Objects : Aimed to test the hypothesis that neonatal testosterone exposure in female mice influences the development of testosterone-related pain inhibitory system and that testosterone administered in adulthood decreases the pain sensitivity. Methods : Thirty androgenized(testosterone propionate $100{\mu}g$ ip within 24 hrs after birth) adult female and twenty five control(normal saline $100{\mu}g$ ip within 24 hrs after birth) adult female mice were injected with testosterone propionate 1mg/kg/day for 3 consecutive days from 84th experimental days. Nociceptive sensitivity was measured before and after treatment of testosterone by tail flick latency on 84th and 86th experimental days. Results : 1) On the 84th experimental day, basal nociceptive sensitivity was significantly higher in the androgenized group($2.7{\pm}0.4$ sec) as compared to the control group($3.3{\pm}1.1$ sec). 2) Testosterone treatment on the 84th experimental day significantly lowered nociceptive sensitivity in both androgenized($5.2{\pm}0.9$ sec) and control groups($4.6{\pm}1.8$ sec). However the effect was significantly greater in the androgenized group. 3) Nociceptive sensitivity on 86th experimental day before administration of testosterone was significantly lower in the androgenized group($4.8{\pm}1.9$ sec) as compared to the control group($3.9{\pm}1.2$ sec). 4) Testosterone treatment on the 86th experimental day significantly lowered the nociceptive sensitivity in both groups, but the androgenized group($5.9{\pm}0.9$ sec) showed significantly lower post-treatment nociceptive sensitivity as compared to the control group($4.9{\pm}1.5$ sec). 5) Nociceptive sensitivity was decreased significantly after injection of testosterone once a day for two consecutive days in the androgenized group(${\Delta}2.1{\pm}1.0$ sec), but not in the control group(${\Delta}0.5{\pm}1.3$ sec). Conclusions : There may be a testosterone-related pain inhibitory system, the development of which is enhanced by exposure to testosterone in the neonatal period, and the activity of which is also mediated by testosterone in the later life.
Park, Yeon-Hee;Yu, Ok-Kyeong;Bae, Cho-Rong;Cha, Youn-Soo
Journal of the Korean Society of Food Science and Nutrition
/
v.44
no.11
/
pp.1599-1606
/
2015
The purpose of this study was to assess the quality characteristics of Moju made with Hovenia dulcis Thunb. and its physiological effects on ICR mice. According to the sensory score, we selected Moju made with 1% Hovenia dulcis Thunb. among Moju made with 0, 0.5, 1, 5, and 10% Hovenia dulcis Thunb. Compared to Moju made without Hovenia dulcis Thunb., Moju made with 1% Hovenia dulcis Thunb. had higher proportions of moisture (86.77 g/100 g) and carbohydrates (11.86 g/100 g). The mean values of the physicochemical analyses were as follows: pH 4.91, acidity 0.28, $^{\circ}Brix$ 12.63, reducing sugar 68.97, alcohol content 0.1, alcohol density 0.998. Moju made with 1% Hovenia dulcis Thunb. did not have effects on DPPH radical scavenging activity; however, superoxide dismutase activity was significantly higher than that of Moju made without Hovenia dulcis Thunb. For assessing physiological activities, 4-week-old male ICR mice were divided into six groups (n=10): normal control group (NC), ethanol-administered group (EC), EC plus low-dose Moju made with 0% Hovenia dulcis Thunb. (MCL), EC plus high-dose Moju made with 0% Hovenia dulcis Thunb. (MCH), EC plus low-dose Moju made with 1% Hovenia dulcis Thunb. (MDL), and EC plus high-dose Moju made with 1% Hovenia dulcis Thunb. (MDH). Serum triglyceride (TG) level was reduced by 11.17% and 19.61% in the MDL and MDH groups, respectively, compared to the EC group. Serum total-cholesterol levels of MDL and MDH groups were significantly lower as compared to the EC group. Serum high-density lipoprotein-cholesterol levels of the MDL and MDH groups were significantly higher than those of the EC group. Liver TG levels were significantly reduced in the MCL and MDL groups. From these results, Moju made with Hovenia dulcis Thunb. demonstrated antioxidant activity and reduction of hyperlipidemia markers. Therefore, Moju made with Hovenia dulcis Thunb. can serve as a non-alcoholic beverage and functional food source.
