• The Korean Journal of Physiology and Pharmacology
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• v.26 no.3
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• pp.165-174
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• 2022

As the mechanism underlying glucose metabolism regulation by oxymatrine is unclear, this study investigated the effects of oxymatrine on pyroptosis in INS-1 cells. Flow cytometry was employed to examine cell pyroptosis and reactive oxygen species (ROS) production. Cell pyroptosis was also investigated via transmission electron microscopy and lactate dehydrogenase (LDH) release. Protein levels were detected using western blotting and interleukin (IL)-1β and IL-18 secretion by enzyme-linked immunosorbent assay. The caspase-1 activity and DNA-binding activity of nuclear factor kappa B (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 protein (Nrf2) were also assessed. In the high glucose and high fat-treated INS-1 cells (HG + PA), the caspase-1 activity and LDH content, as well as Nod-like receptor family pyrin domain containing 3, Gsdmd-N, caspase-1, apoptosis-associated speck-like protein containing a CARD, IL-1β, and IL-18 levels were increased. Moreover, P65 protein levels increased in the nucleus but decreased in the cytoplasm. Oxymatrine attenuated these effects and suppressed high glucose and high fat-induced ROS production. The increased levels of nuclear Nrf2 and heme oxygenase-1 (HO-1) in the HG + PA cells were further elevated after oxymatrine treatment, whereas cytoplasmic Nrf2 and Keleh-like ECH-associated protein levels decreased. Additionally, the elevated transcriptional activity of p65 in HG + PA cells was reduced by oxymatrine, whereas that of Nrf2 increased. The results indicate that the inhibition of pyroptosis in INS-1 cells by oxymatrine, a key factor in its glucose metabolism regulation, involves the suppression of the NF-κB pathway and activation of the Nrf2/HO-1 pathway.

• Korean Journal of Veterinary Research
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• v.37 no.2
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• pp.383-388
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• 1997

This study was designed to investigate the effects of varying concentrations of $CdCl_2$ on the enzyme activities such as LDH and SOD related with the accumulations of cadmium(Cd) in liver and kidney of BALB/c mice. 1. Cd accumulations in liver and kidey were increased in a dose dependent fashion. And also, this pattern was more conspicuous in kidney than that in liver. 2. LDH activities of liver and kidney were increased in a dose dependent fashion except for that of liver in 200 ppm Cd group which was similar to that of 25 ppm Cd group. 3. SOD activities of Cd exposed liver and kidney in Cd-fed mice similar to those of controls except for elevation of SOD activity of liver in 25 ppm Cd group. The results of this study suggest that the activities of various enzymes can be modulated by Cd intoxication. Acknowledgement: This study was financially supported in part by a Research Grant from Bio-Safty Research Institute, Chonbuk National University in 1997(CNU-BSRI, No. 97-03).

• Journal of the East Asian Society of Dietary Life
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• v.24 no.2
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• pp.176-182
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• 2014

Haw (Crataegus pinnatifida Bunge) has been used in traditional medicine for treating various ailments such as obesity and digestive trouble in Far East countries, including Korea. The present study was carried out to investigate the effects of feral haw on hepatic functional enzymes in dyslipidemic rats. Four groups of male rats (Sprague Dawley strain) were fed different diets for 5 weeks: NND (normal-nondyslipidemic diet) group, NNDH (normal-nondyslipidemic diet + haw extract) group, CDD (control-dyslipidemic diet) group and DDH (dyslipidemic diet + haw extract) group. ALP (alkaline phosphatase), LDH (lactate dehydrogenase), AST (aspartate aminotransferase) and ALT (alanine aminotransferase) activities were significantly higher in the CDD group than the NND group. However, haw extract supplement significantly reduced hepatic functional enzyme activities compared to the CDD group. Lipid deposition of the DDH group decreased compared to the CDD group. The size of adipose tissue decreased significantly in the DDH group compared to the CDD group. These results suggest that feral haw could be used as a food resource and functional food material.

