Tianjin Medical Journal

Tianjin Medical Journal ›› 2019, Vol. 47 ›› Issue (12): 1210-1214.doi: 10.11958/20191918

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Effects of cucurbitacin on IL-1β-induced cell injury and metabolism dysfunction in chondrocytes

WANG Xi-bin1, ZUO Rui-ting2   

  1. 1 Department of Spine, 2 Department of Rheumatology, Henan Province Hospital of TCM, Zhengzhou 450002, China
  • Received:2019-06-25 Revised:2019-08-19 Published:2019-12-15 Online:2019-12-15
  • Supported by:
     

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Abstract:

Objective To explore the function of cucurbitacin B (CuB) in cell injury and metabolism dysfunction in
chondrocytes upon interleukin (IL)-1β conditions. Methods Mouse chondrocytes were pre-treated with various doses of
CuB (0.5,1,5,10 and 20 µmol/L), prior to expose to IL-1β (10 µg/L). Cell viability was then determined by CCK-8 assay.
The commercial kits were used to detect lactate dehydrogenase (LDH) and Caspase-3 activity. The cell apoptosis was
evaluated by flow cytometer. The mRNA levels of metabolism dysfunction-related Collagen Ⅱ , aggrecan, matrix
metalloproteinase (MMP)-3 and MMP-13 were analyzed by qRT-PCR. ELISA assay was performed to measure the contents
of MMP-3, MMP-13 and PGE-2. The levels of nitrous oxide (NO) were determined by a commercial kit. Western blot assay
was conducted to investigate the effects of CuB on the activation of NF -
κB signaling in IL-
1β - treated chondrocytes
.
Results CuB dose-dependently ameliorated the suppressive roles of IL-
1β on chondrocyte viability
(P＜0.05).
Simultaneously, CuB suppressed IL-1β-induced LDH release, cell apoptosis and Caspase-3 activity (
P＜0.05). In contrast
to IL-1β - treated groups, administration with CuB antagonized the inhibitory effects of IL-
1β on the mRNA levels of
Collagen Ⅱ and aggrecan
(
P＜0.05). Furthermore, CuB treatment attenuated IL-1β- induced transcripts and releases of
MMP-
3 and MMP-
13 (
P＜
0.05), concomitant with reductions in the production of inflammatory mediator NO and PGE
2
(
P＜0.05
). Additionally
, IL-1β incubation enhanced the expression of p-I
κB and p-p
65 NF - κB (
P＜0.05), which were
reversed following CuB treatment (
P＜0.05). Conclusion CuB may suppress IL-
1β-induced cell injury and metabolism
dysfunction in chondrocytes by blocking the NF-
κB signaling
, implying a potential function in osteoarthritis therapy
.

Key words: chondrocytes, osteoarthritis, interleukin-1beta, NF-kappa B, inflammatory mediator, cucurbitacin B

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