Objective To observe the effect of moxibustion intervention on the expression of toll-like receptor-4(TLR 4)

myeloid differentiation factor 88(MyD 88)

and nuclear factor kappa B p 65(NF-κB p 65)genes of knee-joint synovial cells in rheumatoid arthritis(RA)rats

so as to explore its molecular mechanism underlying improving RA.Methods Forty SD rats were randomly divided into normal control

RA model

moxibustion and medication groups(n=10).The RA model was duplicated by raising the rats in a windy

cold and wet environment

followed by injecting Freund's complete adjuvant(0.15mL)into the rat's foot.Moxibustion was applied to"Shenshu"(BL 23)and"Zusanli"(ST 36)for 20 min

once daily for 15 days.Rats of the medication group were treated by intragastric administration of tripterygium wilfordii(8.75mL/kg)

once daily for 15 days.Pathological changes of the synovial tissues were detected by H.E.stain

the contents of serum TNF-αand IL-1detected by radioimmunoassay

and the expression levels of TLR 4mRNA

MyD 88 mRNA and TRAF-6mRNA of synovial tissue were analyzed by real time-PCR

and the NF-κB p 65 immunoactivity was assayed by immunohistochemistry.Results In comparison with the normal control group

the synovial tissue of the knee-joint was impaired remarkably and infiltrated by numerous inflammatory cells

and the synovial surface got thickening because of hyperplasia in the model group.Following moxibustion and medication

these situations such as synovial infiltration of inflammatory

synovial cell proliferation were alleviated.The serum TNF-αand IL-1contents and synovial TLR 4mRNA

MyD 88 mRNA

TRAF-6mRNA and NF-κB p 65 expression levels were remarkably higher in the model group than in the control group(P<0.01).After moxibustion and medication

the contents of serum TNF-αand IL-1

the expression levels of TLR 4mRNA

MyD 88 mRNA

TRAF-6mRNA and NF-κB p 65 were significantly down-regulated(P<0.01

P<0.05).Conclusion Moxibustion intervention can improve pathological changes of the knee-joint synovial membrane tissue in RA rats

which may be related with its effect in inhibiting abnormal activation of TLR 4-MyD 88-NF-κB pathway in synovial tissue.