• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.8
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• pp.1166-1173
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• 2014

This study investigated the detoxification effects of enzymatic hydrolysate from oyster on acetaminophen-induced toxicity using HepG-2 cells. Oyster hydrolysate was made with 1% Protamex and 1% Neutrase after treatment with transglutaminase (TGPN) or without (PN). Two types of oyster hydrolysate were added to human-derived HepG-2 hepatocytes damaged by acetaminophen, after which the survival rate of HepG-2 cell was measured. In addition, glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) activities in the culture media were evaluated. The survival rates of HepG-2 cells were $136.2{\pm}1.4%$ at $100{\mu}g/mL$ of TGPN and $179.6{\pm}3.8%$ at $200{\mu}g/mL$ of TGPN. These cell survival rates were higher compared to that of the negative control group ($60.7{\pm}3.2%$) treated only with acetaminophen. GOT activity was $38.3{\pm}0.2$ Karmen/mL in the negative control group, whereas it was $19.9{\pm}0.5$ for TGPN ($200{\mu}g/mL$) and $22.0{\pm}2.4$ Karmen/mL for PN ($200{\mu}g/mL$). GOT and GTP activities were shown to be dependent on TGPN concentration, and significant reduction in activities could be conformed. The detoxification efficacy of TGPN was higher compared to that of PN. These results suggest that oyster hydrolysate has potential as a healthy food or pro-drug for liver protection.

• Journal of Life Science
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• v.31 no.9
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• pp.818-826
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• 2021

5-Aminolevulinic acid phosphate (5-ALA-p) is a substance obtained by eluting 5-ALA (a natural delta amino acid) with aqueous ammonia, adding phosphoric acid to the eluate, and then adding acetone to confer properties suitable for use in photodynamic therapy applications. However, its pharmacological efficacy, including potential mechanisms of antioxidant and anti-inflammatory reactions, remains unclear. This study aimed to investigate the effects of 5-ALA-p on oxidative and inflammatory stresses in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Our data showed that 5-ALA-p significantly inhibited excessive phagocytic activity via LPS and attenuated oxidative stress in LPS-treated RAW 264.7 cells. Furthermore, 5-ALA-p improved mitochondrial biogenesis reduced by LPS, suggesting that 5-ALA-p restores mitochondrial damage caused by LPS. Additionally, 5-ALA-p significantly suppressed the release of nitric oxide (NO) and pro-inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and IL-6, which are associated with the inhibition of inducible NO synthase and respective cytokine expression. Furthermore, 5-ALA-p reduced the nuclear translocation of nuclear factor-kappa B (NF-κB) and inhibited phosphorylation of mitogen-activated protein kinases (MAPKs), indicating that the anti-inflammatory effect of 5-ALA-p is mediated through the suppression of NF-κB and MAPK signaling pathways. Based on these results, 5-ALA-p may serve as a potential candidate to reduce inflammation and oxidative stress.

• Radiation Oncology Journal
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• v.21 no.3
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• pp.216-221
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• 2003

Purpose: To investigate the modulation of radiosensitivity by celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on cancer cells over- and under-expressing COX-2. Materials and Methods: A clonogenic radiation survival analysis was performed on A549 human lung and MCF-7 human breast cancer cell lines incubated in both 1 and $10\%$ fetal bovine serum (FBS) containing media. The apoptosis in both cell lines was measured after treatment with radiation and/or celecoxib. Results: Celecoxib enhanced the radiation sensitivity of the A549 cells in the medium containing the $10\%$ FBS, with radiation enhancement ratios of 1.58 and 1.81 respectively, at surviving fractions of 0.1, with $30\muM\;and\;50\muM$ celecoxib. This enhanced radiosensitivity disappeared in the medium containing the $1\%$ FBS. Celecoxib did not change the radiation sensitivity of the MCF-7 cells in either media. The induction of apoptosis by celecoxib and radiation was not synergistic in either cell line. Conclwsion: Celecoxib, a selective COX-2 inhibitor, preferentially enhanced the effect of radiation on COX-2 over-expressing cancer cells compared to the cells with a low expression, and this effect disappeared on incubation of the cells during drug treatment in the medium with suboptimal serum concentration. Apoptosis did not appear to be the underlying mechanism of this radiation enhancement effect due to celecoxib on the A549 cells. These findings suggest radiosensitization by a selective COX-2 inhibitor is COX-2 dependent.