Seo, Eun-Hui;Han, Ying;Park, So-Young;Koh, Hyong-Jong;Lee, Hye-Jeong
Journal of Life Science
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v.20
no.7
/
pp.1019-1026
/
2010
Obesity and being overweight are strongly associated with the development of metabolic disease such as diabetes, hypertension, dyslipidemia. High-fat diet (HFD) is one of the most important factors which cause obesity. In this study, C57BL/6 mice were treated with a HFD for 22 weeks in order to induce obesity and hyperglycemia. Twenty-two weeks later, body weight and plasma glucose level of the HFD group were significantly increased, compared with the normal diet (ND) group. Intra-peritoneal glucose tolerance test (IPGTT) showed glucose intolerance in the HFD group compared with the ND group. These results confirmed that a HFD induced obesity and hyperglycemia in C57BL/6 mice. Plasma levels of triglyceride (TG) and total cholesterol (TC) were increased in the HFD group compared with the ND group. Hepatic levels of TG and TC were also increased by a HFD. To investigate the alteration of lipid metabolism in liver, proteins which are related to lipid metabolism were observed. Among lipid synthesis related enzymes, fatty acid synthase (FAS) and glycerol phosphate acyl transferase (GPAT) were significantly increased in the HFD group. Apolipoprotein B (apoB) and microsomal triglyceride transport protein (MTP), which are related to lipid transport, were significantly increased in the HFD group. Interestingly, protein level and phosphorylation of AMP-activated protein kinase (AMPK), which is known as a metabolic regulator, were significantly increased in the HFD group compared with the ND group. In the present study we suggest that HFD may physiologically increase the proteins which are related with lipid synthesis and lipid transport, but that HFD may paradoxically induce the activation of AMPK.
Sung, Mi-Sun;Jung, Hoe-Yune;Choi, Jun-Hyeok;Lee, Sung-Cheol;Choi, Bo-Hwa;Park, Sung Sun
Journal of Life Science
/
v.24
no.9
/
pp.959-966
/
2014
This study was carried out to develop a functional healthy drink using 60% ethanol of dried Acanthopanax senticosus stem extract (ASE). The preparation, physical activity, anti-oxidant activity, and sensory properties of ASE were investigated. The moisture, crude protein, crude lipid, and ash contents of dried ASE were $6.50{\pm}0.12%$, $5.89{\pm}0.16%$, $1.18{\pm}0.11%$, and $3.03{\pm}0.40%$ respectively. The 1,1-Diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity was $87.42{\pm}1.63%$ at 1/10 folds diluted ASE. In total, 40 male ICR mice were divided into five groups including the control (PBS), positive control (Red ginseng 200 mg/kg/day), and ASE-treated groups at doses of 35, 70, and 140 mg/kg/day for five weeks, respectively. ASE was administrated orally one time per day for five weeks before treadmill exercises, and normal and positive controls were fed PBS and red ginseng extract. In the treadmill test, ASE-treated mice (140 mg/kg/day) could run 1.4 times longer than the control mice. Healthy drinks were prepared with the addition of ASE at levels of 0.97% or 0.49% (A, B, and C type). Among the healthy drinks, the B type (ASE, 0.97%) was revealed to have the highest level of taste and overall acceptability through a sensory evaluation. The brix and pH of the ASE health drink (B type) were 14.9 and 4.51, respectively. These results indicated that the dried stem of Acanthopanax senticosus could be used as a functional material in the health drink industry.
Ultraviolet (UV) irradiation reduces epidermal hydration, which is paralleled by the reduction of natural moisturizing factors (NMFs). Of various NMFs, free amino acids (AAs) are major constituents generated by filaggrin degradation. In this study, we attempted to determine whether dietary supplementation of royal jelly (RJ) in UV-irradiated mice can alters epidermal levels of hydration, filaggrins, and free AAs as well as of peptidylarginine deiminase-3 (PAD3), an enzyme involved in filaggrin degradation processes. Albino hairless mice were fed either a control diet (group UV+: UV irradiated control) or diets with 1% RJ harvested from different areas in Korea (groups RJ1, RJ2, and RJ3) or imported from China (group RJ4) for six weeks in parallel with UV irradiation. A normal control group (group UV-) was fed a control diet without UV irradiation for six weeks. Reduced epidermal levels of hydration, total filaggrins, and PAD3 were observed in group UV+; in group RJ1, these levels were increased to a level similar to that of group UV-. In addition, profilaggrins, two repeat intermediates (2RI), a precursor with two filaggrin repeats, and filaggrin were increased. Although no alteration of AAs was observed in any of the groups, and glutamate and serine, major AAs of NMF in group RJ1 were higher than in group UV+. Despite the increased levels of PAD3, epidermal levels of hydration, filaggrins, glutamate, and serine in groups RJ2, RJ3, and RJ4 were similar to those in group UV+. Dietary supplementation of RJ1 improves epidermal hydration in parallel with enhanced expression and degradation of filaggrin, but not by increased protein expression of PAD3, along with increased generation of glutamate and serine.
