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| 异甘草素对膝骨关节炎模型兔炎症反应影响 |
| The effect of isoliquiritigenin on inflammatory reaction of knee osteoarthritis rabbits by adjusting TXNIP/NLRP3 pathway |
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| DOI：10.3969/j.issn.1006-7108.2026.05.002 |
| 中文关键词: 异甘草素 TXNIP/NLRP3通路 膝骨关节炎 炎症反应 |
| 英文关键词:isoliquiritigenin TXNIP/NLRP3 pathway knee osteoarthritis inflammatory reaction |
| 基金项目:湖北省卫生健康委员会科研项目(WJ2019F005) |
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| 中文摘要: |
| 目的 探讨异甘草素（isoliquiritigenin，ISL）对膝骨关节炎（knee osteoarthritis，KOA）模型兔炎症反应及硫氧还蛋白相互作用蛋白/NOD样受体蛋白3（thioredoxin interacting protein/NOD-like receptor protein 3,TXNIP/NLRP3）通路的影响。方法 构建KOA兔模型，将造模成功兔随机分为KOA组，异甘草素低、高剂量组（ISL-L、ISL-H组），ISL-H+TMAO（TXNIP/NLRP3通路激活剂，氧化三甲胺）组，每组12只，另取12只正常健康兔子作为对照组（Control组）；采用Lequesne MG对各组兔进行行为学评分；X线片观察膝关节情况；ELISA检测血清TNF-α、IL-1β、IL-6水平；HE染色观察膝关节组织病理情况并进行Mankin评分；免疫组化检测MMP-13、Collagen II表达；Western blot检测TXNIP/NLRP3通路相关蛋白表达。结果 KOA组较Control组兔膝关节结构被破坏，胫骨平台关节面粗糙不平，外侧髁间隙变窄，且髁间隆起变锐，骨赘形成，关节软骨表层破损，存在多处裂隙甚至陷窝，软骨细胞固缩坏死、空泡增多，软骨细胞排列稀疏紊乱，软骨基底层可见血管入侵，Lequesne MG评分、Mankin评分、IL-1β、IL-6、TNF-α水平及MMP13、TXNIP、NLRP3、C-caspase-1表达升高，Collagen II表达降低（P<0.05）；ISL-L、ISL-H组较KOA组兔膝关节结构及关节软骨组织病理损伤明显改善，Lequesne MG评分、Mankin评分、IL-1β、IL-6、TNF-α水平及MMP13、TXNIP、NLRP3、C-caspase-1表达降低，Collagen II表达升高（P<0.05）；TMAO处理可部分逆转异甘草素对KOA兔炎症反应的改善作用。结论 异甘草素可减轻KOA兔炎症反应，与抑制TXNIP/NLRP3通路有关。 |
| 英文摘要: |
| Objective To discuss the impacts of isoliquiritigenin (ISL) on inflammatory reaction and thioredoxin interacting protein/NOD-like receptor protein 3 (TXNIP/NLRP3) pathway in knee osteoarthritis (KOA) rabbits. Methods A KOA rabbit model was constructed, and successfully modeled rabbits were randomly assigned into KOA group, low and high dose ISL groups (ISL-L, ISL-H), and ISL-H+TMAO group (activator of the TXNIP/NLRP3 pathway, trimethylamine oxide), with 12 rabbits in each group. Additionally, 12 healthy rabbits were considered as Control group. The Lequesne MG method was used to score the behavior of rabbits. X-ray was used to observe the condition of the knee joint. ELISA was performed to detect serum TNF-α, IL-1β, and IL-6. HE staining was performed to observe the pathological condition of knee joint tissue. The Mankin scoring was performed. Immunohistochemistry was performed to measure MMP-13 and Collagen II. Western blotting was used to measure TXNIP/NLRP3 pathway related proteins. Results Compared to those of rabbits in the Control group, the knee joint structure of rabbits in the KOA group was damaged, the tibial plateau joint surface was rough and uneven, the lateral condyle gap was narrowed, and the intercondylar ridge became sharper. Osteophytes were formed, and the surface of the articular cartilage was damaged, with multiple cracks and even pits. The chondrocytes were reduced in size, necrotic, and vacuolated, and the arrangement of chondrocytes was sparse and disordered. Vascular invasion was observed in the cartilage basal layer. The Lequesne MG score, Mankin score, IL-1β, IL-6, TNF-α, MMP13, TXNIP, NLRP3, and C-caspase-1 increased, while collagen II decreased (P<0.05). Compared to those in the KOA group, the knee joint structure and pathological damage of articular cartilage tissue in the ISL-L and ISL-H groups were significantly improved. The Lequesne MG score, Mankin score, IL-1β, IL-6, TNF-α, MMP13, TXNIP, NLRP3, and C-caspase-1 reduced, while collagen II increased (P<0.05). TMAO treatment partially reversed the improvement effect of isorlicorice on the inflammatory response in KOA rabbits. Conclusion Isoliquiritigenin alleviates the inflammatory reaction in KOA rabbits, which is related to the inhibition of the TXNIP/NLRP3 pathway. |
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