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Protective Effect of Carnosine Against Zn-Mediated Toxicityin Cortical Neuronal Cells
Jin-Joo Hue,Ah-Ram Lee,Yea Eun Lee,Min-Hang Cho,Ki-Nam Lee,남상윤,윤영원,Jae-Hwang Jeong,Sang-Hwa Lee,이범준 한국독성학회 2007 Toxicological Research Vol.23 No.1
Zinc is an endogenous transition metal that can be synaptically released during neuronal activity. However, zinc may contribute to the neuropathology associated with a variety of conditions. Carnosine expressed in glial cells can modulate the effects of zinc on neuronal excitability as a zinc chelator. We hypothesize that carnosine may protect against neurotoxicity of zinc in cortical neuronal cells. The cortical neuronal cells from newborn rats were prepared and exposed to zinc chloride and/or carnosine at various concentrations. Zinc at the doses of 0 to 500 μM decreased neuronal cell viability in a dosedependent manner. Additionally, at the concentrations of 100 and 200 μM, it significantly decreased cell viability in an exposed time-dependent manner (p < 0.05). Treatment with carnosine at the concentrations of 20 and 200 μM significantly increased neuronal cell proliferation by approximately 14% and 20%, respectively, compared to the control (p < 0.05). At the concentrations of 100 and 200 μM zinc, 20 μM carnosine significantly increased the viability of neuronal cells by 18.3% and 12.1%, and 200 μM carnosine also increased it by 33.5% and 28.6%, respectively, compared to the normal control group (p < 0.01). These results suggest that carnosine at a physiologically relevant level may protect against zinc-mediated toxicity in neuronal cells as an endogenous neuroprotective agent
Hue, Jin Joo,Lee, Hu-Jang,Nam, Sang Yoon,Kim, Jong-Soo,Lee, Beom Jun,Yun, Young Won The Korean Society of Veterinary Science 2015 大韓獸醫學會誌 Vol.55 No.1
To investigate kinetics of free $^{177}Lu$ and $^{177}Lu$-labeled thermally cross-linked superparamagnetic iron oxide nanoparticles (TCL-SPION), suspensions were intravenously injected into the tail vein of mice at a dose of $5{\mu}Ci$/mouse or 15 mg/kg body weight, respectively. Free $^{177}Lu$ radioactivity levels were highest in kidney followed by liver and lung 1 day post-injection. $^{177}Lu$-labeled TCL-SPION radioactivity in liver and spleen was significantly higher compared to that of other organs throughout the experimental period (p < 0.05). Radioactivity in blood, brain, and epididymis rapidly declined until 28 days. Based on these results, TCL-SPION could be a safe carrier of therapeutics.
Anti-obesity activity of diglyceride containing conjugated linoleic acid in C57BL/6J ob/ob mice
Jin-Joo Hue,Ki Nam Lee,정재황,이상화,Young Ho Lee,Seong-woon Jeong,남상윤,윤영원,이범준 대한수의학회 2009 Journal of Veterinary Science Vol.10 No.3
This study was to investigate the anti-obesity effects of diglyceride (DG)-conjugated linoleic acid (CLA) containing 22% CLA as fatty acids in C57BL/6J ob/ob male mice. There were four experimental groups including vehicle control, DG, CLA, and DG-CLA. The test solutions of 750 mg/kg dose were orally administered to the mice everyday for 5 weeks. CLA treatments significantly decreased mean body weight in the obese mice throughout the experimental period compared to the control (p < 0.01). All test solutions significantly decreased the levels of triglyceride, glucose and free fatty acids in the serum compared with control (p < 0.05). The levels of total cholesterol were also significantly reduced in DG and DG-CLA groups compared with the control group (p < 0.05). CLA significantly decreased weights of renal and epididymal fats compared with the control (p < 0.05). DG and DGCLA also significantly decreased the epididymal fat weights compared with the control (p < 0.05). A remarkable decrease in the number of lipid droplets and fat globules was observed in the livers of mice treated with DG, CLA, and DG-CLA compared to control. Treatments of DG and CLA actually increased the expression of peroxisome proliferator-activated receptor gamma. These results suggest that DG-CLA containing 22% CLA have a respectable anti-obesity effect by controlling serum lipids and fat metabolism.
Jin-Joo Hue,Ji-Yeon Han,Ki-Nam Lee,Myak Miga,Jong-Soo Kim,Sang Yoon Nam,Byeongwoo Ahn,Young Won Yun,Jae-Hwang Jeong,Beom Jun Lee 한국실험동물학회 2008 Laboratory Animal Research Vol.24 No.4
Phytic acid (PA) has chelating and reducing properties on many divalent transition metals. Its properties may be associated with a role in anticancer activity. In the present study, effects of PA on colon carcinogenesis were investigated in Fe-deficient ICR male mice. Five-week old mice were acclimated for one week and assigned to five experimental groups including normal control, azoxymethane (AOM) only, AOM+low Fe, AOM+low Fe+0.5% PA, and AOM+low Fe+2% PA groups. Animals fed on iron-normal diet (35 ppm Fe) or iron-deficient diet (3 ppm Fe) and PA (0.5% or 2% PA in water) for 8 weeks. Animals received three (0-2nd weeks after starting experiment) injections of AOM (10 ㎎/㎏ bw) to induce colonic aberrant crypt foci (ACF). The total numbers of ACF and aberrant crypt (AC) were measured in the colonic mucosa stained with methylene blue. The blood and serum were analyzed with a blood cell differential counter and an automatic serum analyzer. Low iron diet induced a significant low in hemoglobin and mean corpuscular volume and hemoglobin values, compared with normal diet group (P<0.05). AOM treatment induced total numbers of 81.7 ACF and 102.0 AC per colon in normal iron-diet (AOM alone) group. Low dietary iron (AOM LFe) decreased the numbers of ACF (64.9) and AC (79.8) per colon by 20.6 and 21.8%, respectively, compared with AOM alone group. Treatment of 0.5% PA significantly decreased the numbers of ACF (50.3) and AC (60.5) per colon by 22.5 and 24.2%, respectively, compared with AOM LFe group (P<0.05). PA at 2% also reduced the formation of ACF or AC by 13.3 and 18.3%, respectively, compared with AOM LFe group (P<0.05). No detrimental effects by PA treatment were observed in blood and serum chemistry, body weight, and relative organ weight of mice during the experimental period. These findings suggest that PA may prevent colon carcinogenesis in mice even with iron-deficient status.