• 한국식품영양과학회지
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• 제31권1호
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• pp.124-130
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• 2002

두충잎의 생약 및 식품 자원으로서의 이용성을 증진시킬 목적으로 두충잎의 물추출물을 사염화탄소를 투여한 흰쥐의 간손상에 미치는 영향을 검토하기 위해, 정상군, 사염화탄소군, 두충잎 물추출액 투여군, 사염화탄소 처리 후 두충잎 물추출액을 투여한 군의 4개군으로 나누어 6주간 사육하여 얻은 결과는 다음과 같다. 혈청 중의 AST, ALT, LDH 활성은 사염화탄소 투여에 의해 현저히 증가하였으나 두충잎 물추출물을 함께 투여함으로 정상군과 수준으로 회복되었다. 한편 사염화탄소에 의해 증가된 혈청중의 ALP 활성은 두충잎 투여에 의해 유의성 있게 감소하지 않았다. 혈청 중의 중성지질, 총 콜레스테롤 함량과 LDL콜레스테롤의 함량은 사염화탄소군에서만 유의적인 증가를 나타내었을 뿐 나머지 각군간의 유의적인 차이는 없었다. 한편 혈청 중의 HDL콜레스테롤의 함량은 두충 단독 투여군 및 사염화탄소 투여 후 두충잎 투여군이 정상군 및 사염화탄소 단독 투여군들보다 유의적으로 높게 나타났다. 간조직 중의 총콜레스테롤, 총지질, 중성 지질의 함량은 사염화탄소에 의해 유의적인 증가를 나타내었으나 두충잎 물추출액의 투여로 인해 이들의 함량이 유의성 있는 감소는 관찰되지 않았다. 광학현미경에 의한 간소직 세포의 병리학적인 검사에서는 사염화탄소군에서 간손상시 나타나는 간조직의 지방변화, 풍선양 변성, 호산성 변성, 국소성 괴사, 부위별 괴사가 관찰되었으나 그후 두충잎 투여에서 변화가 나타나지 않아 간 손상이 회복되었음을 알 수 있었다. 이상의 결과에서 두충잎 열수 추출물은 $CCl_4$에 의해 손상된 간기능을 회복시키는데 효과가 있었으며, 특히 혈청지질 개선에 탁월한 효과가 있음을 알 수 있었다.

• 한국가금학회지
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• 제6권1호
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• pp.24-30
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• 1979

1. 도살전의 환경온도(38$^{\circ}C$, 2$0^{\circ}C$, 4$^{\circ}C$, -2$0^{\circ}C$)가 닭 가슴고기의 연도와 근육내 해당작용에 미치는 영향을 연구하였다. 고온구는 현저하게(p＜0.05) 계육의 연도를 저하시켰고 저온구도 다소 연도의 저하를 초래하였다. 고온구는 대조구보다 근육내 glycogen의 함량과 최초 Ph가 높았고 24시간후의 최종 PH는 현저하게 (P＜0.05) 낮았다. 저온구는 대조구와 고온구 사이의 중간수치를 보여주었다. 고기의 절단력(즉 연도)와 근육내 glycogen 함량, 최초 및 최종 근육 산도(PH) 간에는 현저하게 (p＜0.01) 높은 상관관계를 나타냈고 사후 해당속도와 가열처리후의 고기의 수화도 역시 유의한(p＜0.05) 상관관계를 보여 주었다. 근육 혹은 혈청내의 효소(LDH, CPK)의 활력과 고기 연도와는 아무런 상관관계가 없었다. 2. 도살후 가슴고기와 다리고기를 절취하여 각각 다른 보존온도에 방치하여 근섬유의 단축도를 조사하였던 바 4-1$0^{\circ}C$ 사이에서 가장 낮은 단축도를 보여주었다. $0^{\circ}C$에서 보존시 약간의 단축이 있었으나 현저하지 않았고 보존온도가 2$0^{\circ}C$ 이상일 때 온도상승에 따라 비례적으로 단축도의 급격한 증가를 보여주었다. 따라서 계내에서는 저온보다는 고온에서의 근섬유단축이 더 실제적인 중요성을 가지며 도계후 가급적 속히 15$^{\circ}C$이하로 냉각하므로 심한 연도의 저하를 방지할 수 있다.

