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Journal of Cardiovascular Pharmacology 2014-Jan

The effect of 17-methoxyl-7-hydroxy-benzene-furanchalcone on NF-κB and the inflammatory response during myocardial ischemia reperfusion injury in rats.

Straipsnius versti gali tik registruoti vartotojai
Prisijungti Registracija
Nuoroda įrašoma į mainų sritį
Xingmei Liang
Jianchun Huang
Xing Lin
Feizhang Qin
Qingwei Wen
Chunxia Chen
Yingxin Li
Wenyi Ge
Renbin Huang

Raktažodžiai

Santrauka

The aim of this study was to investigate the effect of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC) on nuclear factor-kappa-binding (NF-κB) and the inflammatory response in rats with myocardial ischemia reperfusion injury (MI/RI). Sprague-Dawley rats were randomly divided into 7 groups, and the rat MI/RI model was established by the ligation of the left anterior descending for 30 minutes followed by ligation release for 1 hour. Areas of myocardial infarction were measured using Evans blue-2,3,5-Triphenyltetrazolium chloride (TTC) staining. Levels of malondialdehyde, glutathione peroxidase, and total superoxide dismutase were assessed. Release of interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10) was measured by means of an enzyme-linked immunosorbent assay. NF-κBp65 and intercellular adhesion molecule-1 protein expression and caspase-3 and adenine nucleotide translocator-1 messenger RNA expression were evaluated by immunohistochemistry and reverse transcription polymerase chain reaction, respectively. Pretreatment with MHBFC decreased the infarction areas, the malondialdehyde, IL-1β and IL-6 levels, the expression of caspase-3, NF-κBp65, and intercellular adhesion molecule-1. Further, MHBFC increased total superoxide dismutase and glutathione peroxidase activities, the release of IL-10, and the expression of adenine nucleotide translocator-1 messenger RNA compared with the results of the model group. The experiment showed that MHBFC protected the heart against MI/RI possibly by reducing lipid peroxidation damage while inhibiting the activity of NF-κBp65 and the inflammatory response.

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