基于p38/p53通路探讨温针对膝骨性关节炎模型兔软骨细胞凋亡的影响OA

Objective:To observe the effect of warm needling on the expression of p38,p53,and Caspase-3 in the knee joint chondrocyte of rabbits model with knee osteoarthritis(KOA),and to explore the possible mechanism of warm needling in treating KOA.Methods:Eighteen New Zealand rabbits were randomly divided into a control group,a model group,and a warm needling group,with six rabbits in each group.The KOA model was replicated in the model group and the warm nee-dling group by injecting 0.3 ml of 4%papain into the knee joint cavity.After successful modeling,rabbits in the warm nee-dling group received acupuncture using a disposable sterile acupuncture needle(0.25 mm×25 mm)inserted perpendicularly at the outer knee eye of the left hind limb.After penetrating the skin,the needle was directed toward the inner knee eye.Needle insertion was stopped when the needle tip reached the subcutaneous layer,and even mild reinforcing-reducing ma-nipulation by twisting was applied until desired sensation(needle tightening sensation)was achieved.A thin moxa stick(ap-proximately 1 cm in length,5 mm in diameter)was then attached to the needle handle and ignited.The needle was retained for 20 minutes,once daily,five times per week,for four consecutive weeks.The control group and model group received the same grasping and immobilization as the warm needling group but without any other intervention.After four weeks,behav-ioral assessment was performed using the Lequesne MG index of severity for KOA.Hematoxylin-eosin(HE)staining was used to observe the morphology of knee joint cartilage.Real-time quantitative PCR and Western blot were used to detect the expression of p38,p53,and Caspase-3 protein and mRNA in the knee joint cartilage of rabbits in each group.Results:HE staining showed:in the control group,the knee joint cartilage structure was normal,with a smooth surface,no defects or fis-sures,uniform staining,and regularly arranged chondrocytes.In the model group,the knee joint cartilage surface was rough with defects and fissures,uneven matrix staining,and disordered chondrocyte arrangement.In the warm needling group,the cartilage tissue margin was slightly uneven,with mild defects and fissures,slightly disordered chondrocyte arrangement,and the degree of structural damage was less severe than that in the model group.Compared with the control group,the Lequesne MG score and the expression of p38,p53,and Caspase-3 protein and mRNA in cartilage tissue were significantly increased in the model group,and the differences were statistically significant(P<0.01).Compared with the model group,the Lequesne MG score and the expression of p38,p53,and Caspase-3 protein and mRNA in cartilage tissue were significantly decreased in the warm needling group,and the differences were statistically significant(P<0.01).Conclusion:Warm needling may re-duce chondrocyte apoptosis and alleviate KOA by inhibiting the p38/p53 pathway and decreasing Caspase-3 expression.