• 대한한의학방제학회지
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• 제22권1호
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• pp.123-139
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• 2014

Objectives : This study was performed to investigate the inhibitory effects of Cheongshimyeonja-tang water extracts(CSYJ) on high fat diet-induced obesity and hyperlipidemia in C57BL/6J mice. Methods : The experimental animals were divided into four groups; normal diet-fed control(ND), high fat diet-fed control(HFD), HFD+CSYJ 150 mg/kg(CSYJ 150), and HFD+CSYJ 300 mg/kg(CSYJ 300). Obesity with hyperlipidemia was induced by feeding high fat diet(40%), and CSYJ was administrated orally into mice every day for 5 weeks. The effect of CSYJ on the serological parameters for Obesity with hyperlipidemia was evaluated. Results : CSYJ-treated groups revealed significantly reduced body weight and feed intake, as well as feed efficiency ratio, compared to HFD-fed group in dose-dependent manner. CSYJ reduced significantly the serum levels of triglyceride, total cholesterol and LDL-cholesterol elevated by intake of high fat diet feed, while the increased serum levels of HDL-cholesterol attenuated levels of atherogenic index and cardiac risk factor. It also reduced the blood levels of insulin and leptin in HFD group, and inhibited lipid accumulation in organs such as liver and abdomal adipose tissue. Moreover oral administration of CSYJ decreased significantly the blood level of alanine aminotransferase(ALT), aspartate aminotransferase(AST) and lactate dehydrogenase(LDH), and lipid peroxide(LPO), compared to HFD-fed group in dose-dependent manner. Conclusions : These results indicate that CSYJ could reduce high fat diet-induced obesity and hyperlipidemia, suggesting its clinical usefulness for declining body fat and hyperlipidemia.

• Journal of Microbiology and Biotechnology
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• 제26권4호
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• pp.790-798
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• 2016

Chlamydiae, obligate intracellular bacteria, are associated with a variety of human diseases. The chlamydial life cycle undergoes a biphasic development: replicative reticulate bodies (RBs) phase and infectious elementary bodies (EBs) phase. At the end of the chlamydial intracellular life cycle, EBs have to be released to the surrounded cells. Therefore, the interactions between Chlamydiae and cell death pathways could greatly influence the outcomes of Chlamydia infection. However, the underlying molecular mechanisms remain elusive. Here, we investigated host cell death after Chlamydia infection in vitro, in L929 cells, and showed that Chlamydia infection induces cell necrosis, as detected by the propidium iodide (PI)-Annexin V double-staining flow-cytometric assay and Lactate dehydrogenase (LDH) release assay. The production of reactive oxygen species (ROS), an important factor in induction of necrosis, was increased after Chlamydia infection, and inhibition of ROS with specific pharmacological inhibitors, diphenylene iodonium (DPI) or butylated hydroxyanisole (BHA), led to significant suppression of necrosis. Interestingly, live-cell imaging revealed that Chlamydia infection induced lysosome membrane permeabilization (LMP). When an inhibitor upstream of LMP, CA-074-Me, was added to cells, the production of ROS was reduced with concomitant inhibition of necrosis. Taken together, our results indicate that Chlamydia infection elicits the production of ROS, which is dependent on LMP at least partially, followed by induction of host-cell necrosis. To our best knowledge, this is the first live-cell-imaging observation of LMP post Chlamydia infection and report on the link of LMP to ROS to necrosis during Chlamydia infection.

• The Korean Journal of Physiology and Pharmacology
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• 제15권4호
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• pp.189-194
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• 2011

ATP-sensitive $K^+$ channels ($K_{ATP}$) are major component of preventing ischemia-reperfusion injury. However, there is little information regarding to the expressional difference of $K_{ATP}$ and its function between left and right ventricles. In this study, we measured the lactate dehydrogenase release of rabbit heart slices in vitro and determined the difference of the $K_{ATP}$ expression at the both ventricles by measuring the level of $K_{ATP}$-forming Kir6.2 (OcKir6.2) mRNA using in situ hybridization. The hearts were preconditioned with 15 min hypoxia and reoxygenated for 15 min before a hypoxic period of 60 min, followed by reoxygenation for 180 min. With hypoxic preconditioning (100% $N_2$) with 15 min, left ventricles (LV) showed higher release of LDH comparing with right ventricles (RV). Adding $K_{ATP}$ blocker glibenclamide ($10{\mu}M$) prior to a hypoxic period of 60 min, hypoxic preconditioning effect of RV was more abolished than LV. With in situ hybridization, the optical density of OcKir6.2 was higher in RV. Therefore, we suggest that different $K_{ATP}$ expression between LV and RV is responsible for the different response to hypoxia and hypoxic preconditioning of rabbit hearts.

