Effects of jaceosidin on inflammatory injury in osteoarthritis rats by regulating AMPK/NLRP3 signaling pathway
- VernacularTitle:棕矢车菊素调节AMPK/NLRP3信号通路对骨关节炎大鼠炎性损伤的影响
- Author:
Chao WEI
1
;
Jiang YU
2
;
Guanyun SHENG
3
;
Yi CAI
4
Author Information
1. Dept. of Pain，Jianghan University Affiliated Hospital/ Wuhan Sixth Hospital，Wuhan 430015，China
2. Dept. of Orthopedic Surgery，Jianghan University Affiliated Hospital/Wuhan Sixth Hospital，Wuhan 430015，China
3. Dept. of Orthopaedics，Liuzhou Hospital of Traditional Chinese Medicine，Guangxi Liuzhou 545000，China
4. Dept. of Pain，Wuhan Central Hospital，Wuhan 430014，China
- Publication Type:Journal Article
- Keywords:
jaceosidin;
AMPK/NLRP3 signaling pathway;
osteoarthritis;
inflammation;
extracellular matrix
- From:
China Pharmacy
2025;36(4):421-426
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the effects of jaceosidin on osteoarthritis （OA） of rats by regulating adenosine monophosphate-activated protein kinase （AMPK）/NOD-like receptor protein 3 （NLRP3） pathway. METHODS Rats were randomly separated into OA group， jaceosidin group （33.33 mg/kg）， AMPK inhibitor （Compound C， 20 mg/kg） group， jaceosidin （33.33 mg/kg）+Compound C （20 mg/kg） group， and sham operation group， with 12 rats in each group. Except for the sham operation group， the OA model was induced with modified Hulth method in all other groups. After successful modeling， they were given a relevant dose of jaceosidin or normal saline intragastrically， and Compound C or normal saline intraperitoneally， once a day， for consecutive 8 weeks. Twenty-four h after the last medication， the degree of knee joint swelling in rats from each group was measured. The pathological changes of the articular cartilage tissue in the knee joints， and the Mankin score were assessed. The levels of tumor necrosis factor-α （TNF-α）， interleukin-18 （IL-18）， and IL-6， as well as the protein expressions of collagen Ⅱ， aggrecan （ACAN）， and a disintegrin and metalloproteinase with thrombospondin 5 （ADAMTS5）， phosphorylated AMPK （p-AMPK）， AMPK， NLRP3， cleaved-caspase-1， and cleaved-IL-1β were detected in the articular cartilage tissue of rats’ knees. RESULTS Compared with OA group， the cartilage tissue defect of jaceosidin group was relieved， the cartilage matrix staining was deepened， and the number of chondrocytes was increased. Knee swelling， Mankin score， the levels of TNF- α， IL-18 and IL-6， and protein expressions of ADAMTS5， NLRP3， cleaved-caspase-1 and cleaved-IL-1β in knee cartilage were significantly decreased or down-regulated. Protein expressions of collagen Ⅱ， ACAN and phosphorylation level of AMPK were significantly increased or up-regulated （P＜0.05）. Compound C significantly reversed the improvement effects of jaceosidin on the above indexes of OA rats （P＜0.05）. CONCLUSIONS Jaceosidin may inhibit inflammation and extracellular matrix degradation in OA rats by regulating the AMPK/NLRP3 signaling pathway.
