
Diabetic peripheral neuropathyTanshinone ⅡAc-Jun Nterminal KinasePhosphorylated c-JunPhosphorylated activating transcription factor 2Inflammatory factors
分类号:
R 587.1
DOI:
DOI:10.3969/j.issn.1000-7377.2026.04.005
文献标志码:
A
摘要:
目的:糖尿病周围神经病变(DPN)与炎性反应密切相关,JNK信号通路是炎性反应的关键环节。丹参酮ⅡA(TⅡA)具有抑制炎性反应、保护神经的作用。本研究探讨TⅡA通过调控JNK信号通路干预DPN的分子机制。方法:采用RSC96细胞构建体外模型。实验设对照组、高糖组、TⅡA高、中、低组。采用CCK-8法评估TⅡA对细胞活力的影响。Western blot法检测磷酸化c-Jun氨基末端激酶(p-JNK)、磷酸化c-Jun(p-c-Jun)、磷酸化激活转录因子2(p-ATF-2)及炎症因子(IL-1β、IL-6、TNF-α)的表达水平。ELISA法检测炎性因子的含量。结果:CCK-8结果显示,TⅡA对RSC96细胞活力的影响呈现时间依赖性,随着作用时间的延长,细胞活力增强,以72 h最为显著。浓度方面,2~6 μg/ml范围内,细胞活力显著增强,之后随着浓度上升,细胞增殖活力减弱。WB结果显示,与对照组比较,高糖组p-JNK、p-c-Jun、p-ATF-2、IL-1β、IL-6和TNF-α的蛋白表达水平上调(均P<0.05)。TⅡA干预后,这些指标被显著抑制(均P<0.05)。ELISA实验显示,高糖诱导的细胞上清液中IL-1β、IL-6和TNF-α含量升高,而TⅡA可以逆转这一现象(均P<0.05)。结论:TⅡA可能通过抑制JNK信号通路减少促炎因子的释放,从而发挥对DPN的治疗作用。
Abstract:
Objective:Diabetic peripheral neuropathy (DPN) is closely associated with inflammatory responses,and the JNK signaling pathway is a key link in inflammation.Tanshinone ⅡA (TⅡA) possesses antiinflammatory and neuroprotective effects.This study aims to investigate the molecular mechanism by which TⅡA intervenes in DPN through regulating the JNK signaling pathway.Methods:An in vitro model was established using RSC96 cells.Experiments were divided into control group,high glucose group,and high/medium/low TⅡA concentration groups.The CCK-8 assay was used to evaluate the effect of TⅡA on cell viability.Western blot (WB) was used to detect the expression levels of JNK,p-JNK,p-c-Jun,p-ATF-2,and inflammatory factors (IL-1β,IL-6,TNF-α).The content of inflammatory factors in the cell supernatant was measured by ELISA.Results:CCK-8 results showed that the effect of TⅡA on RSC96 cell viability was timedependent.Cell viability increased with prolonged action time,most significantly at 72 hours.Regarding concentration,within the range of 2~6 μg/ml,cell viability significantly increased;beyond this range,cell proliferation activity decreased with increasing concentration.WB results showed that compared with the control group,the protein expression levels of p-JNK,p-c-Jun,p-ATF-2,IL-1β,IL-6,and TNF-α were upregulated in the high glucose group (all P<0.05).After TⅡA intervention,these indicators were significantly inhibited (all P<0.05).ELISA experiments showed that the contents of IL-1β,IL-6,and TNF-α in the cell supernatant induced by high glucose were increased,and TⅡA reversed this phenomenon (P<0.05).Conclusion:TⅡA may exert therapeutic effects on DPN by inhibiting the JNK signaling pathway and reducing the release of proinflammatory factors.

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备注/Memo

备注/Memo:
国家自然科学基金资助项目(82205017);陕西省自然科学基础研究计划项目(2020JQ515);陕西省中医药管理局课题(2021ZZJC013)
更新日期/Last Update: 2026-04-05