• Nutrition Research and Practice
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• 제14권4호
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• pp.334-351
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• 2020

BACKGROUND/OBJECTIVES: This study was designed to investigate the improvement effect of white ginseng extract (GS-KG9) on D-galactosamine (Ga1N)-induced oxidative stress and liver injury. SUBJECTS/METHODS: Sixty Sprague-Dawley rats were divided into 6 groups. Rats were orally administrated with GS-KG9 (300, 500, or 700 mg/kg) or silymarin (25 mg/kg) for 2 weeks. The rats of the GS-KG9- and silymarin-treated groups and a control group were then intraperitoneally injected Ga1N at a concentration of 650 mg/kg for 4 days. To investigate the protective effect of GS-KG9 against GalN-induced liver injury, blood liver function indicators, anti-oxidative stress indicators, and histopathological features were analyzed. RESULTS: Serum biochemical analysis indicated that GS-KG9 ameliorated the elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in GalN-treated rats. The hepatoprotective effects of GS-KG9 involved enhancing components of the hepatic antioxidant defense system, including glutathione, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT). In addition, GS-KG9 treatment inhibited reactive oxygen species (ROS) production induced by GalN treatment in hepatocytes and significantly increased the expression levels of nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) proteins, which are antioxidant proteins. In particular, by histological analyses bases on hematoxylin and eosin, Masson's trichrome, α-smooth muscle actin, and transforming growth factor-β1 staining, we determined that the administration of 500 mg/kg GS-KG9 inhibited hepatic inflammation and fibrosis due to the excessive accumulation of collagen. CONCLUSIONS: These findings demonstrate that GS-KG9 improves GalN-induced liver inflammation, necrosis, and fibrosis by attenuating oxidative stress. Therefore, GS-KG9 may be considered a useful candidate in the development of a natural preventive agent against liver injury.

• 한국식품영양과학회지
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• 제46권2호
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• pp.161-168
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• 2017

본 연구에서는 산화적 스트레스로 유도한 시신경 세포사멸에 대한 차조기 물 추출물(PFE)의 효과를 확인하였다. Staurosporine으로 분화된 ssdRGC-5 세포에 buthionine과 glutamate(B/G)로 산화적 스트레스를 유도하였으며, LDH release assay, MTT reduction assay를 통하여 PFE가 농도 의존적으로 B/G에 의한 세포사멸을 억제함을 관찰하였다. 세포사멸의 기전을 연구하기 위해 caspase 활성, 세포 내 ROS 생성량, 세포고사 관련 단백질 발현을 관찰한 결과, B/G에 의해 증가한 ROS 생성량, caspase 활성을 PFE가 억제하였고, 세포질로 방출된 cytochrome c와 미토콘드리아로 이동한 Bax도 감소함을 확인하였다. 이상의 결과로부터 차조기는 산화적 스트레스로 유도된 시신경 세포사멸 과정에서 항산화 효과와 미토콘드리아성 세포사멸을 완화함으로써 세포 보호 작용을 나타냄을 확인하였다.

• Clinical and Experimental Pediatrics
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• 제45권8호
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• pp.994-999
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• 2002

목 적: SNL는 아시아 지역의 젊은 성인 여성에 호발하고 소아에서의 보고는 적다. 저자들은 소아 SNL의 임상 양상을 알아보고자 하였다. 방 법: 1995년 2월부터 2002년 1월까지 노원을지병원에서 SNL로 진단된 15세 이하 소아 23례의 임상양상을 고찰하였다. 2례는 절제생검으로 진단하였고 21례는 세침흡인으로 진단하였다. 결 과 : 평균 연령은 $8.1{\pm}3.8$세였고 범위는 14개월에서 14세였다. 남녀비는 1 : 1.6이었다. 10례(10/23)가 2000년에 진단되었다. 증세의 발현은 봄철인 경우가 많았다. 주된 임상 증세는 경부 종괴(22/23), 종괴동통(12/20), 발열(8/18)이었다. 발열 기간은 7례(7/8)에서 2주 미만이었고 림프절 종대 기간은 14례(14/15)에서 5개월 미만이었다. 백혈구 수치의 평균은 $7,664{\pm}3,454/mm^3$였다. ESR은 10례(10/12)에서 증가되어 있었고 LDH는 5례(5/6)에서 경도의 증가 소견이 있었다. CRP는 3례(3/4)에서 양성이었다. 방사선학적으로 측정한 림프절의 최대 직경은 14례(14/15)에서 2 cm이하였다. 원형 탈모증 환아에서 발생한 1례와 1형 당뇨병 환아에서 발생한 1례가 있었다. 전례에서 경과는 양호하였다. 결 론: SNL는 우리나라의 소아에서 드물지 않다고 생각되며 경부 림프절 종대를 주소로 내원하는 환아에서 발열이나 종괴동통의 유무에 상관없이 감별진단에 포함되어야 할 것으로 사료된다.

