PH_I_P: Pharmaceutical Sciences I. Posters
Virág Vass1,2, Erzsébet Szabó1, Ilona Bereczki3, Nóra Debreczeni3,4, Anikó Borbás3, Pál Herczegh3, Árpád Tósaki1
1 Department of Pharmacology, Faculty of Pharmacy, University of Debrecen, H-4032 Debrecen, Nagyerdei krt. 98., Hungary
2 Doctoral School of Pharmaceutical Sciences, University of Debrecen, H-4032 Debrecen, Nagyerdei krt. 98., Hungary
3 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, University of Debrecen, H-4032 Debrecen, Egyetem tér 1, Hungary.
4 Doctoral School of Chemistry, University of Debrecen, H-4032 Debrecen, Egyetem tér 1, Hungary.
Introduction: Hydrogen sulfide (H2S) has been generated by tissues in a small quantity for physiological regulatory processes. Earlier studies proved that H2S and ibuprofen have a beneficial effect against tissue damage, and H2S reduces side effects of non-steroid anti-inflammatory (NSAI) drugs.
Aims: In our study ischemia/reperfusion was generated in isolated rat hearts where we investigated the H2S delivery capacity and cardioprotective effects of a new H2S donor molecule (BM-88).
Methods: Hearts were excised, and perfused in Langendorff mode. BM-88 was administered for 10 min before or after 30 min ischemia, reperfusion was performed for 120 min. The dose effect of BM-88 was determined by gradually increasing the concentration. The released H2S was measured from coronary effluent using electrochemical sensor. The protective effect of BM-88 can be confirmed by the infarct sizes of hearts. Autophagic and apoptotic markers (LC3-I/II, p62, Beclin1) were detected by immunohistochemistry method.
Result: We find that added H2S can be taken up and utilized by heart until 10µmol/ml concentration. BM-88 supports a long lasting H2S delivery in the heart tissues. It is likely that a treatment-induced decrease in infarct area was observed in BM-88 exposed hearts.
Conclusion: Confirming the protective effect of our new molecule may open a possibility for the development of cardioprotective agents with less side effects.
Funding: The work is funded by GINOP-2.3.2-15-2016-00043, NKFIH-K-124719 and supported by the EFOP-3.6.1-16-2016-00022 project. The project is co-financed by the European Union and the European Social Fund.
Debrecen University Faculty of Medicine, Doctoral School of Pharmaceutical Sciences