• Clinical and Experimental Pediatrics
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• v.52 no.12
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• pp.1337-1347
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• 2009

Purpose:Taurine (2-aminoethanesulfonic acid) is a simple sulfur-containing amino acid. It is abundantly present in tissues such as brain, retina, heart, and skeletal muscles. Current studies have demonstrated the neuroprotective effects of taurine, but limited data are available for such effects during neonatal period. The aim of this study was to determine whether taurine could reduce hypoxic-ischemic (HI) cerebral injury via anti-apoptosis mechanism. Methods:Embryonic cortical neurons isolated from Sprague-Dawley (SD) rats at 18 days gestation were cultured in vitro. The cells were divided into hypoxia group, taurine-treated group before hypoxic insult, and taurine-treated group after HI insult. In the in vivo model, left carotid artery ligation was performed in 7-day-old SD rat pups. The pups were exposed to hypoxia, administered an injection of 30 mg/kg of taurine, and killed at 1 day, 3 days, 1 week, 2 weeks, and 4 weeks after the hypoxic insult. We compared the expressions of Bcl-2, Bax, and caspase-3 among the 3 groups by using real- time polymerase chain reaction (PCR) and western blotting. Results:The cells in the taurine-treated group before hypoxic insult, although similar in appearance to those in the normoxia group, were lesser in number. In the taurine-treated group, Bcl-2 expression increased, whereas Bax and caspase-3 expressions reduced. Conclusion:Taurine exerts neuroprotective effects onperinatal HI brain injury due to its anti-apoptotic effect. The neuroprotective effect was maximal at 1-2 weeks after the hypoxic injury.

• Journal of Life Science
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• v.18 no.1
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• pp.1-8
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• 2008

The purpose of this study was to determine the possible additive effects of endurance exercise training (EXER) and selenium (SELE) on the improvements of glucose and lactate transport capacities in diabetic Goto-kakizaki rats. Animals either remained sedentary control (SED) or performed EXER or received SELE [$5{\mu}mol$ kg body wt (-1) day (-1)], or underwent both EXER and SELE (COMBI), which lasted for 6 wk. Compared with sedentary control, EXER alone or the SELE alone group, or the combined treatment group had significant reduction in glucose response measured at 90 min and 120 min during an intraperitoneal glucose tolerance test (IPGTT) and body weight after 6week treatment. EXER alone, or combined group individually had significantly higher glycogen contents in liver compared with SED or SELE groups. EXER alone increased glycogen content in soleus and plantaris compared with SED, and this parameter was increased to greatest extent in the combined treatment groups compared with SED or SELE groups. EXER alone, SELE alone or COMBI, caused significant decreases in the plasma lactates, serum glucose, insulin, total cholesterol and HOMA-IR along with a significant increase in high-density lipoprotein cholesterol compared with SED. In addition, EXER or COMBI individually had significantly lower serum triacylglycerol compared with SED or SELE. With respect to protein expression related to glucose and lactate transport capacities, EXER alone, SELE alone, or COMBI increased in MCT1 and MCT4 protein level in soleus and plantaris. Furthermore, EXER alone, SELE alone or COMBI caused significant increases in mt MCT1 protein level in soleus and plantaris. The findings of the current study suggest that endurance exercise training and selenium treatment may provide therapeutic values to type II diabetic patients with peripheral insulin resistance and hyperlactatecemia by improving glucose and lactate transport capacities, leading to improvements in plasma lactate, serum glucose, insulin and lipid profiles (TC, TG, HDL).

• Journal of Life Science
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• v.29 no.2
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• pp.215-222
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• 2019

Muscle dysfunction may arise from skeletal muscle atrophy caused by aging, injury, oxidative stress, and hereditary disease. Powdered heat-killed Enterococcus faecalis (EF-2001) has anti-allergy, anti-inflammatory, and anti-tumor effects. However, its antioxidant and anti-atrophy effects are poorly characterized. In this study, we examined the effects of EF-2001 on muscle atrophy. To determine the protective effect of EF-2001 on oxidative stress, C2C12 myoblasts were treated with $H_2O_2$ to induce oxidative stress. This induced cell damage, which was reduced by treatment with EF-2001. The mechanism of EF-2001's effect was examined in response to oxidative stress. Treatment with EF-2001 reversed the expression of HSP70 and SOD1 proteins. Also, mRNA levels of Atrogin-1/MAFbx and MuRF1 increased under oxidative stress conditions but decreased following EF-2001 treatment. To evaluate muscle volume, two and three dimensional models of the muscles were analyzed using micro-CT. As expected, muscle volume decreased after sciatic denervation and recovered after oral administration of EF-2001. Therefore, EF-2001 is a candidate for the treatment of muscular atrophy, and future discovery of the additional effects of EF-2001 may yield further applications as a functional food with useful activities in various fields.