The Effect of 17-Methoxyl-7-Hydroxy-Benzene-Furanchalcone on NF-κB and the Inflammatory Response During Myocardial Ischemia Reperfusion Injury in Rats

Abstract

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.

The Combination of Three Components Derived from Sheng MaiSan Protects Myocardial Ischemic Diseases and Inhibits Oxidative Stress via Modulating MAPKs and JAK2-STAT3 Signaling Pathways Based on Bioinformatics Approach

“…Many pharmacological investigations exhibited that the transcription factor NF-κB exerts an essential part in cell proliferation and serves as an important modulator of the inflammatory process. The activity suppression of NF-κB could protect myocardial ischemia reperfusion induced heart injury ( Liang et al, 2014 ). STAT3 has been indicated to be essential for cardioprotective effects such as preservation of LV functional reserve and perfused capillary density, decrease of apoptotic cell death and reduction of infarct size ( Smith et al, 2004 ).…”

Silencing of long non‑coding RNA HRIM protects against myocardial ischemia/reperfusion injury via inhibition of NF‑κB signaling

“…p65 is a major subunit of nF-κB (28). upregulation of nF-κB p65 can enhance activation of the nF-κB signaling pathway (29), and inhibition of nF-kB p65 activity has been shown to protect against Mi/ri in rats (30). Moreover, downregulation of nF-κB attenuated Mi/ri in rats (31).…”

Cardioprotective Effects of Combined Therapy with Hyperbaric Oxygen and Diltiazem Pretreatment on Myocardial Ischemia-Reperfusion Injury in Rats

“…General surgical procedure Ischemia-reperfusion injury was inflicted by occlusion of the left anterior descending coronary artery and then reperfused as previously described [25]. Briefly, the rats were anesthetized using sodium pentobarbital (30 mg/kg, i.p.)…”