• Journal of Embryo Transfer
• /
• v.27 no.2
• /
• pp.71-80
• /
• 2012

Biotechnologies for cloning animals and in vitro embryo production have the potential to produce biomedical models for various researches. Especially, pigs are a suitable model for xenotransplantation, transgenic production and various areas of reproductive research due to its physiological similarities to human. However, utilization of in vitro-produced embryos for transfer remains limited. Despite improvement over past few decades, obstacles associated with the production of good quality embryos in vitro still exist which limit the efficiency of cloning. One of major problems includes improper in vitro maturation (IVM) and culture (IVC). Oxidative stress caused from in vitro culture conditions contributes to inadequate IVM and IVC which leads to poor developmental competence of oocytes, failure of fertilization and embryo development. To reduce the oxidative stress, various antioxidants have been used to IVM and IVC system. However, limited information is available on the effects of resveratrol on livestock reproductions. Resveratrol is a polyphenolic natural product and well known as an antioxidant in foods and beverages (e.g. in grapes and red wine). Resveratrol is known to be cardioprotective, anticarcinogenic, anti-inflammatory, antioxidant and antiapoptotic. This paper will review the effects of resveratrol on in vitro maturation of oocytes and embryo development.

• Biomedical Science Letters
• /
• v.24 no.2
• /
• pp.130-133
• /
• 2018

The aim of this study was to evaluate the protective function of fisetin, a natural flavonoid in zebrafish heart for the treatment of myocardial infarction in coronary and ischemic heart disease. For this purpose, we induced oxidative stress zebrafish (Danio rerio)-Tg (cmlc2: egfp) by $H_2O_2$ and then administered fisetin, the protective effect of fisetin was determined by measuring the heart rate following fisetin administration. After testing the toxicity of fisetin, we found that the heartt increased in a concentration-dependent manner, however there was no difference between the heart rates of embryos and adults. The improved heart rate demonstrated the cardioprotective effect of fisetin. The result showed that fisetin, at concentration of 3and $5{\mu}M$, significantly increased heart rate compared with the heart with $H_2O_2$ alone. This indicates that fisetin plays an important role in the prevention of heart damage and treatment of cardiovascular diseases caused by oxidative stress due to ischemia / reperfusion.

• Biomolecules & Therapeutics
• /
• v.7 no.4
• /
• pp.354-361
• /
• 1999

In this study, the effects of tauroursodeoxycholic acid (TUDCA) on ischemia/ reperfusion injury were investigated on isolated heart perfusion models. Hezrts were perfused with oxygenated Krebs-henseleit solution (pH 7.4, $37^{\cire}C$) on a Langendorff apparatus. After equilibration, isolated hearts were treated with TUDCA 100 and 200 $\mu\textrm{M}$ or vehicle (0.02% DMSO) for 10 min before the onset of ischemia in single treatment group. In 7 day pretreatment group. TUDCA 50, 100 and 200 mg/kg body weight were given orally for 7 days before operation. After global ischemia (30 min), ischemic hearts were reperfused for 30 min. The physiological (i.e. heart rate, left ventricdular developed pressure, coronary flow, double product, time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 810 sec during ischemia, LVDP was 34.0 mmHg at the endpoint of reperfusion and LDH activity in total reperfusion effluent was 34.3 U/L. Single treatment with TUDCA did not change the postischemic recovery of cardiac function, LDH and time to contractur compared with ischemic control group. TUDCA pretreatment showed the tendency to decrease LDH release and to increase time to contracture and coronary flow. Our findings suggest that TUDCA does not ameliorate ischemia/reperfusion-reduced myocardial damage.

