Effects of Wenyangbushen formula on the expression of VEGF, OPG, RANK and RANKL in rabbits with steroid-induced femoral head avascular necrosis

  • Authors:
    • Hong‑Mei Song
    • Ying‑Chen Wei
    • Nan Li
    • Bin Wu
    • Na Xie
    • Kun‑Mu Zhang
    • Shi‑Zhong Wang
    • He‑Ming Wang
  • View Affiliations

  • Published online on: October 23, 2015     https://doi.org/10.3892/mmr.2015.4478
  • Pages: 8155-8161
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The present study aimed to investigate the effects of Wenyangbushen formula on the mRNA and protein expression levels of vascular endothelial growth factor (VEGF), osteoprotegerin (OPG), receptor activator of nuclear factor (NF)‑κβ ligand (RANK), and RANK ligand (RANKL) in a rabbit model of steroid‑induced avascular necrosis of the femoral head (SANFH). The present study also aimed to examine the potential mechanism underlying the effect of this formula on the treatment of SANFH. A total of 136 New Zealand rabbits were randomly divided into five groups: Normal group, model group, and three groups treated with the traditional Chinese medicine (TCM), Wenyangbushen decoction, at a low, moderate and high dose, respectively. The normal group and positive control group were intragastrically administered with saline. The TCM groups were treated with Wenyangbushen decoction at the indicated dosage. Following treatment for 8 weeks, the mRNA and protein expression levels of VEGF, OPG, RANK and RANKL in the femoral head tissues were determined using reverse transcription‑quantitative polymerase chain reaction and western blot analyses, respectively. The data revealed that Wenyangbushen decoction effectively promoted the growth of bone cells, osteoblasts and chondrocytes, and prevented cell apoptosis in the SANFH. The mRNA and protein expression levels of OPG and VEGF were increased, while the levels of RANK and RANKL were reduced in the necrotic tissue of the model group, compared with those in the normal rabbits. Wenyangbushen treatment prevented these changes, manifested by an upregulation in the expression levels of VEGF and OPG, and downregulation in the expression levels of RANK and RANKL in a dose‑dependent manner. It was concluded that treatment with Wenyangbushen formula alleviated necrosis of the femoral head induced by steroids. It was observed to promote bone cell, osteoblast and chondrocyte growth, as well as prevent cell apoptosis. In addition, it upregulated the expression levels of OPG and VEGF, and inhibited the expression levels of RANK and RANKL. These results suggest the potential use of Wenyangbushen formula as a possible approach for the effective treatment of SANFH.
View Figures
View References

Related Articles

Journal Cover

December-2015
Volume 12 Issue 6

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Song HM, Wei YC, Li N, Wu B, Xie N, Zhang KM, Wang SZ and Wang HM: Effects of Wenyangbushen formula on the expression of VEGF, OPG, RANK and RANKL in rabbits with steroid-induced femoral head avascular necrosis. Mol Med Rep 12: 8155-8161, 2015
APA
Song, H., Wei, Y., Li, N., Wu, B., Xie, N., Zhang, K. ... Wang, H. (2015). Effects of Wenyangbushen formula on the expression of VEGF, OPG, RANK and RANKL in rabbits with steroid-induced femoral head avascular necrosis. Molecular Medicine Reports, 12, 8155-8161. https://doi.org/10.3892/mmr.2015.4478
MLA
Song, H., Wei, Y., Li, N., Wu, B., Xie, N., Zhang, K., Wang, S., Wang, H."Effects of Wenyangbushen formula on the expression of VEGF, OPG, RANK and RANKL in rabbits with steroid-induced femoral head avascular necrosis". Molecular Medicine Reports 12.6 (2015): 8155-8161.
Chicago
Song, H., Wei, Y., Li, N., Wu, B., Xie, N., Zhang, K., Wang, S., Wang, H."Effects of Wenyangbushen formula on the expression of VEGF, OPG, RANK and RANKL in rabbits with steroid-induced femoral head avascular necrosis". Molecular Medicine Reports 12, no. 6 (2015): 8155-8161. https://doi.org/10.3892/mmr.2015.4478