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조미라,박정우,정인상,이규양,유성은,정훈종,윤여표,권석형,신화섭 대한약학회 2005 Archives of Pharmacal Research Vol.28 No.1
We evaluated the antiplatelet effects of two classes of ATP-sensitive potassium hannel openers (KATP openers) on washed human platelets, and the study's emphasis was on the role of mitochondrial KATP in platelet aggregation. Collagen-induced platelet aggregation was inhibited in a dose dependent manner by lemakalim and SKP-450, which are potent cardio-nonselective KATP openers, and also by cardioselective BMS-180448 and BMS-191095 (IC50: 1,130, >1,500, 305.3 and 63.9 µM, respectively), but a significantly greater potency was noted for the cardioselective KATP openers. The latter two KATP openers also inhibited platelet aggregation induced by thrombin, another important blood-borne platelet activator, with similar rank order of potency (IC50: 498.0 and 104.8 µM for BMS-180448 and BMS-191095, respectively). The inhibitory effects of BMS-191095 on collagen-induced platelet aggregation were significantly blocked by a 30-min pretreatment of platelets with lyburide (1 µM) or sodium 5-hydroxydecanoate (5-HD, 100 µM), a nonselective and selective mitochondrial KATP antagonist, respectively, at similar magnitudes; this indicates the role of mitochondrial KATP in the antiplatelet activity of BMS-191095. However, glyburide and 5-HD had no effect when they were added to the platelet cuvette immediately prior to the addition of BMS-191095. These findings indicate that cardioselective mitochondrial KATP openers like BMS-191095 are able to exert cardioprotective effects in cardiac schemia/reperfusion injury via dual mechanisms directed at the inhibition of platelet aggregation and the protection of cardiomyocytes, and both these mechanisms are mediated by mitochondrial KATP.
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박은석,강도현,강준철,장용창,이민주,정훈종,이규양,김대은,김보경,신화섭 대한약학회 2017 Archives of Pharmacal Research Vol.40 No.5
Oxidative stress plays a critical role in cardiacinjury during ischemia/reperfusion (I/R). Despite a potentcardioprotective activity of KR-33889, a novel poly (ADPribose)polymerase inhibitor, its underlying mechanismremains unresolved. This study was designed to investigatethe protective effects of KR-33889 against oxidative stressinducedapoptosis in rat cardiomyocytes H9c2 cells andisolated rat hearts. H2O2 caused severe injury to H9c2 cells,mainly due to apoptosis, as revealed by TUNEL assay. However, KR-33889 pretreatment significantly attenuatedH2O2-induced apoptosis of H9c2 cells, which wasaccompanied by decrease in expression of both cleavedcaspase-3 and Bax and increase in Bcl-2 expression and theratio of Bcl-2/Bax. KR-33889 also significantly enhancedthe expression of anti-oxidant enzymes including hemeoxygenase-1, Cu/Zn-superoxide dismutase (SOD), Mn-SOD, and catalase, thereby inhibiting production of intracellularROS. Furthermore, KR-33889 reversed H2O2-induceddecrease in phosphorylation of Akt, GSK-3b, ERK1/2, p38 MAPK, and SAPK/JNK during most H2O2 exposuretime. In globally ischemic rat hearts, KR-33889 inhibitedboth I/R-induced decrease in cardiac contractility andapoptosis by increasing Bcl-2, decreasing both cleavedcaspase-3 and Bax expression, and enhancing expression ofanti-oxidant enzymes. Taken together, these results suggestthat KR-33889 may have therapeutic potential to preventI/R-induced heart injury in ischemic heart diseases mainlyby reducing oxidative stress-mediated myocardialapoptosis.
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