Open Access

Ulinastatin attenuates diabetes‑induced cardiac dysfunction by the inhibition of inflammation and apoptosis

  • Authors:
    • Wen‑Ke Wang
    • Qing‑Hua Lu
    • Xin Wang
    • Ben Wang
    • Juan Wang
    • Hui‑Ping Gong
    • Lin Wang
    • Hao Li
    • Yi‑Meng Du
  • View Affiliations

  • Published online on: July 19, 2017     https://doi.org/10.3892/etm.2017.4824
  • Pages: 2497-2504
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ulinastatin exhibits anti-inflammatory activity and protects the heart from ischemia/reperfusion injury. However, whether ulinastatin has a protective effect in diabetic cardiomyopathy is yet to be elucidated. The aim of the present study was to investigate the protective effects of ulinastatin against diabetic cardiomyopathy and its underlying mechanisms. A C57/BL6J mice model of diabetic cardiomyopathy was used and mice were randomly assigned to three groups: Control group, diabetes mellitus (DM) group and DM + ulinastatin treatment group. Cardiac function was assessed using echocardiography and the level of inflammatory cytokine high mobility group box 1 (HMGB1) expression was measured using histopathological examination and reverse transcription‑quantitative polymerase chain reaction. The levels of tumor necrosis factor (TNF)‑α and interleukin (IL)‑6 were measured using western blotting and ELISA. The apoptosis rate in the myocardium was assessed by TUNEL assay. Caspase‑3 activation, expression of B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2 associated x (Bax) were measured using western blotting, as was the activity of the mitogen activated protein kinase (MAPK) signaling pathway. The results indicated that ulinastatin significantly improved cardiac function in mice with DM. Ulinastatin treatment significantly downregulated HMGB1, TNF‑α and IL‑6 expression (P<0.05) and significantly reduced the percentage of apoptotic cardiomyocytes (P<0.05) via reduction of caspase‑3 activation and the ratio of Bax/Bcl‑2 in diabetic hearts (P<0.05). In addition, ulinastatin attenuated the activation of the MAPK signaling pathway. In conclusion, ulinastatin had a protective effect against DM‑induced cardiac dysfunction in a mouse model. This protective effect may be associated with the anti‑inflammatory and anti‑apoptotic abilities of ulinastatin via the MAPK signaling pathway.

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September-2017
Volume 14 Issue 3

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

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Copy and paste a formatted citation
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Spandidos Publications style
Wang WK, Lu QH, Wang X, Wang B, Wang J, Gong HP, Wang L, Li H and Du YM: Ulinastatin attenuates diabetes‑induced cardiac dysfunction by the inhibition of inflammation and apoptosis. Exp Ther Med 14: 2497-2504, 2017.
APA
Wang, W., Lu, Q., Wang, X., Wang, B., Wang, J., Gong, H. ... Du, Y. (2017). Ulinastatin attenuates diabetes‑induced cardiac dysfunction by the inhibition of inflammation and apoptosis. Experimental and Therapeutic Medicine, 14, 2497-2504. https://doi.org/10.3892/etm.2017.4824
MLA
Wang, W., Lu, Q., Wang, X., Wang, B., Wang, J., Gong, H., Wang, L., Li, H., Du, Y."Ulinastatin attenuates diabetes‑induced cardiac dysfunction by the inhibition of inflammation and apoptosis". Experimental and Therapeutic Medicine 14.3 (2017): 2497-2504.
Chicago
Wang, W., Lu, Q., Wang, X., Wang, B., Wang, J., Gong, H., Wang, L., Li, H., Du, Y."Ulinastatin attenuates diabetes‑induced cardiac dysfunction by the inhibition of inflammation and apoptosis". Experimental and Therapeutic Medicine 14, no. 3 (2017): 2497-2504. https://doi.org/10.3892/etm.2017.4824