क्लिनिकल एवं प्रायोगिक कार्डियोलॉजी

क्लिनिकल एवं प्रायोगिक कार्डियोलॉजी
खुला एक्सेस

आईएसएसएन: 2155-9880

अमूर्त

KB-R7943 Reduces Necrosis and Apoptosis in Hyperlipidemic Animals through the Activation of K+ATP Channels

Yongkui Ren, Yunfei Cai and Dalin Jia

Reverse-mode activation of the Na+-Ca2+ exchanger (NCX) at the time of reperfusion following ischemia contributes to Ca2+ overload and cardiomyocyte injury, KB-R7943, as a selective reverse-mode NCX inhibitor, reduces lethal reperfusion injury under normal conditions, but its effectiveness under certain pathological states is in dispute. In the present study, we sought to determine the effect of KB-R7943 in hyperlipidemic animals and assess if the K+ ATP are involved in the protective mechanisms. Anesthetized rats were randomized into five groups, as follows, and were subjected to 25min global ischemia (GI) followed by 120 min reperfusion (R). Normally fed animals: a Control group (NC) with no additional intervention. Cholesterol fed (6weeks) animals: a Chol group (HC) with no additional interventions, a KB-R7943 group (HKB) treated with KB-R7943, a KB-R7943 and glybenclamide group (HGKB) treated with KB-R7943 and glybenclamide (K+ ATP, blocker, 0.3μM), a glybenclamide group (HGLY) treated with glybenclamide
The infarct size was measured by triphenyltetrazolium. The infarct size was 35±5.0% in NC, 46±8.7% in HC and 47±8.5% in HGLY (NC vs. HC, P<0.05; HC vs. HGLY, P>0.05). KB-R7943 reduced the infarct size (28.6±3.3% in HKB vs. HC, P<0.05), In addition, KB-R7943 attenuated apoptotic cell (HKB vs. HC, p<0.05), glybenclamide abolished the effect reached by KB-R7943. Thus, diet-induced hypercholesterolemia enhances myocardial injury; KB-R7943 reduces infarct size and apoptosis in hyperlipidemic animals through the activation of K+ ATP channels.

अस्वीकरण: इस सार का अनुवाद कृत्रिम बुद्धिमत्ता उपकरणों का उपयोग करके किया गया था और अभी तक इसकी समीक्षा या सत्यापन नहीं किया गया है।
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