• Tuberculosis and Respiratory Diseases
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• v.44 no.5
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• pp.1063-1071
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• 1997

Backgroung : The efficacy of oral corticosteroids in the treatment of chronic asthma is undisputed, but their long-term use is associated with adverse side-effects, including supression of the hypothalamic-pituitary adrenal axis function, osteoporosis, weight gain, hypertension and impaired glucose tolerance. The introduction of inhaled corticosteroids in the early 1970's represented a significant therapeutic advance in the management of asthma, since these compounds combined high topical potency with low systemic activity. Fluticasone propionate is a new topically active synthetic glucocorticosteroid that combinds a high degree of efficacy with negligible systemic bioavailability. This study was perfomed to determine the effect of inhaled fluticasone propionate on the adreocortical supression in patients with bronchial asthma or chronic obstructive pulmonary disease. Method : The adrenocortical function was assessed by measurement of plasma cortisol concentration at 8 o'clock in morning and free cortisol in 24 hour urine collection at interval. Absolutely, no steroid was taken during pretreatment period of 10days. There after each subject inhaled fluticasone aerosol, in daily doses of 500 or 1000micrograms for 12days. The dose was delivered by metered dose inhaler(MDI). Results : The serum cortisol and 24hour urinary free cortisol were not decreased during the treatment period in patients with inhaled fluticasone propionate in daily doses of 500 micrograms. In contrast, serum cortisol was significantly decreased on 9th and 12th day(p less than 0.05). And, 24hour urinary free cortisol was also significantly decreased on 3rd and 12th day of treatement period(p less than 0.05) in patients with inhaled fluticasone in daily doses of 1000 micrograms. Conclusion : These results suggested that endogenous cortisol secretion was not supressed after short-term inhalation of fluticasone in daily dose of 500 micrograms, but in daily dose of 1000 micrograms, the endogenous cortisol secretion was supressed.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.87-100
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• 1994

It has been known for some time that dopamine-containing cells are existed in sympathetic ganglia, i.e., small, intensely fluorescent cells. However, its role and mechanism of action as a peripheral neurotransmitter are poorly understood so far. In the present study, an attempt was made to examine the effect of apomorphine, which is known to be a selective agonist of dopaminergic $D_2$. receptor on secretion of catecholamines (CA) from the isolated perfused rat adrenal gland. The perfusion of a low concentration of 10uM apomorphine into an adrenal vein for 20 min produced significant reduction in CA secretion induced by 5.32 mM ACh, 56 mM KCl, 100 uM DMPP and 100 uM McN-A-343. Increasing apomorphine concentration to 30 uM led to more markedly decreased CA secretion as compared to the case of 10 uM apomorphine and also did inhibit clearly CA release by $10^{-5}M$ Bay-K-8644. Furthermore, in adrenal glands preloaded with a higher dose of 100 uM apomorphine, CA releases evoked by ACh, excess $K^+$, DMPP and McN-A-343 were almost abolished by the drug. The perfusion of $3.3{\pm}10^{-5}M$ metoclopramide, which is well-known as a selective dopaminergic $D_2$ antagonist, produced significantly inhibitory effect of CA release by ACh, DMPP and McN-A-343 but did not affect that by excess $K^+$. However, preloading of 30uM apomorphine in the presence of metoclopramide did not modify the CA secretory effect of excess $K+$ and DMPP. These experimental results demonstrate that apomorphine causes dose-dependent inhibition of CA secretion by cholinergic receptor stimulation and also by membrane depolarization from the isolated perfused rat adrenal gland, suggesting that these effects appear to be exerted by inhibiting influx of extracellular calcium into the rat adrenal medullary chromaffin cells through activation of inhibitory dopaminergic receptors.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.67-73
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• 1994

