Puerarin attenuates inflammation and oxidation in mice with collagen antibody-induced arthritis via TLR4/NF-κB signaling.
Puerarin is an important active ingredient in the root of kudzu vine due to its pharmacological properties. The aim of the present study is to contribute to the existing knowledge of the effect of puerarin in the attenuation of inflammation and oxidation in mice with collagen antibody-induced arthritis via toll‑like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling. Arthritis was induced using injection of anti‑type II collagen antibodies. Treatment with puerarin was observed to significantly decrease clinical scoring of the collagen antibody‑induced arthritis and suppress oxidative stress and the inflammatory response in mice. Furthermore, puerarin was demonstrated to inhibit mRNA expression of matrix metalloproteinase‑9 and protein expression of TLR4 following collagen antibody-induced arthritis in mice. The effect of puerarin may be associated with the suppression of NF‑κB activity in collagen antibody‑induced arthritis mice. Furthermore, upregulation of phosphorylated (p)‑Janus kinase 2 and p‑signal transducer and activator of transcription 3 protein expression was suppressed by puerarin. The results of the present study indicate, for the first time, the effect of puerarin to attenuate inflammation and oxidation in mice with collagen antibody‑induced arthritis via TLR4/NF-κB signaling.
Department of Orthopedics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China.
Changxing
C
Wang
Department of Orthopedics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China.
Weidong
W
Wang
Department of Orthopedics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China.
Xiaping
X
Jin
Department of Orthopedics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China.
Jianguo
J
Shen
Department of Orthopedics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China.
Weifeng
W
Hu
Department of Orthopedics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China.
Tao
T
Jiang
D000818:Animals; D001169:Arthritis, Experimental / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D001323:Autoantibodies / Q000276:immunology; D003094:Collagen / Q000009:adverse effects / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D015870:Gene Expression; D018836:Inflammation Mediators / Q000378:metabolism; D007529:Isoflavones / Q000737:chemistry / Q000494:pharmacology*; D053614:Janus Kinase 2 / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects; D010766:Phosphorylation; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism*
D001323:Autoantibodies; D016207:Cytokines; D018836:Inflammation Mediators; D007529:Isoflavones; D016328:NF-kappa B; D050796:STAT3 Transcription Factor; D051197:Toll-Like Receptor 4; D008315:Malondialdehyde; D003094:Collagen; D013482:Superoxide Dismutase; D053614:Janus Kinase 2; D020780:Matrix Metalloproteinase 9; C033607:puerarin