Protection against acute radiation-induced lung injury: A novel role for the anti-angiogenic agent Endostar

  • Authors:
    • Kai Zhang
    • Shenghui Yang
    • Ying Zhu
    • Anwei Mo
    • Dan Zhang
    • Li Liu
  • View Affiliations

  • Published online on: May 4, 2012     https://doi.org/10.3892/mmr.2012.903
  • Pages: 309-315
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Radiotherapy is commonly used to treat thoracic malignancies, but often causes severe lung injury. Currently there are no effective protective strategies against radiation‑induced lung injury (RILI). This study aimed to evaluate the ability of an angiogenesis antagonist, Endostar, against RILI, and the underlying mechanism in a mouse model. A total of 108 C57BL/6 female mice were randomized into 4 groups (n=27): i) control group; ii) Endostar group, animals were administered 7.75 ml/kg Endostar through intraperitoneal injection; iii) irradiation group, RILI was induced by exposing the animals to a single external irradiation on the thoraces (6 MV X-ray, 12 Gy); and iv) irradiation plus Endostar group, animals were subjected to Endostar treatment and irradiation as in groups 2 and 3. A total of 3 animals from each of the 4 groups were sacrificed at 1, 6, 12, 24 and 72 h and at 2, 4, 8 and 24 weeks following treatment. Clinical signs and pathology of RILI were examined. The expression of transforming growth factor-β 1 (TGF-β1) in lungs was analyzed by real-time quantitative polymerase chain reaction (RT-QPCR) and immunohistochemistry. Compared with the control group, irradiation induced evident interstitial edema and a significant increase in inflammatory cells in the lungs (P<0.05). Correlated with these changes, a notable increase in TGF-β1 mRNA level and a robust increase in TGF-β1 immunoreactivity were observed in lung tissues in a time-dependent manner following irradiation (P<0.05). Endostar administration effectively attenuated the magnitude of the increase in inflammatory cells as well as the elevation of TGF-β1 expression in lung tissues after RILI (P<0.05). In conclusion, radiation induced an increased expression of the inflammatory mediator TGF-β1 and the associated pathogenesis in the lung, while Endostar was able to at least partially attenuate RILI through downregulating the expression of TGF-β1 in mice. Our findings suggest that Endostar may be a novel protective agent against RILI.
View Figures
View References

Related Articles

Journal Cover

August 2012
Volume 6 Issue 2

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
Zhang K, Yang S, Zhu Y, Mo A, Zhang D and Liu L: Protection against acute radiation-induced lung injury: A novel role for the anti-angiogenic agent Endostar. Mol Med Rep 6: 309-315, 2012.
APA
Zhang, K., Yang, S., Zhu, Y., Mo, A., Zhang, D., & Liu, L. (2012). Protection against acute radiation-induced lung injury: A novel role for the anti-angiogenic agent Endostar. Molecular Medicine Reports, 6, 309-315. https://doi.org/10.3892/mmr.2012.903
MLA
Zhang, K., Yang, S., Zhu, Y., Mo, A., Zhang, D., Liu, L."Protection against acute radiation-induced lung injury: A novel role for the anti-angiogenic agent Endostar". Molecular Medicine Reports 6.2 (2012): 309-315.
Chicago
Zhang, K., Yang, S., Zhu, Y., Mo, A., Zhang, D., Liu, L."Protection against acute radiation-induced lung injury: A novel role for the anti-angiogenic agent Endostar". Molecular Medicine Reports 6, no. 2 (2012): 309-315. https://doi.org/10.3892/mmr.2012.903