Na-Ca exchange transports calcium ion either into (reverse mode Na-Ca exchange) or out of the cell (forward mode Na-Ca exchange) according to the direction of driving force produced by the changes in ratio of intra- and extra-cellular Na concentrations. Thus, Na-Ca exchange is regarded as the regulator of myocardial contraction. However, the existence of reverse mode Na-Ca exchange and its role in myocardial contraction is still questioned. Present study was performed to identify the presence of reverse mode Na-Ca exchange and its possible involvement in the regulation of myocardial contraction in rat heart. Using the left atria of rat, contraction was induced by electrical field stimulation (EFS, 0.5 msec duration and supramaximal voltage). Changing of the stimulation frequencies from resting 4 Hz to 0.4, 1 or 8 Hz caused typical negative staircase effect in twitch tension, but $^{45}Ca$ uptake showed bimodal increase. When the stimulation frequency was abruptly changed from 4 Hz to 0.4 Hz the atrial twitch tension showed three phased-enhancement, that is, the initial rapid increase (the first phase) followed by rapid decrease (the second phase) and stabilization (the third phase). $^{45}Ca$ uptake was equivalent to tension, i.e. initial significant increase in first 30 second and then decrease. Benzamil treatment abolished the first phase of increase in a dose dependent manner from $10^{-5}\;to\;3{\times}10^{-4}M.$ Bay k 8644 $(3{\times}10^{-5}M)$ treatment enhanced the inotropy induced by frequency reduction and abolished the second and third phase decreases. Benzamil treatment also suppressed the contraction stimulated by Bay K 8644. Although the contraction at 4 Hz stimulation was completely abolished by verapamil $3{\times}10^{-5}\;M$ pretreatment, the contraction reappeared as soon as the stimulation frequency was changed into 0.4 or 1 Hz and interstingly,$^{45}Ca$ uptake were significantly higher than no treatment. From these results, it is concluded that reduction of stimulation frequency causes calcium influx by the reverse mode Na-Ca exchange, resulting in initial rapid increase of twitch tension. then it turns into forward mode exchange to efflux the calcium, resulting in decrease of the twitch tension in left atria of rat.

• Journal of Life Science
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• v.21 no.11
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• pp.1612-1618
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• 2011

The present study was undertaken to analyze the effects of different types of treatment on excess post exercise oxygen consumption (EPOC), flexibility, free radical and antioxidants in women using a horseback riding therapeutic device. Subjects were trained in regular horseback riding exercises for 12 weeks (3 times/wk). The effects of this exercise were examined by means of a single session of horseback riding that lasted for 30 min. 21 women were recruited from a public health center and divided into 3 groups (passive recovery group, passive+massage recovery group, and dynamic recovery group). 3 types of recovery patterns were determined after a single trial of horseback riding exercise. Their flexibility were determined pre-and post-training by Paired T test, and ANOVA were used to analyze the data. The results were as follows: Among the 3 groups, the dynamic recovery group showed the highest levels of EPOC compared to the other groups, and also showed higher levels of anti-oxidants, as did the passive+massage recovery group compared to the passive recovery group. Moreover, horseback riding exercise greatly increased flexibility in the women. In conclusion, regular horseback riding training is recommended to enhance the flexibility of women and dynamic recovery is recommended to enhance EPOC and anti-oxidants after a single bout of exercise. Further study is needed in this area.

