Open Access

Hydroxytyrosol protects against myocardial ischemia reperfusion injury by inhibiting mitochondrial permeability transition pore opening

  • Authors:
    • Jiaxin Miao
    • Zijun Huang
    • Shuang Liu
    • Xuying Li
    • Pengyu Jia
    • Yuxuan Guo
    • Nan Wu
    • Dalin Jia
  • View Affiliations

  • Published online on: November 27, 2018     https://doi.org/10.3892/etm.2018.7016
  • Pages: 671-678
  • Copyright: © Miao 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

Hydroxytyrosol (HT), a phenolic compound extracted from olive oil, is reported to protect against myocardial ischemia reperfusion injury (MIRI), but its mechanism has not been fully elucidated. The mitochondria permeability transition pore (MPTP) is an important therapeutic target for MIRI. The present study aimed to investigate the role of MPTP in the cardioprotection of HT. Isolated rat hearts were mounted on a Langendorff apparatus and subjected to 30 min of ischemia followed by 120 min of reperfusion to mimic a MIRI model. Isolated hearts were pretreated with different doses of HT (10, 100 and 1,000 µM) for 10 min prior to ischemia. Myocardial infarct size was detected using TTC staining. Changes in myocardial cell structure were observed using hematoxylin and eosin staining. MPTP opening was detected spectrophotometrically. Myocardial cell apoptosis was observed with terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assays. The expression of apoptosis‑associated proteins was measured by western blot analysis. The data revealed that HT (100 and 1,000 µM) treatment significantly alleviated pathological damage in ischemic myocardium and reduced myocardial infarct size compared with the untreated control. However, no significant difference was observed in the 10 µM HT treatment group compared with the untreated control. It was further revealed that HT decreased the B cell lymphoma‑2 (Bcl‑2)‑like protein 4 (Bax)/Bcl‑2 ratio, suppressed MPTP opening and subsequently decreased the expression of cytochrome c, cleaved caspase‑9 and ‑3, thereby inhibiting apoptosis. Additionally, the beneficial effects of HT on MIRI were reversed by atractyloside, which induces MPTP opening. In conclusion, the present study demonstrated that HT inhibited MPTP opening, partially via modulation of Bax and Bcl‑2, thereby protecting against MIRI and thereby providing a pharmacological basis for future research and treatment of MIRI.
View Figures
View References

Related Articles

Journal Cover

January-2019
Volume 17 Issue 1

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
Miao J, Huang Z, Liu S, Li X, Jia P, Guo Y, Wu N and Jia D: Hydroxytyrosol protects against myocardial ischemia reperfusion injury by inhibiting mitochondrial permeability transition pore opening. Exp Ther Med 17: 671-678, 2019
APA
Miao, J., Huang, Z., Liu, S., Li, X., Jia, P., Guo, Y. ... Jia, D. (2019). Hydroxytyrosol protects against myocardial ischemia reperfusion injury by inhibiting mitochondrial permeability transition pore opening. Experimental and Therapeutic Medicine, 17, 671-678. https://doi.org/10.3892/etm.2018.7016
MLA
Miao, J., Huang, Z., Liu, S., Li, X., Jia, P., Guo, Y., Wu, N., Jia, D."Hydroxytyrosol protects against myocardial ischemia reperfusion injury by inhibiting mitochondrial permeability transition pore opening". Experimental and Therapeutic Medicine 17.1 (2019): 671-678.
Chicago
Miao, J., Huang, Z., Liu, S., Li, X., Jia, P., Guo, Y., Wu, N., Jia, D."Hydroxytyrosol protects against myocardial ischemia reperfusion injury by inhibiting mitochondrial permeability transition pore opening". Experimental and Therapeutic Medicine 17, no. 1 (2019): 671-678. https://doi.org/10.3892/etm.2018.7016