Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart.

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ÜSTÜNOVA S., TAKIR S., YILMAZER N., Bulut H., ALTINDİREK D., HATIRNAZ NG Ö., ...Daha Fazla

In vivo (Athens, Greece), cilt.34, sa.5, ss.2507-2516, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 34 Sayı: 5
  • Basım Tarihi: 2020
  • Doi Numarası: 10.21873/invivo.12067
  • Dergi Adı: In vivo (Athens, Greece)
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE
  • Sayfa Sayıları: ss.2507-2516
  • Anahtar Kelimeler: Hydrogen sulfide, nitric oxide, isolated heart, ischemia/reperfusion injury, oxidative damage, ISCHEMIA-REPERFUSION INJURY, H2S PROTECTS, SYNTHASE, EXPRESSION, INHIBITION, FAILURE, HYPERTENSION, MICE
  • Acıbadem Mehmet Ali Aydınlar Üniversitesi Adresli: Evet

Özet

Background/Aim: This study was designed to provide further evidence for the interactions between hydrogen sulfide (H2S) and nitric oxide (NO) in ischemia/reperfiision (I/R) injury. Materials and Methods: Rat hearts were studied with the Langendorff technique using the H2S donor sodium hydrosulfide (NaHS, 40 mu M) and the cystathionine gamma-lyase (CTH or CSE) inhibitor DL-propargylglycine (PAG, 1 mM). NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME, 30 mg/kg, 7 days) was administered before the isolation. The hearts were homogenized for biochemical and molecular analysis. Results: NaHS reversed I/R-induced cardiac performance impairment, increased tissue nitric oxide production and decreased tissue markers for cardiac injury, while L-NAME inhibited these effects. The expression of CTH was increased with PAG, which was suppressed by L-NAME. Conclusion: H2S and NO increase each other's production suggesting their interaction and cooperation in cardioprotection against I/R injury.