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高良姜素调控JAK3/STAT3通路对大鼠类风湿性关节炎的影响
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| 篇名： | 高良姜素调控JAK3/STAT3通路对大鼠类风湿性关节炎的影响 |
| TITLE： | Effects of galangin on rheumatoid arthritis in rats by regulating the JAK3/STAT3 pathway |
| 摘要： | 目的 探讨高良姜素调控Janus激酶3（JAK3）/信号转导及转录激活因子3（STAT3）通路对大鼠类风湿性关节炎（RA）的影响。方法取50只雄性SD大鼠，通过皮下注射由牛Ⅱ型胶原、费氏完全佐剂构成的乳剂以构建诱导性关节炎模型。将造模成功的大鼠随机分为模型组，高良姜素低、中、高剂量组（1、5、15mg/kg）和甲氨蝶呤组（阳性对照，2mg/kg），每组10只；另取10只正常大鼠，作为正常组。从造模第15天起，各组大鼠灌胃相应药液或含0.5%吐温80的生理盐水，每天1次，连续28d。比较灌胃前及灌胃后各组大鼠的关节炎指数（AI）评分和足跖趾容积；末次给药后24h，检测其血清中白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）、IL-4、IL-10水平，观察踝关节滑膜组织病理变化，并检测其踝关节滑膜组织中UNC-51样激酶1（ULK1）、Beclin-1、微管相关蛋白1轻链3（LC3）、B细胞淋巴瘤2（Bcl-2）、Bcl-2相关X蛋白（Bax）、胱天蛋白酶3（caspase-3）、JAK3、磷酸化JAK3（p-JAK3）、STAT3、磷酸化STAT3（p-STAT3）蛋白的表达情况以及LC3阳性区域的荧光强度。结果与模型组相比，各药物组大鼠踝关节滑膜组织细胞增生、炎症细胞浸润等病理变化均有所改善；其AI评分和足跖趾容积（灌胃后28d），IL-6、TNF-α水平，Bcl-2蛋白的表达水平和JAK3、STAT3的磷酸化水平均显著降低（P＜0.05）；IL-4、IL-10水平，ULK1、Beclin-1、Bax、caspase-3、LC3蛋白的表达水平和LC3阳性区域的荧光强度均显著升高（P＜0.05），且高良姜素的作用具有剂量依赖性（P＜0.05）。结论高良姜素可诱导RA大鼠滑膜组织细胞持续自噬、促进细胞凋亡、抑制滑膜细胞增生、减轻持续性炎症反应，上述抗RA作用可能与其抑制JAK3/STAT3通路有关。 |
| ABSTRACT： | OBJECTIVE To investigate the effects of galangin on rheumatoid arthritis （RA） in rats by regulating the Janus kinase 3 （JAK3）/signal transducer and activator of transcription 3 （STAT3） pathway. METHODS Fifty male SD rats were taken， and an emulsion composed of bovine type Ⅱ collagen and Freund’s complete adjuvant was injected subcutaneously to establish an induced arthritis model. The rats that were successfully modeled were randomly divided into model group， low， medium and high dose groups of galangin （1， 5， 15 mg/kg）， and methotrexate group （positive control， 2 mg/kg）， with 10 rats in each group. Another 10 normal rats were taken as the normal group. Starting from the 15th day of modeling， each group of rats was gavaged with the corresponding drug solution or normal saline containing 0.5% Tween 80 once a day for 28 consecutive days. The arthritis index （AI） scores and paw volume of rats were compared before and after gavage administration. Twenty-four hours after the last administration， the serum levels of interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， IL-4 and IL-10 were determined， the pathological changes in ankle joint synovial tissue were observed， and the protein expressions of UNC-51 like kinase 1 （ULK1）， Beclin-1， microtubule-associated protein 1 light chain 3 （LC3）， B cell lymphoma 2 （Bcl-2）， Bcl-2-associated X protein （Bax）， caspase-3， JAK3， phosphorylated JAK3 （p-JAK3）， STAT3 and phosphorylated STAT3 （p-STAT3） in the synovial tissue of the ankle joint were detected， as well as the fluorescence intensity of LC3-positive areas. RESULTS Compared with the model group， the pathological changes such as cellular proliferation of ankle joint synovial tissue and infiltration of inflammatory cells in rats of each administration group showed improvement. Moreover， their AI scores and paw pad volumes （on day 28 after gavage）， the levels of IL-6 and TNF-α， the protein expression of Bcl-2， and the phosphorylation levels of JAK3 and STAT3 were all significantly reduced （ P ＜0.05）. The levels of IL-4 and IL-10， the protein expressions of ULK1， Beclin-1， Bax， caspase-3 and LC3， as well as the fluorescence intensity of LC3-positive areas， were all significantly increased （ P ＜0.05）. Moreover， the effect of galangin was in a dose-dependent manner （ P ＜0.05）. CONCLUSIONS Galangin can induce sustained autophagy in synovial tissue cells of RA rats， promote cell apoptosis， inhibit synovial cell proliferation， and alleviate persistent inflammatory responses. The above anti-RA effects may be related to the inhibition of the JAK3/STAT3 pathway. |
| 期刊： | 2026年第37卷第06期 |
| 作者： | 黄燕；王伟明；刘海英；战艺；陈曦；于得泓 |
| AUTHORS： | HUANG Yan，WANG Weiming，LIU Haiying，ZHAN Yi，CHEN Xi，YU Dehong |
| 关键字： | 高良姜素；类风湿性关节炎；自噬；凋亡；滑膜细胞增生；炎症反应；JAK3/STAT3通路 |
| KEYWORDS： | galangin； rheumatoid arthritis； autophagy； apoptosis； synovial cell proliferation； inflammatory response； JAK3/ |
| 阅读数： | 3 次 |
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