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膝痹宁Ⅱ方经JAK2/STAT3通路缓解KOA大鼠滑膜炎症及纤维化的机制研究
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| 篇名： | 膝痹宁Ⅱ方经JAK2/STAT3通路缓解KOA大鼠滑膜炎症及纤维化的机制研究 |
| TITLE： | Mechanism study of Xibining Ⅱ formula in alleviating synovial inflammation and fibrosis in KOA rats via JAK2/STAT3 pathway |
| 摘要： | 目的 基于Janus激酶2（JAK2）/信号转导及转录激活因子3（STAT3）通路，探讨膝痹宁Ⅱ方缓解膝骨关节炎（KOA）大鼠滑膜炎症及纤维化的作用机制。方法将75只雄性SD大鼠随机分为假手术组（Sham组）、KOA组、膝痹宁Ⅱ低剂量组（XBNⅡ-L组，4g/kg）、高剂量组（XBNⅡ-H组，8g/kg）、膝痹宁Ⅱ高剂量联合STAT3激活剂Colivelin三氟乙酸盐（C-TFA）组[C-TFA组，8g/kg膝痹宁Ⅱ+1.0mg/（kg·d）C-TFA]，每组15只。除Sham组外，其余各组采用前交叉韧带离断法建立KOA模型。造模成功后，各药物组分别给予相应药物灌胃和（或）腹腔注射，每日1次，持续28d。末次给药后，评估各组大鼠膝关节滑膜组织病理改变并进行指标计算；检测血清炎症因子水平，检测膝关节滑膜组织中磷酸化JAK2（p-JAK2）、磷酸化STAT3（p-STAT3）蛋白阳性表达，滑膜组织JAK2/STAT3通路相关蛋白及mRNA表达。结果与Sham组相比，KOA组大鼠滑膜衬里细胞显著增生且排列紊乱，Krenn评分，纤维化占比，p-JAK2、p-STAT3阳性面积百分比，p-JAK2/JAK2、p-STAT3/STAT3和Ⅰ型胶原蛋白、α-平滑肌肌动蛋白的表达水平，JAK2、STAT3、Ⅰ型胶原蛋白、α-平滑肌肌动蛋白mRNA的表达水平，以及血清白细胞介素1β、白细胞介素18水平均显著升高（P＜0.05）。与KOA组相比，XBNⅡ-L组、XBNⅡ-H组大鼠上述病理改变明显改善，各指标均显著下降（P＜0.05），且XBNⅡ-H组的改善效果显著优于XBNⅡ-L组（P＜0.05）。与XBNⅡ-H组相比，C-TFA组上述病理损伤加重，各指标均显著恶化（P＜0.05）。结论膝痹宁Ⅱ方可减轻KOA大鼠滑膜炎症与纤维化，其机制可能与抑制JAK2/STAT3通路激活有关。 |
| ABSTRACT： | OBJECTIVE To investigate the mechanism of Xibining Ⅱ formula in alleviating synovial inflammation and fibrosis in knee osteoarthritis （KOA） rats based on Janus kinase 2 （JAK2）/signal transducer and activator of transcription 3 （STAT3） pathway. METHODS Seventy-five male SD rats were randomly divided into sham operation group （Sham group）， KOA group， Xibining Ⅱ low-dose group （XBNⅡ-L group， 4 g/kg）， Xibining Ⅱ high-dose group （XBNⅡ-H group， 8 g/kg）， and Xibining Ⅱ high-dose combined with STAT3 activator Colivelin trifluoroacetate （C-TFA） group [C-TFA group， 8 g/kg Xibining Ⅱ+ 1.0 mg/（kg·d） C-TFA]， with 15 rats in each group. Except for the Sham group， the KOA model was established by anterior cruciate ligament transection in the other groups. After successful modeling， each group was given corresponding drugs by intragastric administration and （or） intraperitoneal injection once daily for 28 consecutive days. After the last medication， the pathological changes of synovial tissue of knee joint in each group were evaluated and the indicators were calculated. The levels of serum inflammatory factors were detected. The positive expressions of phosphorylated JAK2 （p-JAK2） and phosphorylated STAT3 （p-STAT3） in synovial tissue of the knee joint were detected. The expressions of JAK2/STAT3 pathway-related proteins and mRNAs in synovial tissue were detected. RESULTS Compared with the Sham group， the synovial lining cells in the KOA group showed significant proliferation and disordered arrangement； the Krenn score， fibrosis ratio， positive area percentage of p-JAK2 and p-STAT3， p-JAK2/JAK2 and p-STAT3/STAT3， protein expression of Collagen-Ⅰ and α -smooth muscle actin， the mRNA expression of JAK2， STAT3， Collagen-Ⅰ and α -smooth muscle actin， as well as serum levels of interleukin-1β and interleukin-18 were significantly increased （ P ＜0.05）. Compared with the KOA group， the above pathological changes were significantly improved in each dose group of Xibining Ⅱ formula， and all indicators were significantly decreased （ P ＜0.05）， with the XBNⅡ-H group showing better effects than the XBNⅡ-L group （ P ＜0.05）. Compared with the XBNⅡ-H group， the above pathological damages were aggravated in the C-TFA group， and all indicators were significantly worsened （ P ＜0.05）. CONCLUSIONS Xibining Ⅱ formula can alleviate synovial inflammation and fibrosis in KOA rats， and its mechanism may be related to inhibiting the activation of JAK2/STAT3 pathway. |
| 期刊： | 2026年第37卷第14期 |
| 作者： | 宋佳宸；吴鹏；张立；刘德仁；施蕾；刘江宇；史尧天；茆军 |
| AUTHORS： | SONG Jiachen，WU Peng，ZHANG Li，LIU Deren，SHI Lei，LIU Jiangyu，SHI Yaotian，MAO Jun |
| 关键字： | 膝痹宁Ⅱ方; 膝骨关节炎; 滑膜纤维化; 滑膜炎症; JAK2/STAT3通路 |
| KEYWORDS： | Xibining Ⅱ formula; knee osteoarthritis; synovial fibrosis; synovial inflammation; JAK2/STAT3 pathway |
| 阅读数： | 1 次 |
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