• Journal of Life Science
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• v.18 no.10
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• pp.1342-1347
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• 2008

The purpose of present study was to investigate the protective effect of silkworm excrement powder (SEP) on alcohol-induced hepatotoxicity in rats. Semisynthetic diet supplemented with SEP (3%, w/w) given to alcohol-feeding rats for 30 days, then blood and tissues were collected, processed and used for alcohol concentration mensuration, various biochemical estimations and histopathological examination. Chronic alcohol administration resulted in significantly increase in the activities of the clinically important liver marker enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST), $\gamma$-glutamyl transpeptidase ($\gamma$-GTP) and lactate dehydrogenase (LDH). Also, a highly significant increase in the blood alcohol level by alcohol treatment was observed. But alcohol-induced elevation of ALT and LDH levels markedly prevented and the level of blood alcohol decreased in SEP treated rats as compared to alcohol-administered control rats. SEP supplementation showed highly decreased the concentrations of total lipid, triglyceride and cholesterol in serum, as compared with alcohol treated control rats. Alcohol treatment induced the marked accumulation of large lipid droplets, hepatocytes necrosis and inflammation in the liver, but SEP administration attenuated to alcohol-induced accumulation of lipid droplets and hepatocyte necrosis. The results indicated that SEP may exert a protective effect against alcoholic hepatotoxicity through decreasing the activity of hepatic marker enzymes.

• Journal of Chest Surgery
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• v.29 no.4
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• pp.365-372
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• 1996

In an attempt to evaluate the effect of St. Thomas' hospital cardioplegic solution (STH) I and II on the cultured rat myocardial cells, beating rate, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (Irtrazolium MTT) and lactate dehydrogenase activity were investigated, and also light and electron microscopic studies were carried out. After rat myocardial cells were cultured for 72 hours, cells were treated with STH I or with STH H solution for 30 and 120 min. and thereafter myocardial cells were cultured in control medium for 24 hours. The results obtained were as follows : 1. Beating rate was 154 times per min. in control group, 141 times per min. in STH I solution(for 2. 120 min.)-treated group and 145 times in STH ll solution (for 120 min.)-treated group. MTT absorbances by MTT assay were 102% in STH I solution (for 120 min.)-treated group and 93% in STH ll solution (for 120 min.)-treated group compared with control group. 3. The amount of lactate dehydrogenase released into the medium were 123% in STH I solution (for 120 min.)-treated group and 109% in STH H solution (for 120 min.)-treated group compared with control group. 4. In the light microscopy examination, myocardial cells showed no differences between experimental and control groups in their number and shape. 5. In the electron microscopy examination, myocardial cells treated with STH I solution showed fewer destroyed mitochondria compared to STH ll solution-treated group. These results suggest that both 51. Thomas'cardioplegic solution STH 1 and STH H have no cytotoxicity on cultured rat myocardial cells, but STH H solution has more protective effect on myocardial cells compared to STH I solution.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.42 no.1
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• pp.87-94
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• 2016

Skin damage is mainly caused by environmental factors such as ultraviolet light, heat, and smoking. It is known that reactive oxygen species production is commonly involved in the pathogenesis of skin damage induced by these factors, causing skin aging. Pyrus pyrifolia Nakai continues to be a popular and highly consumed fruit in many countries with known beneficial effects including antitumor, antioxidative, and anti-inflammatory effects. However, there is no evidence of a therapeutic effect of Pyrus pyrifolia extract (PPE) against skin aging via inhibition of mitochondria-mediated apoptosis. In this study, we investigated PPE protective effect against photoaging induced by UVB ($50mJ/cm^2$) in HS68 human dermal fibroblasts. Lactate dehydrogenase assay showed that PPE significantly protected HS68 cells against UVB-induced damage in a dose-dependent manner. Other assays using DCF-DA demonstrated that PPE protected HS68 cells by regulating reactive oxygen species production. PPE also regulated mitochondrial dysfunction and mitochondrial membrane potential induced by UVB, and inhibited UVB-induced caspase-3 activity. These results indicate that PPE protects human dermal fibroblasts from UVB-induced damage by regulating the oxidative defense system.

• Journal of Digital Convergence
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• v.11 no.4
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• pp.339-350
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• 2013

The decreased body, liver, kidney, spleen and testis weights of guinea pigs by TCDD (2,3,7,8-tetracholorodibenzo-${\rho}$-dioxin) treatment (TT) were statistically significantly increased after treating red ginseng saponin fraction (SF) (p>0.01). After treated with SF, the decreased hematocrits values and numbers of RBC and platelet, activity of amylase and lactate dehydrogenase, levels of uric acid, total protein and albumin by TT were increased, and the increased numbers of WBC, levels of triglyceride, total cholesterol (TC), LDL-cholesterol, HDL-cholesterol, creatinine, blood urea nitrogen, calcium and phosphorus, activities of creatinine kinase, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase were decreased after treated with SF. And they all had a statistical significance (p>0.01) except for RBC, WBC, platelet, blood glucose, TC, calcium and albumin. From these results, we knew that SF mollified the acute toxicity induced by TCDD in guinea pigs.