• 사상체질의학회지
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• 제21권3호
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• pp.138-153
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• 2009

1. Objectives: Yeolda-Hanso tang (YH) has long been used as traditional herbal formula in Korea as various diseases. Now we modified Yeolda-Hanso tang (YH) for neurodegenerative diseases treatment and named New-Yeolda-Hanso tang (NYH). We investigated neuroprotective effects of NYH on NGF-differentiated PC12 cells cytotoxicity induced by $\beta$-Amyloid peptide (A$\beta$25-35) and evaluated the ability of NYH to prevent and treat for neurodegenerative diseases via autophagy enhancement. 2. Methods and Results: 1) Protective effect of NYH on PC12 cells cytotoxity induced by A$\beta$25-35. PC12 cells survival was measured by MTT and lactate dehydrogenase (LDH) assay. $20{\mu}M$ $\beta$-Amyloid peptide (A$\beta$25-35) induced cytotoxicity on NGF-differentiated PC12 cells. NYH attenuated the cytotoxic effects of A$\beta$25-35 in a dose-dependent manner. 2) Pharmacological induction of Autophagy by NYH in PC12 cells Autophagy induction and activation was measured by immunoblot assay. Marker of autophagy, LC3 II expression and the ratio of LC3-II/I was slightly increased in the protein treated with YH, and significantly augmented in the protein treated with NYH. NYH-induced increase of LC3-II protein level was inhibited by 3MA. 3) Induction of Autophagy by NYH on A$\beta$25-35-induced injury in PC12 cells In MTT assay, $100{\mu}g/ml$ re-treated NYH attenuated $20{\mu}M$ A$\beta$25-35-induced cytotoxicity in PC12 cells. Protection effect of NYH was blocked by autophagy inhibitor 3MA. In immunoblot assay, $1200{\mu}g/ml$ pre-treated NYH activated autophagy in $20{\mu}M$ A$\beta$25-35-induced cytotoxicity in PC12 cells. The observed effect was partially blocked by 3MA. 3. Conclusions: All the results indicated that NYH possesses neuroprotective potential partially mediated by autophagy enhancement and NYH may be considered to be a promising new herbal formula to prevent and treat for neurodegenerative diseases including Alzheimer's disease (AD).

• Toxicological Research
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• 제24권2호
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• pp.119-127
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• 2008

The objectives of this study were to examine the lung injury and inflammation caused by manual metal arc stainless steel(MMA-SS) welding fume inhalation and to evaluate the recovery process. Sprague-Dawley rats were exposed to MMA-SS welding fumes for 2 h per day in a whole-body exposure chamber, with a total suspended particulate(TSP) concentration of $51.4{\pm}2.8mg/m^3$(low dose) or $84.6{\pm}2.9mg/m^3$(high dose) for 30 days. The animals were sacrificed after 30 days of exposure as well as after a 30-day recovery period. To assess the inflammatory or injury responses, cellular and biochemical parameters as well as cytokines were assayed in the bronchoalveolar lavage fluid(BALF). MMA-SS welding fume exposure led to a significant elevation in the number of alveolar macrophages(AM) and polymorphonuclear cells(PMN). Additionary, the values of $\beta$-n-acetyl glucosaminidase($\beta$-NAG) and lactate dehydrogenase(LDH) in the BALF were increased in the exposed group when compared to controls. After 30 days of recovery from exposure, a significant reduction in inflammatory parameters of BALF was observed between the exposed and recovered groups. Slight, but significant elevations were noted in the number of AM and PMN in the recovered groups, and AM that had been ingested fume particles still remain in the lungs. In conclusion, these results indicated that welding fumes induced inflammatory responses and cytotoxicity in the lungs of exposed rats. Fume particles were not fully cleared from lungs even after a 30-day recovery period.