Warm-needling moxibusion inhibits NLRP3 inflammasome activation and improves cartilage injury in a rabbit model of knee osteoarthritis

doi:10.12307/2023.429

Abstract

Abstract: BACKGROUND: Warm-needling moxibusion has a significant clinical effect on knee osteoarthritis, but its therapeutic mechanism remains unclear.
OBJECTIVE: To observe the effect of warm-needling moxibusion on the expression of NLRP3, matrix metalloproteinases 3, 13, and type I collagen in cartilage tissue of rabbit knee osteoarthritis.
METHODS: Forty 6-month-old male New Zealand rabbits were randomly divided into blank group, model group, warm-needling moxibusion group, and NLRP3 inhibitor group, with 10 rabbits in each group. Except for the blank group, osteoarthritic models of the right hind limb were established in the other three groups using plaster cast fixation. After modeling, intervention with warm-needling moxibusion in the warm-needling moxibusion group was performed once a day and lasted for 4 weeks; in the NLRP3 inhibitor group, MCC950, an NLRP3 inhibitor, was injected into the knee joint cavity, once a week, for four times in total. Lequesne MG score was used for behavioral evaluation, hematoxylin-eosin staining was used to observe the morphological structure of cartilage tissue, and the expression of NLRP3, matrix metalloproteinases 3, 13, and type I collagen in chondrocytes was detected by immunohistochemistry and western blot.
RESULTS AND CONCLUSION: Lequesne MG score: Compared with the blank group, Lequesne MG score increased in the other three groups after modeling (P < 0.05). After treatment, the Lequesne MG scores were significantly decreased in the warm-needling moxibusion group and NLRP3 inhibitor group compared with the model group (P < 0.05). Hematoxylin-eosin staining: compared with the blank group, the number of chondrocytes was decreased, the structural integrity was destroyed, and the Mankin’s score was significantly increased in the model group (P < 0.05). Compared with the model group, the distribution of chondrocytes was more uniform, the structure of cartilage layer was relatively clear, and the Mankin’s score was decreased in the warm-needling moxibusion group and NLRP3 inhibitor group (P < 0.05). Immunohistochemistry and western blot detection: compared with the blank group, the expression of NLRP3, matrix metalloproteinases 3 and 13 was significantly increased (all P < 0.05), and the expression of type I collagen was significantly down-regulated in the model group (P < 0.05). Compared with the model group, the expression of NLRP3, matrix metalloproteinases 3 and 13 were significantly decreased in the warm-needling moxibusion group and NLRP3inhibitor group (all P < 0.05), and the expression of type I collagen was significantly up-regulated (P < 0.05). To conclude, warm-needling moxibusion can inhibit the activation of NLRP3 inflammatory promoter, down-regulate the release of inflammatory factors, matrix metalloproteinases 3 and 13, reduce the inflammatory amplification reaction, and delay the degradation of type I collagen, thereby reducing cartilage injury and local damage of articular cartilage due to knee osteoarthritis.

Key words: warm-needling moxibusion, knee osteoarthritis, NLRP3 inflammasome, cartilage injury, matrix metalloproteinase

CLC Number:

Wu Yongli, Li Long, Liu Junwei, Liu Di, Wang Duo. Warm-needling moxibusion inhibits NLRP3 inflammasome activation and improves cartilage injury in a rabbit model of knee osteoarthritis[J]. Chinese Journal of Tissue Engineering Research, 2023, 27(20): 3202-3208.

Figures/Tables 9

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