Tea catechins attenuate chronic ventricular remodeling after myocardial ischemia in rats

Suzuki, Jun–ichi; Ogawa, Masahito; Maejima, Yasuhiro; Isobe, Kazuya; Tanaka, Hiroyuki; Sagesaka, Yuko M.; Isobe, Mitsuaki

doi:10.1016/j.yjmcc.2006.10.006

Cited by 34 publications

(25 citation statements)

References 41 publications

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“…The chest wall and the skin were then closed with a 3-0 silk suture. [12][13][14][15][16][17][18] This investigation conforms with the Guide for the Care and Use of Laboratory Animals of Tokyo Medical and Dental University. Animals used in this study were maintained in accordance with the Guide for the Care and Use of Laboratory Animals published by the US National Institute of Health (NIH Publication No.…”

Section: Methodsmentioning

confidence: 81%

“…M-mode views were used to measure the LV dimensions according to the American Society for Echocardiography leading edge method. [12][13][14][15][16][17][18] LV end-diastolic dimension (LVDd) and end-systolic dimension (LVDs), and fractional shortening (%FS= [(LVDd−LVDs) / LVDd]×100) were calculated from the M-mode recordings. Measurement of area at risk and infarct size: On day 1 after reperfusion, the anesthetized rats were intubated and thoracotomy was repeated.…”

Section: -18)mentioning

confidence: 99%

“…The hearts were then sliced transversely into 4 slices, and incubated in 2.0% triphenyl tetrazolium chloride (TTC) (Sigma, Tokyo) for 15 minutes at 37°C to verify the viable and necrotic area in the ischemic myocardium (area at risk, AAR) as described earlier. [12][13][14][15][16][17][18] Each slice was weighed and photographed, and the areas of infarction, AAR, and left ventricle were evaluated using computerassisted planimetry (Scion Image β4.0.2) by observers blinded to the treatment protocol. The volumes of each area were determined by the following process: volume of AREA = (A1 × Wt1) + (A2 × Wt2) + (A3 × Wt3) + (A4 × Wt4) where A is the percentage of each area by planimetry from subscripted numbers 1-4 indicating sections and Wt is the weight of the same numbered sections.…”

Section: -18)mentioning

confidence: 99%

“…The area ratio (affected/LV as a percentage) was calculated as described previously. [12][13][14][15][16][17][18] Values for 3 ventricular regions were averaged for each heart, and the mean percentage of affected area for each group was calculated. All data were analyzed in a blind fashion by two independent investigators and averaged.…”

Section: -18)mentioning

confidence: 99%

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Effects of Pharmacological Suppression of Plasminogen Activator Inhibitor-1 in Myocardial Remodeling After Ischemia Reperfusion Injury

et al. 2011

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SummaryPlasminogen activator inhibitor-1 (PAI-1) contributes to cardiac ventricular remodeling because migration of inflammatory cells and attenuation of extracellular matrix degradation are caused by plasmin and matrix metalloproteinase. However, the roles of PAI-1 in myocardial ischemia reperfusion (I/R) injury and the following inflammatory response have not yet been well elucidated. To clarify the role of PAI-1 in myocardial I/R injury, we used a specific PAI-1 inhibitor (IMD-1622) in a rat model. The left anterior descending coronary artery was ligated and reperfusion was performed by loosening the suture after 30 minutes of arterial occlusion. A single administration of IMD-1622 (20 mg/kg) or vehicle was given intraperitoneally and then the rats were sacrificed on day 1 or day 14 after I/R. Blood pressure, echocardiograms, histopathology, and molecular examination were performed. The examinations revealed that PAI-1 inhibitor showed limited effects on cardiac dysfunction and ventricular remodeling after I/R. We conclude that the pharmacological inhibition of PAI-1 may not affect ventricular remodeling after myocardial I/R injury. (Int Heart J 2011; 52: 388-392)

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Section: Methodsmentioning

confidence: 81%

Section: -18)mentioning

confidence: 99%

Section: -18)mentioning

confidence: 99%

Section: -18)mentioning

confidence: 99%

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Effects of Pharmacological Suppression of Plasminogen Activator Inhibitor-1 in Myocardial Remodeling After Ischemia Reperfusion Injury

et al. 2011

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“…In our study, the antioxidant effect of LUT has not been revealed directly, but the increase of eNOS in brain and other tissues and decrease of iNOS, shows that LUT has an indirect antioxidant effect. There are also many studies reporting that iNOS can create an oxidative stress (32,33).…”