• Journal of Haehwa Medicine
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• v.5 no.2
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• pp.501-501
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• 1997

당뇨병성(糖尿病性) 주위신경병변(周圍神經病變)은 당뇨병(糖尿病)에서 가장 많이 볼 수 있는 삼대합병증(三大合倂症) 중(中)의 하나이다. 환자(患者)의 임상표현(臨床表現)은 사고(四股) 및 구간부(軀幹部)가 마목(麻木)하고,동통(疼痛)이 칼로 베는 듯하거나 침(鍼)으로 찌르는 듯하여 참기 힘들며, 환자(患者)로 하여금 작업능력(作業能力)을 상실(喪失)하게 하고 휴식(休息)과 수안(睡眼)에 엄중(嚴重)한 영향(影響)을 준다. 지금까지 국내외(國內外)에서는 아직 효과적(效果的)인 치료방법(治療方法)이 없다. 우리는 임상(臨床)에서 관찰(觀察)해 본 결과(結果), 이 병(病)의 임상표현(臨床表現)인 "사고마목(四股麻木), 자통(刺痛), 야간가중(夜間加重), 통처고정(痛處固定)"의 특징(特徵)이 중의임상(中醫臨床)에서 표현(表現)되는 "혈어형(血瘀型)" 동통(疼痛)과 완전(完全)히 상동(上同)하였다. 우리는 "활혈화어(活血化瘀), 통락지통(通絡止痛), 거어생신(祛瘀生新)"을 치료원칙(治療原則)으로 중약복방(中藥復方) 제제(制劑) "당말녕(糖末寧)"을 제조(製造)하여 이 병(病)을 치료(治療)하는데 만족(滿足)스러운 임상치료효과(臨床治療效果)를 거두었다. 전체(全體)의 병례(病例)는 모두 우리 과(科)의 입원환자(入院患者)로써 모두 45례(例)인데, 병기(病機)에 따라 양조(兩組)로 나누었다. 관찰조(觀察組) 30례(例) 중(中)에는 남성(男性)이 19례(例)이고 여성(女性)이 12례(例)이며, 年齡(연령)은 25세(歲)에서 68세(歲)까지로 평균연령(平均年齡)이 49.8세(歲)이다. I형(型) 당뇨병(糖尿病)이 10례(例)이고 II형(型) 당뇨병(糖尿病)이 20례(例)이며, 당뇨병(糖尿病)의 병정(病程)은 6개월(個月)에서 17년(年)사이로 평균(平均) 7.1 년(年)이다. 주위신경병변(周圍神經病變)의 병정(病程)은 2주(周)에서 3년(年)까지로 평균(平均) 1년(年)이다. 대조조(對照組)는 15례(例)로 남성(男性)이 8례(例)이고 여성(女性)이 7례(例)이며, 연령(年齡)은 20세(歲)에서 65세(歲)까지로 평균(平均) 49세(歲)이다. I형(型) 당뇨병(糖尿病)이 7례(例)이고 II형(型) 당뇨병(糖尿病)이 8례(例)이며, 橋民病의 병정(病程)은 3개월(個月)에서 12년(年)까지로 평균(平均) 7.5년(年)이다. 주위신경병변(周圍神經病變)의 병정(病程)은 1개월(個月)에서 3년(年)까지로 평균병정(平均病程)은 11.6개월(個月)이다. 양조(兩組)사이의 병정(病程)은 현저(顯著)한 차이는 없으나 서로 비교(比較)해 볼만하다. 당말녕(糖末寧)은 주(主)로 삼궁(三芎),원호(元胡), 당귀(當歸), 계혈승 등(等)의 약물(藥物)로 조성(組成)되었고, 약제실(藥劑室)에서 濃縮液(농축액)(매(每) ml당(當) 생약량(生藥量) 2.5g 함유(含有))으로 제조(製造)하였다. 관찰조(觀察組)는 매차례(每次例) 당말녕(糖末寧) 50ml를 하루 세번씩 복용(服用)하였고; 대조조(對照組)는 비타민 $B_1$, 비타민 $B_6$을 각각(各各) 20mg씩 하루 세차례 복용(服用)하였다. 양조(兩組) 모두 사주(四周)를 한번의 치료료정(治療療程)으로 하였다. 우리는 모두 45례(例)의 환자(患者)를 관찰(觀察)하였는데, 그 중(中) 관찰조(觀察組)가 30례(例)이고 대조조(對照組)가 15례(例)이다. 임상표현(臨床表現) 분급(分級)과 신경근전도(神經筋電圖)(운동신경(運動神經)과 감각신경(感覺神經)의 전도(電圖) 속도(速度))를 치료(治療) 전(前)과 후(後)의 대조지표(對照指標)로 하였고. 매(每) 4주(周)를 한개의 료정(療程)으로 총(總) 1-2개(個)의 료정(療程)을 진행(進行)하여 比較硏究(비교연구)하였다. 총유효율(總有效率)은 96.7%이고 총현효율(總顯效率)은 50%로써 대조조(對照組)보다 뚜렷하게 높았다. 치료전(治療前) MNCV와 SNCV를 측정(測定)한 것은 당말녕(糖末寧)이 당뇨병(糖尿病) 주위신경병변(周圍神經病變) 환자(患者)의 신경전도속도(神經電圖速度)를 명확(明確)하게 개선(改善)하였음을 표현(表現)하고 있다. 신경근전도(神經筋電圖)에서 자발전위(自發電位)는 눈에 띄게 감소(減少)되고 소력수축(小力收縮)의 평균시한(平均時限)은 명확(明確)히 연장(延長)되었으며 다상전위(多相電位)는 명확(明確)하게 증가(增加)되었는데, 이는 신경지측(神經支測)이 재생(再生)되고 회복(恢復)하였음을 설명(說明)하고 있다. 중약복방제제(中藥復方制劑) "당말녕(糖末寧)"이 본병(本病)을 치료(治療)하는 기전(機轉)은 여러 방면(方面)일 것이다. 그 중(中) 微循環(미순환)을 개선(改善)하고 적혈구(赤血球)의 변형성(變形性)을 향상(向上)하여 신경세포(神經細胞)에 혈액(血液)과 산소공급(酸素供給) 및 영양공급(營養供給)을 향상(向上)함으로써 神經損傷(신경손상)의 수정(修整)과 회복(恢復)을 촉진(促進)하는 것이 주요(主要)한 일환(一環)이 될 것이다.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.7 no.1
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• pp.77-91
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• 1996

