Abstract

To investigate the effect and mechanism of Tripterygium wilfordii polyglycosides on rheumatoid arthritis rats by regulating the signal transducer and activator of transcription 3 pathways. 45 specific-pathogen free male Sprague-Dawley rats were randomly divided into normal control group, model group and Tripterygium wilfordii polyglycosides group with 15 rats in each group. The histopathological changes of the synovium of the ankle joint of rats in each group, on the 12th, 20th and 28th d were compared. On the 12th d, the degree of tissue swelling in the model group was significantly higher than that in the normal control group (p<0.05); there was no significant difference in the degree of toe swelling between the Tripterygium wilfordii polyglycosides group and the model group (p>0.05). At 20 d and 28 d, the degree of toe swelling in the model group was significantly higher than that in the normal control group (p<0.05); the swelling degree of toes in Tripterygium wilfordii polyglycosides group was significantly lower than that in model group (p<0.05). The serum interleukin-6 level in model group was significantly higher than that in normal control group and interleukin-10 level was significantly lower than that in normal control group (p<0.05). The level of interleukin-6 in serum of rats in Tripterygium wilfordii polyglycosides group was significantly lower than that in model group and the level of interleukin-10 was significantly higher than that in model group (p<0.05). The expression levels of phosphorylated Janus kinase 2 and phosphorylated signal transducer and activator of transcription 3 protein in model group were significantly higher than those in normal control group; the expression levels of phosphorylated Janus kinase 2 and phosphorylated signal transducer and activator of transcription 3 protein in Tripterygium wilfordii polyglycosides group were significantly lower than those in the model group (p<0.05). Tripterygium wilfordii polyglycosides has the effect of anti-rheumatoid arthritis and its mechanism may be through regulating the Janus kinase 2/ signal transducer and activator of transcription 3 signal pathways by reducing the expression level of phosphorylated Janus kinase 2 and phosphorylated signal transducer and activator of transcription 3 proteins.

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