Section: Discussionmentioning

confidence: 99%

EffectsofLuteolinonLiver,KidneyandBraininPentylentetrazol-Induced Seizures: Involvement of Metalloproteinases and NOS Activities

Birman¹,

Dar²,

Kapucu³

et al. 2012

Balkan Med J

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Objective: Flavonoids are an important group of recognized antioxidants in plants. Luteolin (LUT) is a natural flavonoid in the plant kingdom. This study was aimed to investigate the effects of the LUT in the liver, kidney and brain of pentylentetrazol (PTZ)-induced seizure and the relationship between nitric oxide synthases (iNOS, eNOS) and matrix metalloproteinases (MMP2, MMP9).Materials and Methods: LUT (10 mg/kg) was given intraperitoneally during two weeks prior to seizure induction. A single dose PTZ 80 mg/kg i.p. was administered and seizures were observed and evaluated with regard to latency, frequency and stage for one hour.Results: Seizure frequen cy after PTZ administration was significantly decreased in LUT pretreated rats (p<0.05). An increase of immunhistochemical reactions of iNOS and MMP2, but a decrease of eNOS activity, were observed in rat hippocampus and peripheral tissues during the PTZ induced seizures. LUT pretreatment reversed the iNOS and MMP2 activity to the control levels and significantly increased the eNOS activity (p<0.001).Conclusion: LUT seems to have an effective role in reducing the seizure frequency and a protective role on peripheral organ injury in animal models of seizure. The protective effect of LUT in seizures and the seizure induced peripheral tissue damage warrant further investigations.

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Green tea polyphenols improve cardiac muscle mRNA and protein levels of signal pathways related to insulin and lipid metabolism and inflammation in insulin‐resistant rats

Qin

Polansky

Dawson

et al. 2010

Molecular Nutrition Food Res

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Epidemiological studies indicate that the consumption of green tea polyphenols (GTP) may reduce the risk of coronary artery disease. To explore the underlying mechanisms of action at the molecular level, we examined the effects of GTP on the cardiac mRNA and protein levels of genes involved in insulin and lipid metabolism and inflammation. In rats fed a high-fructose diet, supplementation with GTP (200 mg/kg BW daily dissolved in distilled water) for 6 wk, reduced systemic blood glucose, plasma insulin, retinol-binding protein 4, soluble CD36, cholesterol, triglycerides, free fatty acids and LDL-C levels, as well as the pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and IL-6. GTP did not affect food intake, bodyweight and heart weight. In the myocardium, GTP also increased the insulin receptor (Ir), insulin receptor substrate 1 and 2 (Irs1 and Irs2), phosphoinositide-3-kinase (Pi3k), v-akt murine thymoma viral oncogene homolog 1 (Akt1), glucose transporter 1 and 4 (Glut1 and Glut4) and glycogen synthase 1 (Gys1) expression but inhibited phosphatase and tensin homolog deleted on chromosome ten (Pten) expression and decreased glycogen synthase kinase 3beta (Gsk3beta) mRNA expression. The sterol regulatory element-binding protein-1c (Srebp1c) mRNA, microsomal triglyceride transfer protein (Mttp) mRNA and protein, Cd36 mRNA and cluster of differentiation 36 protein levels were decreased and peroxisome proliferator-activated receptor (Ppar)gamma mRNA levels were increased. GTP also decreased the inflammatory factors: Tnf, Il1b and Il6 mRNA levels, and enhanced the anti-inflammatory protein, zinc-finger protein, protein and mRNA expression. In summary, consumption of GTP ameliorated the detrimental effects of high-fructose diet on insulin signaling, lipid metabolism and inflammation in the cardiac muscle of rats.

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Tea catechins attenuate chronic ventricular remodeling after myocardial ischemia in rats

Cited by 34 publications

References 41 publications

Effects of Pharmacological Suppression of Plasminogen Activator Inhibitor-1 in Myocardial Remodeling After Ischemia Reperfusion Injury

Effects of Pharmacological Suppression of Plasminogen Activator Inhibitor-1 in Myocardial Remodeling After Ischemia Reperfusion Injury

EffectsofLuteolinonLiver,KidneyandBraininPentylentetrazol-Induced Seizures: Involvement of Metalloproteinases and NOS Activities

Green tea polyphenols improve cardiac muscle mRNA and protein levels of signal pathways related to insulin and lipid metabolism and inflammation in insulin‐resistant rats

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