In order to elucidate the biological etiology and the effects of comorbidity on biological variables in tic disorders, plasma serotonin (5-hydroxlfryptamine, 5-HT) and 5-hydroxy- indoleacetic acid (5-HIAA) we.e measured in 87 tic disorders and 30 control subjects. The 87 tic disorder were composed of 45 Tourette's disorder(TS), 22 chronic motor tic disorders (CMT) and 20 transient tic disorders (TTD). Among these patients,43 patients were pure tic disorder (PT), 28 subject also had attention deficit hyperactivity disorder (T+ADHD) and 16 subjects had obsessive compulsive disorders (T+ OCD) as comorbid disorders. The results are summarized as follows : 1) Plasma 5-HT levels showed significant positive correlations with plasma 5-HIAA levels (Pennon r=0.77, p<0.05). 2) Plasma 5-HT and 5-HIAA levels showed no significant correlation with age in tic disorders. 3) Plasma 5-HIAA and 5-HT levels showed no significant correlations with age in control subjects. 4) There was significant difference in plasma 5-HT levels among TS, CMT, TTD and control groups (ANOVA F=34.48, df=3, 113, p<0.01), and post-hoc test using Scheffe method showed significant differences between control and TS, control and CMT, control and ITD groups. But, post-hoc test showed no significant differences between TS and CMT, TS and TTD, CMT and TTD groups. 5) There was significant difference in plasma 5-HIAA levels among TS, CMT, TTD and control groups (ANOVA F=26.48, df=3, 113, p<0.01), and post-hoc test using Scheffe method showed significant differences between control and TS, control and CMT, control and TTD groups. But, post-hoc test showed no significant differences between TS and CMT, TS and TTD, CMT and TID groups.f) There was significant difference in plasma 5-HT and 5-HIAA levels among PT, T+ADHD, T+OCD and contol groups (ANOVA 5-HT, F=37.59, df=3, 113, p<0.01, 5-HIAA, F=27.37, df=3, 113, p<0.01), and post-hoc test using Scheffe method showed signiscant differences between control and PT, control and T+ADHD and control and T+OCB. But, post-hoc test showed no significant differences between PT and T+ADHD, PT and T+ OCD and T+ADHD and T+ OCD. These results show that decreased 5-HT and 5-HIAA levels may play a role in the genesis of tic disorders, but these findings have no significant correlations with the severity of tic disorders. And the comorbid disorders of tics may have minimal effects on the biochemical abnormalities. Future studies must be focused on the effects of serotonin agonists and antagonists on tic disorders and molecular biological methodology may enhance to elucidate the mechanisms of these abnormal findings.