• Advances in Traditional Medicine
• /
• v.8 no.3
• /
• pp.311-315
• /
• 2008

The objective of the study was to investigate the antihyperlipidemic activity of alcoholic extract of Pongamia pinnata Linn. (PPAE) leaves in rats fed with high fat diet (HFD). PPAE was administered orally in the divided doses of 250 and 500 mg/kg/day for 30 days in HFD fed rats. Body weights were observed and the analysis of serum lipid profile was carried out on day 30. Marked decrease in the body weight, total cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL) and very low density lipoprotein (VLDL) whereas significant increase in the levels of high density lipoprotein (HDL) were observed after treatment with PPAE. However, PPAE in a dose of 250 mg/kg did not show significant (P < 0.05) increase in HDL levels. The PPAE also lowered TC: HDL-c and LDL: HDL-c ratios significantly suggesting it's antihyperlipidemic and cardioprotective potential. The present work reveals that PPAE at the dose of 500 mg/kg/day exhibited significant (P < 0.01) antihyperlipidemic effects.

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.6
• /
• pp.579-586
• /
• 1999

Complement-mediated neutrophil activation has been hypothesized to be an important mechanism of reperfusion injury. It has been proposed that C1 esterase inhibitor (C1 INH) may prevent the complement- dependent activation of polymorphonuclear leukocytes (PMNs) that occurs within postischemic myocardium. Therefore, The effect of C1 INH was examined in neutrophil dependent isolated perfused rat heart model of ischemia (I) (20 min) and reperfusion (R) (45 min). Administration of C1 INH (5 mg/Kg) to I/R hearts in the presence of PMNs $(100{\times}10^6)$ and homologous plasma improved coronary flow and preserved cardiac contractile function (p＜0.001) in comparison to those I/R hearts receiving only vehicle. In addition, C1 INH significantly (p＜0.001) reduced PMN accumulation in the ischemic myocardium as evidenced by an attenuation in myeloperoxidase activity. These findings demonstrate the C1 INH is a potent and effective cardioprotective agent inhibits leukocyte-endothelial interaction and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion.

• International Journal of Oral Biology
• /
• v.41 no.4
• /
• pp.175-181
• /
• 2016

Tyrosol, a phenylethanoid and a derivative of phenethyl alcohol, possesses various biological properties, such as anti-oxidative and cardioprotective activity. Olive oil is the principal source of tyrosol in the human diet. However, so far the anti-cancer activity of tyrosol has not yet been well defined. This study therefore undertakes to examine the cytotoxic activity and the mechanism of cell death exhibited by tyrosol in KB human oral cancer cells. Treatment of KB cells with tyrosol induced the cell growth inhibition in a concentration- and a time-dependent manner. Furthermore, the treatment of tyrosol induced nuclear condensation and fragmentation of KB cells. Tyrosol also promoted proteolytic cleavage of procaspase-3, -7, -8 and -9, increasing the amounts of cleaved caspase-3, -7, -8 and -9. In addition, tyrosol increased the levels of cleaved PARP in KB cells. These results suggest that tyrosol induces the suppression of cell growth and cell apoptosis in KB human oral cancer cells, and is therefore a potential candidate for anti-cancer drug discovery.

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 1998.11a
• /
• pp.199-199
• /
• 1998

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on retrograded aortic perfusion model. Hearts from Sprague-Dawley rats were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, 37) on a Langendorff apparatus. After equilibration, hearts were treated with ursodeoxycholic acid 10, 20, 40 and 800 M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. Following 25 min of global ischemia, ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular diastolic pressure, coronary flow and time to contracture formation) and biochemical (lactate dehydrogenase, LDH) endpoints were evaluated. In vehicle group, time to contracture formation (TTC) value was 19.5 min during ischemia, LVDP was 20.8 mmHg at the endpoint of reperfusion and LDH activity in reperfusate was 59.7 U/L. Cardioprotective effects of UDCA following ischemia/reperfusion consisted of a reduced TTC (EC$\_$25/ = 16.10 M), reduced LDH release and enhanced recovery of contractile function during reperfusion. Especially, the treatments of UDCA 80 M remarkably increased LVDP (68.1 mmHg) and reduced LDH release (33.2 U/L). Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage, in agreement with physiological and biochemical parameters.