Recent studies reported that obesity upregulated the expression of neuronal nitric oxide synthase (nNOS) and regulated particular behavior patterns in animal models. They also reported that ameliorated the increase in nNOS expression and decreased depression and anxiolytic effects. Thus, exercise seems to be an effective strategy for improving brain function by downregulating nNOS. However, the immune response differs greatly, depending on the exercise intensity. The aim of the present study was to investigate differences in brain nNOS expression in obese C57BL/6 mice that performed exercise of different intensities. Obesity was induced in 6-wks-old mice (n=35) by feeding a 60%-fat diet for 6-wks. A control (CON) group (n=14) was fed a normal diet. At the end of the induction 6-wks period of obesity, seven animals in the CON group and obesity-induced group were sacrificed to confirm obesity induction (preliminary experiments and confirmation of visceral fat accumulation). The remaining animals were then used in an 8-wks exercise intervention. Other than the CON (n=7), the obesity-induced animals were divided into the following groups: high-fat diet (HFD, n=7), HFD-low intensity (HFD-LI, n=7, 12 m/min for 75 min), HFD-moderate intensity (HFD-MI, n=7, 15 m/min for 60 min), and HFD-high intensity (HFD-HI, n=7, 18 m/min for 50 min). The exercise was performed on an animal treadmill. The expression of the nNOS protein in the hippocampus was significantly higher in the HFD group as compared with that in the CON group (p<0.01). However, there was no difference in the hippocampal expression of the nNOS protein in the other exercise groups as compared with that in the CON group. In contrast, nNOS expression in the HFD-HI group was significantly lower than that in the HFD-LI group (p<0.05). The expression of phosphorylated Akt (pAkt) was significantly higher in all the exercise groups as compared with that in the CON and HFD groups. There was no difference in the expression of pAkt in the cerebral cortex among groups, and the expression of pAkt in the cerebellum was significantly higher in the HFD-HI group as compared with that in the CON group (p<0.05). There were also no between-group differences in pAkt expression in the cerebellum among the various exercise groups. In conclusion, nNOS seems to be overexpressed in response to obesity, and it appears to be downregulated by exercise. Relatively high-intensity exercise may be effective in improving brain function by downregulating nNOS.
In previous studies, ovarian follicle in rat has been used a higher radiation dose than that for cancer radiotherapy in clinical practice. The aim of this study was to evaluate the effect of radiation dose used for cancer radiotherapy on ovarian follicle atresia in rat. Mice of 4-week-old female were whole body irradiated with 2 cGy or 2 Gy (Mevatron 67, Siemens, Germany) and sacrificed by cervical dislocation. Ovaries were collected at 24 hours after irradiation to observe the degree of follicular atresia. Ovaries were fixed in neutral formaldehyde solution for 24 hours and embedded with paraffin. Cutted in $5{\mu}m$ thickness with microtome and stained with hematoxylin and eosin (H&E) and TUNEL immunohistochemical stain, and examined histologically under a light microscope. All data were presented as mean ${\pm}SD$, calculating the ratio of normal or atretic follicles to total ovarian follicles. Statistical analysis was performed by the Mann Whitney test using the SPSS ver 19.0. Ratio of atretic to total follicles of 2 Gy group was significantly higher than control or 2 cGy groups (p<0.05). Ratio of normal to total follicles of 2 Gy group was significantly lower than control group in preantral follicle (64.0 vs. 87.7, p=0.027). Ratio of normal to total follicles of 2 cGy group was significantly increased more than control or 2 Gy groups in antral follicle, and there were no significant difference between control and 2 Gy groups (p=0.522). Radiation dose of 2 Gy for cancer radiotherapy have a significant effect on ovarian follicle atresia in rat.