• 한국유가공학회:학술대회논문집
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• 2007.09a
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• pp.49-58
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• 2007

Inflammatory process leads to the well-known mucosal damage and therefore a further disturbance of the epithelial barrier function, resulting abnormal intestinal wall function, even further accelerating the inflammatory process[1]. Despite of the records, etiology and pathogenesis of IBD remain rather unclear. There are many studies over the past couple of years have led to great advanced in understanding the inflammatory bowel disease(IBD) and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses including increased serum concentrations of different cytokines. Therefore, targeted molecules can be specifically eliminated in their expression directly on the transcriptional level. Interesting therapeutic trials are expected against adhesion molecules and pro-inflammatory cytokines such as TNF-${\alpha}$. The future development of immune therapies in IBD therefore holds great promises for better treatment modalities of IBD but will also open important new insights into a further understanding of inflammation pathophysiology. Treatment of cytokine inhibitors such as Immunex(Enbrel) and J&J/Centocor(Remicade) which are mouse-derived monoclonal antibodies have been shown in several studies to modulate the symptoms of patients, however, theses TNF inhibitors also have an adverse effect immune-related problems and also are costly and must be administered by injection. Because of the eventual development of unwanted side effects, these two products are used in only a select patient population. The present study was performed to elucidate the ability of TNF-${\alpha}$ antibodies produced in sheep colostrums to neutralize TNF-${\alpha}$ action in a cell-based bioassay and in a small animal model of intestinal inflammation. In vitro study, inhibitory effect of anti-TNF-${\alpha}$ antibody from the sheep was determined by cell bioassay. The antibody from the sheep at 1 in 10,000 dilution was able to completely inhibit TNF-${\alpha}$ activity in the cell bioassay. The antibodies from the same sheep, but different milkings, exhibited some variability in inhibition of TNF-${\alpha}$ activity, but were all greater than the control sample. In vivo study, the degree of inflammation was severe to experiment, despite of the initial pilot trial, main trial 1 was unable to figure out of any effect of antibody to reduce the impact of PAF and LPS. Main rat trial 2 resulted no significant symptoms like characteristic acute diarrhea and weight loss of colitis. This study suggested that colostrums from sheep immunized against TNF-${\alpha}$ significantly inhibited TNF-${\alpha}$ bioactivity in the cell based assay. And the higher than anticipated variability in the two animal models precluded assessment of the ability of antibody to prevent TNF-${\alpha}$ induced intestinal damage in the intact animal. Further study will require to find out an alternative animal model, which is more acceptable to test anti-TNF-${\alpha}$ IgA therapy for reducing the impact of inflammation on gut dysfunction. And subsequent pre-clinical and clinical testing also need generation of more antibody as current supplies are low.