• Journal of Ginseng Research
• /
• v.33 no.4
• /
• pp.268-277
• /
• 2009

Ginsenosides are among the most well-known traditional herbal medicines frequently used for the treatment of cardiovascular symptoms in South Korea. The anti-ischemic effects of compound K (CK), a metabolite of ginsenoside Rb1, on ischemia-induced isolated rat hearts were investigated through the analyses of the changes in the hemodynamics (blood pressure, aortic flow, coronary flow, and cardiac output) and the measurement of the infarct region. The subjects in this study were divided into four groups: the normal control, the CK-alone group, the ischemia-induced group without any treatment, and the ischemia-induced group treated with CK. No significant differences in perfusion pressure, aortic flow, coronary flow, and cardiac output were found between the groups before ischemia was induced. The oxygen and buffer supply was stopped for 30 min to induce ischemia 60 min after reperfusion in the isolated rat hearts, and the CK was administered 5 min before ischemia induction. The CK treatment significantly prevented decreases in perfusion pressure, aortic flow, coronary flow, and cardiac output under ischemic conditions. In addition, the hemodynamics (except for the heart rate) of the group treated with CK significantly recovered 60 min after reperfusion, unlike in the control group. CK significantly limited the infarct. These results suggest that CK treatment has distinct anti-ischemic effects in an exvivo model of an ischemia-reperfusion-induced rat heart.

• Journal of Ginseng Research
• /
• v.42 no.3
• /
• pp.356-360
• /
• 2018

The fermentation of medicinal herbs facilitated by microbes is assumed to exert promising therapeutic efficacy on the absorption, bioavailability, and pharmacological effects by speeding up the making or conversion of active constituents into their metabolites. We examined the cardioprotective potential of fermented ginseng, GBCK25, against high-fat diet (HFD)-induced metabolic and functional illnesses as following the essential analysis such as electrocardiographic parameters, alterations of body and organ weights, and echocardiographic studies. The results exhibited that body weights were significantly reduced and the gain of different organ weights were partly eased by GBCK25 treatment. Echocardiography results proposed the amelioration of heart function through normalized levels of left ventricle systolic pressure, ejection fraction, and fractional shortening. These outcomes deliver straight confirmation that GBCK25 could be a potential nutraceutical source for the relief of HFD-induced obesity mediated cardiac dysfunctions.

• The Korean Journal of Physiology and Pharmacology
• /
• v.23 no.1
• /
• pp.37-45
• /
• 2019

To study the effect of nicorandil pretreatment on ketone body metabolism and Acetyl-CoA acetyltransferase (ACAT1) activity in hypoxia/reoxygenation (H/R)-induced cardiomyocytes. In our study, we applied H9c2 cardiomyocytes cell line to evaluate the cardioprotective effects of nicorandil. We detected mitochondrial viability, cellular apoptosis, reactive oxygen species (ROS) production and calcium overloading in H9c2 cells that exposed to H/R-induced cytotoxicity. Then we evaluated whether nicorandil possibly regulated ketone body, mainly ${\beta}$-hydroxybutyrate (BHB) and acetoacetate (ACAC), metabolism by regulating ACAT1 and Succinyl-CoA:3-ketoacid coenzyme A transferase 1 (OXCT1) protein and gene expressions. Nicorandil protected H9c2 cardiomyocytes against H/R-induced cytotoxicity dose-dependently by mitochondria-mediated anti-apoptosis pathway. Nicorandil significantly decreased cellular apoptotic rate and enhanced the ratio of Bcl-2/Bax expressions. Further, nicorandil decreased the production of ROS and alleviated calcium overloading in H/R-induced H9c2 cells. In crucial, nicorandil upregulated ACAT1 and OXCT1 protein expressions and either of their gene expressions, contributing to increased production of cellular BHB and ACAC. Nicorandil alleviated cardiomyocytes H/R-induced cytotoxicity through upregulating ACAT1/OXCT1 activity and ketone body metabolism, which might be a potential mechanism for emerging study of nicorandil and other $K_{ATP}$ channel openers.