Protective effect of cardioplegia with poly (ADP-ribose) polymerase-1 inhibitor against myocardial ischemia-reperfusion injury: in vitro study of isolated rat heart model. (February 2013)

• Record Type: Journal Article
• Authors: Yamazaki, Kazuhiro; Tanaka, Seigo; Sakata, Ryuzo; Miwa, Senri; Oriyanhan, Wnimonk; Takaba, Kiyoaki; Minakata, Kenji; Marui, Akira; Ikeda, Tadashi; Toyokuni, Shinya; Komeda, Masashi; Ueda, Kunihiro
• Is Part Of: Journal of enzyme inhibition and medicinal chemistry. Volume 28:Number 1(2013:Feb.)
• Page Start: 143
• Page End: 147
• Publication Date: 2013-02
• Subjects: Enzyme inhibitors -- Periodicals; Enzyme Inhibitors -- periodicals; Biochemistry -- periodicals; 572.7
• DOI: 10.3109/14756366.2011.642373
• Languages: English
• ISSNs: 1475-6366

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p>Poly(ADP-ribose) polymerase (PARP)-1 inhibitor has been suggested to attenuate the ischemia-reperfusion injury. We investigated the protective effect of the cardioplegia with a PARP-1 inhibitor, 4-hydoxyquinazoline (4-HQ), against myocardial ischemia-reperfusion injury. Isolated rat hearts were perfused on a Langendorff apparatus and cardioplegically arrested for 90 min by perfusion with St. Thomas' Hospital solution (ST-solution). In the Group ST (<italic>n</italic> = 8), the hearts were arrested with the ST-solution alone. The Group HQ (<italic>n</italic> = 8) were treated with the ST-solution containing 4-HQ (10 µM) for cardioplegia. During reperfusion, the Group HQ showed significantly greater functional recovery of +dp/dt_max (<italic>p</italic> = 0.005) and lower enzymatic leakage (<italic>p</italic> &lt; 0.01). NAD⁺ levels were also preserved higher in the Group HQ (<italic>p</italic> &lt; 0.01). Immunohistochemical study revealed lesser extents of oxidative stress and apoptosis, in the Group HQ. Thus, addition of 4-HQ in the cardioplegia may provide a new intervention for myocardial protection against ischemia-reperfusion injury by decreasing NAD⁺ consumption and suppressing oxidative stress.</p> </abstract>