Mechanism of the Protective Effect of Yulangsan Flavonoid on Myocardial Ischemia/Reperfusion Injury in Rats

Abstract

Aims: Effect and mechanism of Yulangsan flavonoid (YLSF) on rat myocardial ischemia/reperfusion injury (MI/RI) has been investigated. Methods: Sprague-Dawley (SD) rats were randomly divided into seven groups (sham group, model group and NS group: 2 mL of normal saline/kg body weight was administered; diltiazem group: 5 mg of diltiazem hydrochloride/kg body weight was administered; YLSFL, YLSFM and YLSFH groups: 20, 40 and 80 mg of YLSF/kg body weight was administered) and the MI/RI model was established. Myocardial infarct area, levels of myocardial enzymes and nitric oxide synthase (NOS) were measured. Caspase-3 and adenine nucleotide translocator-1 (ANT1) mRNA expression were evaluated by reverse transcription polymerase chain reaction (RT-PCR). Pathological structure and cardiocyte ultrastructure were also analysed. Results: Compared with the MI/RI group, pretreatment with YLSF or diltiazem hydrochloride decreased the infarct area, levels of inducible nitric oxide synthase (iNOS), caspase-3 as well as the leakage of myocardial enzyme and increased activities of total nitric oxide synthase (tNOS) as well as constitutive nitric oxide synthase (cNOS). Cellular edema and the infiltration of inflammatory cells were alleviated. Conclusions: The experiment showed that YLSF protected the heart against MI/RI, possibly by reducing lipid peroxidation damage, regulating NOS activity and modulating the apoptosis genes expression.

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“…The I/R model was established according to previously reported studies [20][21][22][23]. Briefly, animals were anesthetized i.p.…”

“…After storage for 10 min at -20°C, the heart was cut into 5 or 6 transverse slices (1 mm thickness) across the long axis. Then, the slices were stained with 1% triphenyltetrazolium chloride (TTC, Amresco, USA) in citrate buffer solution (ph=7.4) for 10 min at 37°C, to delineate the area at risk (AAR) [20][21][22][23]. Afterwards, all slices were fixed with 4% paraformaldehyde, photographed and analyzed.…”

RNAi-Mediated Down-Regulation of CD47 Protects against Ischemia/Reperfusion-Induced Myocardial Damage via Activation of eNOS in a Rat Model

“…At physiological concentrations, NO promotes angiogenesis, inhibits leukocyte and platelet adherence, and induces vasodilatation [5,6]. Inhibition of NO production exacerbates myocardial damage in I/R model, whereas overexpression of NO has a cardio-protective role in I/R events [7][8][9]. Endothelial nitric oxide synthase (eNOS), a major source of NO, has also been show+n to ameliorate MIRI in vivo.…”

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“…The prevention and management of I/R injury are key steps in coronary heart disease treatment and are becoming important issues in ischemic heart disease [6,7]. Following pregassing with 95% N 2 and 5% CO 2 for a minimum of 5 min, the ischemic buffer (1 mM NaH 2 PO 4 , 24 mM NaHCO 3 , 2.5 mM CaCl 2 , 118 mM NaCl, 16 mM KCl, 0.5 mM sodium EDTA, 20 mM sodium lactate, pH 6.8, 37°C) was added to the cells, which were then placed in a sealed chamber containing the deoxygenation reagent, leading to the consumption of O 2 and the production of CO 2 .…”