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2017 ; 6
(8
): 1130-1136
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Anti-inflammatory and anti-osteoarthritis effects of tectorigenin
#MMPMID28642243
Wang CL
; Li D
; Wang CD
; Xiao F
; Zhu JF
; Shen C
; Zuo B
; Cui YM
; Wang H
; Gao Y
; Hu GL
; Zhang XL
; Chen XD
Biol Open
2017[Aug]; 6
(8
): 1130-1136
PMID28642243
show ga
Osteoarthritis (OA) is a common and dynamic disease of the joints, including the
articular cartilage, underlying bones and synovium. In particular, OA is
considered as the degeneration of the cartilage. Tectorigenin (Tec) is known to
affect many biological processes; however, its effects on articular chondrocytes
remain unclear. This study aimed to assess the effects of Tec on articular
cartilage. In vitro, Tec inhibited the expression levels of type X collagen,
cyclooxigenase-2, matrix metalloproteinase (MMP)-3 and MMP-13, but enhanced the
expression of Runx1, type II collagen and aggrecan in the presence of IL-1?.
Meanwhile, Tec inhibited apoptosis through the Bax/Bcl-2/caspase-3 pathway,
upregulating p-Bad, downregulating the Bax/Bcl-2 ratio, and activating caspase-3
compared with IL-1? treatment only. Moreover, this process was partially
regulated by NF-?B P65. In vivo, the chondroprotective effects of Tec were
assessed by establishing a model of surgically induced OA. Tec-treated joints
exhibited fewer osteoarthritic changes than saline-treated joints. Meanwhile,
1.5??g/kg Tec treatment produced a greater protective effect than 0.75??g/kg Tec.
The Osteoarthritis Research Society International (OARSI) scoring system,
employed to assess histopathological grading of the models, as well
immunohistochemistry for Aggrecan Neoepitope and MMP-3, further confirmed the
results. In conclusion, this study showed that Tec plays a chondroprotective role
in the OA process by preventing articular cartilage degeneration and chondrocyte
apoptosis via the NF-?B P65 pathway.