Daidzein administration in vivo reduces myocardial injury in a rat ischemia/reperfusion model by inhibiting NF-kB activation

Kim, Jong Woo; Jin, Yong; Kim, Young Min; Rhie, Sangho; Kim, Hye Jung; Seo, Han Geuk; Lee, Jae Heun; Ha, Yeong Lae; Chang, Ki Churl

doi:10.1016/j.lfs.2008.12.005

Cited by 99 publications

(58 citation statements)

References 26 publications

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“…However, NF-B is modulated by I-B kinase and subsequent degradation of I-B ␣ in turn [22,23] . A number of isoflavones have also been shown to block the NF-B activation [24][25][26] . Thus, the ability of puerarin to inhibit the phosphorylation and degradation of I-B ␣ will cause the accumulation of both I-B ␣ and p65 NF-B in the cytosol, thereby reducing the amount of p65 NF-B Fluorescence-labeled monocytic THP-1 cells were added to the HUVEC monolayers and allowed to adhere for 30 min.…”

Section: Discussionmentioning

confidence: 99%

Puerarin Inhibits Adhesion Molecule Expression in TNF-α-Stimulated Human Endothelial Cells via Modulation of the Nuclear Factor ĸB Pathway

Zhang

Yang

et al. 2009

Pharmacology

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Background: The isoflavone puerarin is the most abundant isoflavone-C-glucoside extracted from the root (radix puerariae) of the plant Pueraria lobata and possesses many biological activities. In this report, the ability of puerarin to modulate intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and endothelial leukocyte adhesion molecule 1 (E-selectin), and to induce changes in the nuclear factor ĸB (NF-ĸB) pathway in human umbilical vein endothelial cells (HUVECs) was examined. Methods: The protein and mRNA levels of tumor-necrosis-factor-α (TNF-α)-induced ICAM-1, VCAM-1 and E-selectin were determined in HUVECs. Inhibitor ĸB (I-ĸB) phosphorylation and p65 NF-ĸB expression in HUVECs were also examined. Results: Puerarin inhibited the expression of TNF-α-induced ICAM-1, VCAM-1 and E-selectin proteins and mRNAs in HUVECs. Subsequently, we determined that the inhibition of ICAM-1, VCAM-1 and E-selectin expression was due to a dose-dependent suppression of phosphorylation and degradation of I-ĸB, which resulted in a reduction of p65 NF-ĸB nuclear translocation. Conclusion: These data suggested that the effect of puerarin-mediated inhibition of TNF-α-induced ICAM-1, VCAM-1 and E-selectin expression is attributed to suppressed NF-ĸB activation on the transcriptional level.

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Section: Discussionmentioning

confidence: 99%

Puerarin Inhibits Adhesion Molecule Expression in TNF-α-Stimulated Human Endothelial Cells via Modulation of the Nuclear Factor ĸB Pathway

Zhang

Yang

et al. 2009

Pharmacology

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“…Furthermore, NF-kappaB is known to protect against apoptosis via transcription of specific inhibitory proteins [57,58]. Other studies report that NF-kappaB is an integral part of apoptosis and tissue injury, notably under conditions of I/R in rats [59]. Reduced hepatocellular apoptosis and necrosis after H/R by GTE were accompanied by reduced JNK phosphorylation and NF-kappaB activation (Figs.…”

Section: Discussionmentioning

confidence: 82%

Plant polyphenols attenuate hepatic injury after hemorrhage/resuscitation by inhibition of apoptosis, oxidative stress, and inflammation via NF-kappaB in rats

et al. 2011

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“…In most situations, NFκB is activated by I/R, and the inhibition of NFκB activation results in a cardioprotective effect in cardiac I/R models [26]. However, NFκB activation is an obligatory step in ischemic late preconditioning, and preconditioning-induced cardioprotection is abolished when NFκB activation is inhibited [17].…”

Section: Discussionmentioning

confidence: 99%

MiR-31 Downregulation Protects Against Cardiac Ischemia/Reperfusion Injury by Targeting Protein Kinase C Epsilon (PKCe) Directly

Wang

Men

Yang

et al. 2015

Cell Physiol Biochem

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Background: Various miRNAs have been shown to participate in cardiac ischemia/reperfusion injury (I/R). miR-31 was identified as the most strikingly upregulated miRNA after acute myocardial infarction; therefore, the underlying role and mechanism of miR-31 in cardiac I/R was investigated. Methods: miR-31 expression was detected after cardiac I/R in mice. The cardioprotective effect of miR-31 downregulation was assessed in vitro and in vivo. The functional target gene and its downstream molecule were determined. Results: miR-31 expression increased after I/R. miR-31 downregulation increased cell viability and SOD activity and decreased LDH activity and MDA content in vitro. Additionally, miR-31 downregulation alleviated myocardial infarct size in vivo. PKCe was identified as the functional target gene of miR-31, and NFκB was identified as its downstream molecule that was involved in the miR-31-mediated cardioprotective effect. Conclusion: miR-31 expression increased throughout the cardiac I/R process, and miR-31 downregulation induced a cardioprotective effect via a miR-31/PKCe/NFκB-dependent pathway.

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Daidzein administration in vivo reduces myocardial injury in a rat ischemia/reperfusion model by inhibiting NF-kB activation

Cited by 99 publications

References 26 publications

Puerarin Inhibits Adhesion Molecule Expression in TNF-α-Stimulated Human Endothelial Cells via Modulation of the Nuclear Factor ĸB Pathway

Puerarin Inhibits Adhesion Molecule Expression in TNF-α-Stimulated Human Endothelial Cells via Modulation of the Nuclear Factor ĸB Pathway

Plant polyphenols attenuate hepatic injury after hemorrhage/resuscitation by inhibition of apoptosis, oxidative stress, and inflammation via NF-kappaB in rats

MiR-31 Downregulation Protects Against Cardiac Ischemia/Reperfusion Injury by Targeting Protein Kinase C Epsilon (PKCe) Directly

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