Park, Chi-Bong;Kim, Hwi-Yool;Jeun, Sin-Soo;Han, Young-Min;Han, Duk-Young;Kang, Young-Woon;Choe, Bo-Young
Progress in Medical Physics
/
v.14
no.4
/
pp.259-267
/
2003
In vivo $^1$H magnetic resonance spectroscopy (MRS) at 4.7 T was applied to investigate the cerebral metabolite changes of mice brain before and after experimental brain trauma. In vivo $^1$H MR spectra were acquired from a voxel covering right parietal cortex in normal brain, used as control subjects. After experimental brain trauma using the fluid percussion injury (FPI) method, $^1$H MR spectra were acquired from the same lesion three days after trauma. Metabolite ratios of the injured lesion were compared to those of controls. After trauma, N-acetylaspartate (NAA)/creatine (Cr) ratio, as a neuronal marker was decreased significantly versus controls, indicating neuronal loss. The ratio of NAA/Cr in traumatic brain contusion was 0.90$\pm$0.11, while that in normal control subjects was 1.13$\pm$0.12 (P=0.001). Choline (Cho)/Cr ratio had a tendency to rise in experimental brain contusion (P=0.02). Cho/Cr ratio after trauma was 0.91$\pm$0.17 while that before traumas was 0.76$\pm$0.15. Cho/Cr ratio was increased and this might indicate a inflammatory activity. However, no significant difference of [(glutamate+glutamine) (Glx)]/Cr was established between experimental traumatic brain injury models and normal controls. Lactate (Lac)/Cr ratio was appeared as a sign of shifted posttraumatic energy metabolism and increased versus controls. These findings strongly suggest that in vivo $^1$H MRS may be a useful modality for clinical evaluation of traumatic contusion and could aid in better understanding the neuropathologic process of traumatic contusion induced by FPI. In the present study, in vivo $^1$H MRS was proved to be a useful non-invasive method for in vivo diagnosis and monitoring of posttraumatic metabolism in models of brain contusion.
Purpose : Ginkgo biloba extract(GBE) is known to increase the peripheral blood circulation. This study was designed to evaluate the effect of GBE on the acute normal tissue radiation reaction. Materials and Methods : mice were divided into two groups, radiation alone and two doses GBE plus radiation, for both acute skin reaction and jejunal crypt assay. GBE was given i.p. one hour before irradiation with priming dose given one day earlier. Thirty to Fifty Gy for acute skin reaction and 11 to 14 Gy for jejunal crypt were irradiated to right hind leg and whole body, respectively. Results : Radiation doses($RD_{50}$) for Peak skin score of 2.0 were 44.2Gy (40.6-48.2Gy) for radiation alone and 44.4Gy(41.6-47.4Gy) for two doses GBE plus radiation, showing no effect of GBE on acute radiation skin damage. The numbers of regenerating jejunal crypts per circumference were also almost the same for each radiation dose level(p=0.57-0.94), and the mean lethal doses($D_o$) were 1.800y(1.57-2.09Gy) for radiation alone and 1.88Gy(1.65-2.18Gy) for two doses GBE plus radiation, indicating no effect of GBE on jejunal crypt cell survival after radiation. Conclusion : GBE doesn't increase acute normal tissue radiation reaction in this model system. As GBE was verified to enhance radiation effect on tumor, high therapeutic gain is expected when GBE is combined with radiation therapy.
This experiment was performed to evaluate the morphological responses of the gastric chief cells of the mouse, inoculated with Ehrlich carcinoma cells in the inguinal area, following administration of BCG (Bacillus Calmette-Guerin). Healthy adult ICR mice weighing 25 gm each were divided into normal and experimental groups (experimental control group and BCG treated group). In the experimental groups, each mouse was inoculated with $1x10^7$ Ehrlich carcinoma cells subcutaneously in the inguinal area. From next day after inoculations, 0.2 mL of saline or BCG (0.5 mL/25 g B.W.: $0.03{\times}10^8{\sim}0.32{\times}10^8$ CFU) were injected subcutaneously to the animals every other day, respectively. The day following the last injection, each mouse was sacrificed. Pieces of the tissue were taken from the stomach, prefixed with 2.5% glutaraldehyde-1.5% paraformaldehyde solution, followed by post-fixation with 1% osmium tetroxide solution. The ultrathin sections were stained with uranyl acetate and lead citrate. The size of zymogen granule and the size of the mitochondrion of the gastric chief cells were observed and calculated. In the BCG treated group, most chief cells did not show any difference in ultrastructure, except that myelin figures were more frequently observed, in comparison with that of nornmal control group. The size of zymogen granule in the gastric chief cells of normal control, experimental control and BCG-treated groups were $0.98({\pm}0.108){\mu}m,\;1.05({\pm}0.092){\mu}m\;and\;0.93({\pm}0.053){\mu}m$, respectively. And the mitochondrial size of the gastric chief cells of normal control, experimental control and BCG-treated groups were $0.80({\pm}0.130){\mu}m,\;0.83({\pm}0.143){\mu}m\;and\;0.72({\pm}0.078){\mu}m$, respectively. From the above results, it was concluded that BCG may slightly suppress function of the gastric chief cells.
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