[1]毛珍△,江润,张涛,等.芍药苷对类风湿关节炎大鼠滑膜组织炎症的改善作用[J].中国中医骨伤科杂志,2026,34(04):14-21.[doi:10.20085/j.cnki.issn1005-0205.260403]
　MAO Zhen,JIANG Run,ZHANG Tao,et al.The Ameliorative Effect of Paeoniflorin on Synovial Tissue Inflammation in Rats with Rheumatoid Arthritis[J].Chinese Journal of Traditional Medical Traumatology & Orthopedics,2026,34(04):14-21.[doi:10.20085/j.cnki.issn1005-0205.260403]
点击复制

芍药苷对类风湿关节炎大鼠滑膜组织炎症的改善作用()

《中国中医骨伤科杂志》[ISSN:1005-0205/CN:42-1340/R]

卷:
第34卷
期数:
2026年04期
页码:
14-21
栏目:
基础研究
出版日期:
2026-04-10

文章信息/Info

Title:
The Ameliorative Effect of Paeoniflorin on Synovial Tissue Inflammation in Rats with Rheumatoid Arthritis
文章编号:
1005-0205(2026)04-0014-08
作者:
毛珍1△; 江润1; 张涛1; 刘健1; 王龙2
1武汉市蔡甸区人民医院(武汉,430100)
2武汉市第一医院
Author(s):
MAO Zhen1△; JIANG Run1; ZHANG Tao1; LIU Jian1; WANG Long2
1Wuhan Caidian District People's Hospital,Wuhan 430100,China; 2Wuhan First Hospital,Wuhan 430022,China.
关键词:
芍药苷;  类风湿关节炎;  滑膜组织;  磷酸肌醇激酶/蛋白激酶/核转录因子-κB
Keywords:
paeoniflorin;  rheumatoid arthritis;  synovial tissue;  PI3K/Akt/NF-κB
分类号:
R285.5
DOI:
10.20085/j.cnki.issn1005-0205.260403
文献标志码:
A
摘要:
目的:基于PI3K/Akt/NF-κB通路观察芍药苷对类风湿关节炎大鼠滑膜组织炎症的改善作用及其机制。方法:将60只SD雄性大鼠随机分为空白组、模型组、PI3K抑制剂组、芍药苷组、芍药苷+PI3K激动剂组,每组12只。除空白组外,其余组采用Ⅱ型胶原诱导类风湿关节炎大鼠模型。观察各组大鼠不同时间点体重和关节肿胀度; 采用苏木精-伊红(HE)染色和番红O-固绿染色观察大鼠病理形态; 用ELISA法检测大鼠血清中TNF-α、IL-6、IL-1β、IL-10含量; 采用Western Blot法检测大鼠滑膜组织中PI3K、Akt、NF-κB p65、TNF-α、IL-6、IL-10蛋白表达; 采用RT-PCR检测大鼠滑膜组织PI3K、Akt、NF-κB p65、TNF-α、IL-6、IL-10 mRNA表达。结果:与模型组比较,第21天和第28天芍药苷+PI3K激动剂组大鼠体重上升、关节肿胀度降低,差异有统计学意义(P<0.05); 芍药苷组和PI3K抑制剂组大鼠体重上升、关节肿胀度显著降低,差异有统计学意义(P<0.01)。与模型组比较,芍药苷+PI3K激动剂组大鼠关节软骨轻度损伤,软骨细胞增多; 芍药苷组和PI3K抑制剂组大鼠关节软骨损伤改善,软骨下骨结构未见明显受损。与模型组比较,芍药苷+PI3K激动剂组大鼠血清TNF-α、IL-6和IL-1β水平降低,IL-10水平升高,差异有统计学意义(P<0.05); 芍药苷组和PI3K抑制剂组大鼠TNF-α、IL-6和IL-1β水平明显降低,差异有统计学意义(P<0.01); IL-10水平显著升高,差异有统计学意义(P<0.01)。Western Blot法检测和RT-PCR显示,与模型组比较,芍药苷+PI3K激动剂组大鼠PI3K、Akt、NF-κB p65、TNF-α、IL-6蛋白表达及基因水平降低,差异有统计学意义(P<0.05); IL-10蛋白表达及基因水平升高,差异有统计学意义(P<0.05); 芍药苷组和PI3K抑制剂组水平变化显著,差异有统计学意义(P<0.01)。结论:芍药苷可以调控PI3K/Akt/NF-κB信号通路,从而改善类风湿关节炎大鼠滑膜组织炎症。
Abstract:
Objective:To observe the effect and mechanism of paeoniflorin on synovial tissue in rats with rheumatoid arthritis(RA),focusing based on the PI3K/Akt/NF-κB signaling pathway.Methods:Sixty male SD rats were randomly divided into the blank group,model group,PI3K inhibitor group,paeoniflorin group,and paeoniflorin +PI3K agonist group,with 12 rats in each group.Except for the blank group,the other groups were established with type Ⅱ collagen-induced rat rheumatoid arthritis models.Body weight and joint swelling degree of rats in each group were monitored at different time points; pathological changes in joint tissues were assessed by hematoxylin-eosin(HE)and Safranin O-Fast Green Staining.The contents of TNF-α,IL-6,IL-1β and IL-10 in rat serum were detected by ELISA.The protein expressions of PI3K,Akt,NF-κB p65,TNF-α,IL-6 and IL-10 in the synovial tissue of rats were detected by Western Blot.The mRNA expressions levels of PI3K,Akt,NF-κB p65,TNF-α,IL-6 and IL-10 in rat synovial tissue were quantified by RT-PCR.Results:Compared with the model group,the body weight of the paeoniflorin +PI3K agonist group increased and the degree of joint swelling decreased on the 21st and 28th day(P<0.05).The body weight of the paeoniflorin group and the PI3K inhibitor group increased,and the degree of joint swelling was significantly reduced(P<0.01).Compared with the model group,the paeoniflorin +PI3K agonist group exhibited mild articular cartilage injury and an increased number of chondrocytes.In the paeoniflorin group and the PI3K inhibitor group,the articular cartilage injury was improved,and no obvious damage was observed in the subchondral bone structure.Compared with the model group,the levels of serum TNF-α,IL-6 and IL-1β in the paeoniflorin +PI3K agonist group decreased,while the level of IL-10 increased(P<0.05),and the levels of TNF-α,IL-6 and IL-1β in the paeoniflorin group and the PI3K inhibitor group significantly decreased(P<0.01).The level of IL-10 was significantly increased(P<0.01).Western Blot and RT-PCR showed that,compared with the model group,the paeoniflorin+ PI3K agonist group exhibited decreased protein expressions and gene levels of PI3K,Akt,NF-κB p65,TNF-α,and IL-6 decreased(P<0.05),while the protein expression and gene level of IL-10 increased(P<0.05).The levels in the paeoniflorin group and the PI3K inhibitor group changed significantly(P<0.01).Conclusion:Paeoniflorin can regulate the PI3K/Akt/NF-κB signaling pathway,thereby improving synovial tissue inflammation in rats with rheumatoid arthritis.

