Objective:

2

To illustrate the molecular mechanisms underlying the therapeutic effects of electroacupuncture (EA) on knee osteoarthritis (OA).

Methods:

2

Twenty-seven six-month-old New Zealand white rabbits were allocated into three groups in accordance with a random number table: normal group (no surgery-induced OA; without treatment)

model group (surgery-induced OA; without treatment) and EA group [surgery-induced OA; received treatment with EA at acupoints Dubi (ST 35) and Neixiyan (EX-LE 5)

30 min twice a day]. After eight consecutive weeks of treatment

the histopathological alterations in cartilage were observed using optical microscopy and transmission electron microscopy

cartilage degeneration was evaluated by modified Mankin's score principles

the synovial fluid concentration of interleukin-1β (IL-1β)

interleukin-6 (IL-6)

tumor necrosis factor-α (TNF-α) and matrix metalloproteinase-3 (MMP-3) were evaluated by enzyme-linked immunosorbent assay

and the protein expression levels of IL-1β

IL-6

TNF-α

MMP-3

IκB kinase-β (IKK-β)

nuclear factor of α light polypeptide gene enhancer in B-cells inhibitor α (IκB-α) and nuclear factor-κB (NF-κB) p65 were quantified by Western blot analysis.

Results:

2

EA treatment significantly improved cartilage structure arrangement and reduced cellular degeneration. The IL-1β

IL-6

TNF-α and MMP-3 of synovial fluid in the EA-treated group were significantly decreased compared with the model group (all

P

<

0.01). Compared with the model group

the IL-1β

IL-6

TNF-α

MMP-3

IKK-β and NF-κB p65 protein expressions in cartilage of EA-treated group were significantly decreased (all

P

<

0.01)

whereas IκB-α expression was significantly up-regulated (

P

<

0.01).

Conclusion:

2

EA treatment may delay cartilage degeneration by down-regulating inflammatory factors through NF-κB signaling pathway

which may

in part

explain its clinical efficacy in the treatment of knee OA.