Open Access

Warm sparse‑dense wave inhibits cartilage degradation in papain‑induced osteoarthritis through the mitogen‑activated protein kinase signaling pathway

  • Authors:
    • Munan Lin
    • Yanhong Lin
    • Xihai Li
    • Wenna Liang
    • Shuiliang Wang
    • Jiansheng Liu
    • Xianxiang Liu
    • Lidian Chen
    • Yin Qin
  • View Affiliations

  • Published online on: August 22, 2017     https://doi.org/10.3892/etm.2017.4984
  • Pages: 3674-3680
  • Copyright: © Lin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Cartilage degradation is an important in the patho­genesis of osteoarthritis (OA). Abnormal activation of the mitogen‑activated protein kinase (MAPK) signaling pathway in chondrocytes promotes an inflammatory response, resulting in the release of chondral matrix‑degrading enzymes that accelerate the degradation of cartilage. As a non‑pharmaceutical and non‑invasive physical therapy regimen, warm sparse‑dense wave (WSDW) has been successfully used for the treatment of OA. However, it remains unclear whether WSDW inhibits cartilage degradation in OA through the MAPK signaling pathway. The present study investigated the effects of WSDW on papain‑induced OA in rat knee joints. Papain‑induced OA was established in rats, which were subsequently divided into a model group and three experimental groups that received a WSDW with the following ratios: WSDW=1:1, WSDW=1:2 and WSDW=2:1. After 12 weeks of treatment, cartilage degradation was evaluated by Mankin scoring of paraffin‑embedded sections stained with hematoxylin and eosin. The changes in cartilage structure were observed by transmission electron microscopy, and the expressions of RAS, extracellular signal‑regulated kinase (ERK), p38 and p53 were measured by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. WSDW was demonstrated to improve the arrangement of collagen fibers, inhibit the tidemark replication and delay cartilage degradation in papain‑induced OA. The expressions of RAS, ERK, p38 and p53 in the WSDW (1:2) and (2:1) groups were significantly decreased when compared with the model group (P<0.01). Furthermore, amongst the WSDW groups, the inhibitory effects of the WSDW (1:2) group were typically greater than those of the WSDW (1:1) and (2:1) groups. The results indicate that WSDW may inhibit cartilage degradation in papain‑induced OA in rat knee joints by regulating the MAPK signaling pathway.

Related Articles

Journal Cover

October-2017
Volume 14 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Lin M, Lin Y, Li X, Liang W, Wang S, Liu J, Liu X, Chen L and Qin Y: Warm sparse‑dense wave inhibits cartilage degradation in papain‑induced osteoarthritis through the mitogen‑activated protein kinase signaling pathway. Exp Ther Med 14: 3674-3680, 2017
APA
Lin, M., Lin, Y., Li, X., Liang, W., Wang, S., Liu, J. ... Qin, Y. (2017). Warm sparse‑dense wave inhibits cartilage degradation in papain‑induced osteoarthritis through the mitogen‑activated protein kinase signaling pathway. Experimental and Therapeutic Medicine, 14, 3674-3680. https://doi.org/10.3892/etm.2017.4984
MLA
Lin, M., Lin, Y., Li, X., Liang, W., Wang, S., Liu, J., Liu, X., Chen, L., Qin, Y."Warm sparse‑dense wave inhibits cartilage degradation in papain‑induced osteoarthritis through the mitogen‑activated protein kinase signaling pathway". Experimental and Therapeutic Medicine 14.4 (2017): 3674-3680.
Chicago
Lin, M., Lin, Y., Li, X., Liang, W., Wang, S., Liu, J., Liu, X., Chen, L., Qin, Y."Warm sparse‑dense wave inhibits cartilage degradation in papain‑induced osteoarthritis through the mitogen‑activated protein kinase signaling pathway". Experimental and Therapeutic Medicine 14, no. 4 (2017): 3674-3680. https://doi.org/10.3892/etm.2017.4984