参考文献/References:

[1] 高志,吴傲,胡仲翔,等.类风湿性关节炎中氧化应激与免疫浸润的生物信息学分析[J].南方医科大学学报,2025,45(4):862-870.
[2] 杨豫正,姚晓玲,罗丰,等.雷公藤治疗类风湿关节炎作用机制的生物信息学分析及实验验证[J].中医杂志,2025,66(7):724-733.
[3] ZHANG L L,WEI W.Anti-inflammatory and immunoregulatory effects of paeoniflorin and total glucosides of paeony[J].Pharmacology & Therapeutics,2020,207:107452.
[4] 代鑫,王莹,任鑫悦,等.芍药苷对溃疡性结肠炎小鼠氧化应激的影响及机制[J].中国药房,2025,36(4):427-433.
[5] 孙韬,李赛菲,屈正皓,等.基于PI3K/AKT/NF-κB通路探讨芍药苷对四氯化碳暴露诱导的肝纤维化小鼠的保护作用及机制[J].河南医学高等专科学校学报,2025,37(2):121-127.
[6] 王亚娜,许晓琳,马文华,等.芍药苷调节PI3K/AKT/NF-κB信号通路对血栓闭塞性脉管炎大鼠的治疗作用研究[J].中国临床药理学杂志,2024,40(6):854-858.
[7] 杜红丽,张晨宇,赵清.黄芩素通过调节HIF-1α/VEGF信号通路抑制类风湿关节炎大鼠的炎症反应和病理性血管生成[J].中国病理生理杂志,2022,38(12):2213-2219.
[8] CHEN Y J,LIU Y X,WU J Y,et al.A two-herb formula inhibits hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes[J].Scientific Reports,2021,11(1):3850.
[9] WU B,HE Y,YANG D,et al.Identification of hub genes and therapeutic drugs in rheumatoid arthritis patients[J].Clinical Rheumatology,2021,40(8):3299-3309.
[10] 杨越,张解玉,张馨文,等.清热活血方对胶原诱导性关节炎模型大鼠H3K18la及JAK2/STAT3信号通路的影响[J].中医杂志,2025,66(19):2045-2051.
[11] 周闻,杨宏伟.靶向铁死亡治疗类风湿关节炎的分子机制及天然药物筛选[J].中国组织工程研究,2026,30(23):6051-6061.
[12] 杨斐,郑晓娟,柴宝.炎症性肠病患者肠道菌群特点及其与CD8+CD28+/CD8+CD28-T细胞免疫的相关性分析[J].北京医学,2024,46(9):727-732.
[13] 张仲博,郑福增,王上增,等.芍药苷对膝骨性关节炎模型大鼠炎症及NF-κB/NLRP3信号通路的影响[J].中国免疫学杂志,2025,41(8):1826-1832.
[14] 冯智明,尤宜洁,郝军舰.芍药苷调节TXNIP/NLRP3信号通路对血栓闭塞性脉管炎大鼠炎症反应的影响[J].中国老年学杂志,2025,45(15):3793-3797.
[15] 王文茜,王阶.芍药苷调节SDF-1/CXCR4信号通路对冠心病大鼠心肌损伤的影响[J].中国免疫学杂志,2025,41(6):1455-1460.
[16] LIU H,ZHU Y L,GAO Y T,et al.NR1D1 modulates synovial inflammation and bone destruction in rheumatoid arthritis[J].Cell Death & Disease,2020,11:129.
[17] GEORGE B,GUI B,RAGURAMAN R,et al.AKT1 transcriptomic landscape in breast cancer cells[J].Cells,2022,11(15):2290.
[18] RANEK M J,KOKKONEN-SIMON K M,CHEN A N,et al.PKG1-modified TSC2 regulates mTORC1 activity to counter adverse cardiac stress[J].Nature,2019,566(7743):264-269.
[19] FATIMA M,HUANG F,FU X.Emerging influence of RNA post-transcriptional modifications in the synovial homeostasis of rheumatoid arthritis[J].Frontiers in Immunology,2024,15:1494873.
[20] GU Y J,JIN S D,WANG F,et al.Clinicopathological significance of PI3K,Akt and survivin expression in gastric cancer[J].Biomedicine & Pharmacotherapy,2014,68(4):471-475.
[21] 吴桐,赵思超,白敏,等.复方升降平喘止咳丸通过调控PI3K/AKT/NFκB信号通路抑制BA大鼠细胞凋亡和炎症反应[J/OL].海南医科大学学报,1-19[2025-09-25].https://doi.org/10.13210/j.cnki.jhmu.20250916.001.
[22] 龙莉,林思,秦慧真,等.凤尾草水提物对LPS致小鼠炎症及PI3K/Akt/NF-κB信号通路的影响[J/OL].中成药,1-7[2025-09-20].https://link.cnki.net/urlid/31.1368.R.20250820.0917.002.
[23] 张欣慰,梁天宇.升血小板胶囊调控PI3K/Akt/NF-κB信号通路抑制氧化应激、炎症反应治疗放射性皮炎的疗效分析[J].辽宁中医药大学学报,2025,27(10):29-33.
(收稿日期:2025-09-21)

备注/Memo

备注/Memo:
基金项目:武汉市卫生计生科研基金资助项目(WZ24Q02)
武汉市蔡甸区人民医院院内科研项目(XHJBYY-KXYJJJ-QNXM-05,XHJBKXYJJJ-MSXM-03)
△通信作者 E-mail:517994770@qq.com
更新日期/Last Update: 2026-04-15