• Journal of Life Science
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• v.20 no.11
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• pp.1595-1602
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• 2010

Oxidation of low density lipoprotein (LDL) has been recognized as an important role in the initiation and progression of atherosclerosis. In this study, effects of allylmercaptan, a major metabolite compound of garlic, was studied on endothelial cell injury induced by oxidized low density lipoprotein (ox-LDL). The antioxidative activity of allylmercaptan was investigated by monitoring a thiobarbituric acid substance (TBARS). Allylmercaptan inhibited LDL oxidation induced by $Cu^{2+}$ at concentrations of 0.1, 1 and 10 mM in a dose dependent manner. Lactate dehydrogenase (LDH) release, as an index of cell injury, and intracellular glutathione levels were determined. Pulmonary artery endothelial cells were preincubated with allylmercaptan at $37^{\circ}C$ and 5% $CO_2$ for 24 hr, washed, and then exposed to 0.1 mg/ml oxidized LDL for 24 hr. Preincubation of endothelial cells with allylmercaptan significantly prevented the LDH release and depletion of GSH. Peroxides were measured directly in 24 well plates using a fluorometric assay. Allylmercaptan inhibited release of peroxides induced by ox-LDL in pulmonary artery endothelial cells. In a free system, allylmercaptan was shown to scavenge hydrogen peroxide. The data indicate that allylmercaptan can protect pulmonary artery endothelial cells from injury caused by oxidized LDL, and suggest that allylmercaptan may be useful for the prevention of atherosclerosis.

• Journal of Life Science
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• v.19 no.8
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• pp.1119-1124
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• 2009

Hyperlipidemia has been reported to be associated with the development of fatty liver. Palmitic acid, a major saturated fatty acid, is involved in the development of diverse diseases. The activation of mitogen activated protein kinases (MAPKs), such as Jun N-terminal kinase (INKs) and p38 MAPK is implicated in the apoptosis in diverse cells. Thus, this study was conducted to investigate the effects of palmitic acid on apoptosis and its relationship between JNK and p38 MAPK in cultured rat hepatocytes. In the present study, palmitic acid (>50 uM) decreased cell proliferation and increased lactate dehydrogenase activity in hepatocytes, which was blocked by the treatment of SP600125 (a JNK inhibitor) and SB203580 (a p38 MAPK inhibitor). Indeed, palmitic acid decreased Bcl-2 expression but increased Bax expression in rat hepatocytes, which was blocked by the treatment of SP600125 and SB203580. In addition, palmitic acid decreased glutathione (GSH) content and increased lipid peroxide formation, which was blocked by the treatment of SP600125 and SB203580. Western immunoblotting analysis also revealed that palmitic acid increased JNK and p38 MAPK. In conclusion, palmitic acid induced apoptosis through oxidative stress via JNK and p38 MAPK activation in rat hepatocytes.

• Korean Journal of Food Science and Technology
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• v.11 no.4
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• pp.224-231
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• 1979

The safety of the sweetening component of stevia was studied by administrating it to the rats. The $LD_{50}$ determined by intraperitoneal injection was 3,400 mg/Kg as the stevia extract containing 50 % stevioside, i.e. $LD_{50}$ of stevioside was more than 1,700 mg/Kg. Oral administration of large quantities of the stevia extract for 56 days resulted in no effect on the growth of rats. The analyses of total blood (RBC, WBC, Hb and Hct), 17 blood serum components including total protein, glucose, cholesterol, GOT, and 11 items of findings on the liver tissues including nuclear deterioration of liver cells, proliferation of Kupffer cells, fibrosis of portal area showed no significant differences between control and treatments except lactate dehydrogenase activity after 56 day-oral administration of the extract. From the results obtained, it was supposed that the stevia extract/stevioside revealed no acute or sub-acute toxic effects on rats.