Effect of polydatin on cartilage degeneration in knee osteoarthritis rats by regulating Janus kinase 3/signal transducer and activator of transcription 3 signaling pathway
Objective To investigate the effect of polydatin on cartilage degeneration in knee oste-oarthritis rats by regulating Janus kinase 3(JAK3)/signal transducer and activators of transcription 3(STAT3)signaling pathway.Methods Fifty rats were randomly separated into a Sham surgery group,a model group,a low-dose polydatin group,a high-dose polydatin group,and a high-dose polydatin+Colive-lin group by random number table method.There were 10 rats in each group.The improved Mankin score was applied to evaluate the degree of cartilage degeneration.Enzyme-linked immunosorbent assay(ELISA)was applied to detect the levels of interleukin(IL)-1β,IL-6,tumor necrosis factor-α(TNF-α),C-termi-nal telopeptide of type Ⅰ collagen(CTX-Ⅰ),and CTX of type Ⅱ collagen(CTX-Ⅱ)in joint tissue and serum.The hematoxylin-eosin(HE)staining and safranine O-solid green staining were applied to observe the morphological changes of articular cartilage tissue.TdT-mediated dUTP nick-end labeling(TUNEL)was applied to observe the apoptosis of chondrocytes.Western blotting was applied to detect matrix metallo-proteinase(MMP)-3,MMP-13,JAK3,and STAT3 proteins in articular cartilage tissue.The data were compared with single factor analysis of variance.Results Compared with the Sham surgery group,the cartilage of the model group was severely degenerated,and the facial mask like structure on the cartilage surface was obviously damaged.Compared with the model group,the degeneration of cartilage and the de-struction of facial mask like structure on the surface of cartilage in the low and high dose polydatin groups were obviously reduced.Mankin score,serum IL-1β,IL-6,TNF-α,CTX-Ⅰ,CTX-Ⅱ levels,apoptosis rate,MMP-3,MMP-13,phosphorylated JAK3(p-JAK3)/JAK3,phosphorylated STAT3(p-STAT3)/STAT3 protein expression in cartilage tissue of rats in high-dose polydatin group were lower than those in model group[(5.30±1.13)point vs.(12.90±2.36)point,(11.49±1.57)pg/ml vs.(28.61± 3.85)pg/ml,(3.18±0.52)pg/ml vs.(7.59±1.16)pg/ml,(6.23±1.14)pg/ml vs.(16.83± 1.94)pg/ml,(15.78±1.71)pg/ml vs.(28.53±3.65)pg/ml,(10.86±1.39)pg/ml vs.(19.61± 2.37)pg/ml,(6.76±0.78)％vs.(21.83±1.84)％,(0.41±0.03)vs.(0.74±0.06),(0.81± 0.07)vs.(1.24±0.11),(0.46±0.04)vs.(0.87±0.08),(0.57±0.05)vs.(1.05±0.09),t=9.185,13.021,10.970,14.897,10.003,10.071,23.846,15.556,14.749,14.496,14.743,P＜0.05].The activator Colivelin could partially reverse the protective effect of polydatin on the cartilage of rats with knee osteoarthritis.Conclusion Polydatin can reduce inflammatory reaction by inhibiting JAK3/STAT3 signaling pathway,thereby improving cartilage degeneration in rats with knee osteoarthritis.
PolydatinJanus kinase 3/signal transducer and activator of transcription 3 signaling pathwayKnee osteoarthritisCartilage degeneration
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