• 동의생리병리학회지
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• 제21권3호
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• pp.688-699
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• 2007

This experiment was designed to investigate the effect of the SST hot water extract & ultra-fine Powder on Alzheimer's Disease Model Induced by ${\beta}$A. The effects of the SST hot water extract on expression of IL-1${\beta}$, IL-6, TNF-${\alpha}$, NOS-II, COX-2 mRNA and production of IL-l${\beta}$, IL-6, TNF-${\alpha}$, NO in BV2 microglial cell line treated by lipopolysacchaide(LPS). The effects of the SST hot water extract & ultra-fine powder on (1) the behavior (2) expression of IL-1${\beta}$, TNF-${\alpha}$, MDA, (3) Glucose, AChE in serum (4) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}$A were investigated. The SST hot water extract suppressed the expression of IL-1${\beta}$, IL-6 and TNF-a mRNA ${\alpha}$in BV2 microglia cell line treated with LPS. The SST hot water extract suppressed the production of IL-1${\beta}$, IL-6, TNF-${\alpha}$, NO in BV2 microglial cell line treated with LPS. The SST hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}$A in the Morris water maze experiment, which measured stop-through latency. The SST ultra-fine powder suppressed the expression of TNF-a protein significantly in the microglial cell of mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced the MDA and suppressed the over-expression of CD68, CD11b in the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder decreased AChE significantly in the serum of the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced the tau protein, GFAP, and presenilin1, 2 of hippocampus in the mice with Alzheimer's disease induced by ${\beta}$A. These results suggest that the SST hot water extract & ultra-fine powder may be effective for the prevention and treatment of A1zheimer's disease. Investigation into the clinical use of the SST hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

• 대한본초학회지
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• 제33권1호
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• pp.17-26
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• 2018

Objective : In this study, we investigated the effect of SAL5(mixing extracts of Schisandra chinensis Baillon, Artemisia capillaris Thunb., and Aloe vera Linne) on chronic ethanol-induced fatty liver model. Methods : Sprague-Dawley male rats were fed Liber-DeCarli (normal), ethanol liquid diet (control), SAL5 (200 mg/kg). We administrated the SAL5 on chronic ethanol-induced fatty liver model for 5 weeks. We measured alkaline phosphtase (ALP), alanine transminase (ALT), aspartate transminase (AST) and ${\gamma}-glutamyl$ transpeptase (${\gamma}-GTP$) in serum and triglyceride (TG), superoxide dismutase (SOD), catalase, glutathione (GSH) and malondialdehyde (MDA) level in liver. Liver histopathology was examined by Hematoxylin-eosin and Oil red O staining of the fixed liver tissues. Real-time PCR was performed to measure the mRNA expression of inflammatory cytokines and MMP-2, MMP-9. Results : SAL5 administration resulted in significantly decreased liver marker enzymes activities of alanine transminase (ALT), ${\gamma}-glutamyl$ transpeptase (${\gamma}-GTP$) in serum and triglyceride (TG) activities in liver. The control group decreased the activities of superoxide dismutase (SOD), catalase (CAT) with the reduced level of glutathione (GSH) in liver. On the other hand, SAL5 group increased the activities of SOD, CAT and the level of GSH. SAL5 delayed the development of an alcoholic fatty liver by reversing fat accumulation in the liver, as evidenced in histological observations. The gene expression of mRNA were significantly decreased at the $IL-1{\beta}$, $TNF-{\alpha}$, NOS-II and MMP-2 by SAL5. Conclusions : These results indicate that SAL5 might have protective effect chronic ethanol-induced fatty liver models.

• Biomolecules & Therapeutics
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• 제31권1호
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• pp.97-107
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• 2023

Aristolochic acid (AA), extracted from Aristolochiaceae plants, plays an essential role in traditional herbal medicines and is used for different diseases. However, AA has been found to be nephrotoxic and is known to cause aristolochic acid nephropathy (AAN). AA-induced acute kidney injury (AKI) is a syndrome in AAN with a high morbidity that manifests mitochondrial damage as a key part of its pathological progression. Melatonin primarily serves as a mitochondria-targeted antioxidant. However, its mitochondrial protective role in AA-induced AKI is barely reported. In this study, mice were administrated 2.5 mg/kg AA to induce AKI. Melatonin reduced the increase in Upro and Scr and attenuated the necrosis and atrophy of renal proximal tubules in mice exposed to AA. Melatonin suppressed ROS generation, MDA levels and iNOS expression and increased SOD activities in vivo and in vitro. Intriguingly, the in vivo study revealed that melatonin decreased mitochondrial fragmentation in renal proximal tubular cells and increased ATP levels in kidney tissues in response to AA. In vitro, melatonin restored the mitochondrial membrane potential (MMP) in NRK-52E and HK-2 cells and led to an elevation in ATP levels. Confocal immunofluorescence data showed that puncta containing Mito-tracker and GFP-LC3A/B were reduced, thereby impeding the mitophagy of tubular epithelial cells. Furthermore, melatonin decreased LC3A/B-II expression and increased p62 expression. The apoptosis of tubular epithelial cells induced by AA was decreased. Therefore, our findings revealed that melatonin could prevent AA-induced AKI by attenuating mitochondrial damage, which may provide a potential therapeutic method for renal AA toxicity.

• 한국자원식물학회지
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• 제35권5호
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• pp.565-573
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• 2022

치주조직에 존재하는 주요한 세포의 한 형태인 인체 치은섬유아세포는 다양한 구강유해세균으로부터 염증이 유발되어지며, 그중 대표적으로 치주염 원인균인 P. gingivalis의 내독소인 LPS-PG로부터 염증성 자극에 반응하여 다양한 염증매개 물질을 분비한다. 본 연구에서는 치주염을 일으키는 주요한 원인균 중 하나인 P. gingivalis로 부터 분리한 LPS-PG를 이용하여 인체 치은섬유아세포주인 HGF-1 세포에 염증을 유도한 후 LRE에 대한 항염증 및 항산화 효과를 분석하였다. 실험 결과, LRE는 LPS-PG 유도에 따라 iNOS에 의한 NO 생성과 COX-2에 의한 PGE₂와 같은 염증 매개 인자의 발현 및 생성 억제와 함께 염증성 싸이토카인(TNF-α, IL-1β및 IL-6)의 생성 또한 억제하였다. 신호전달계에서 염증성 전사인자의 발현 경로를 확인하기 위하여 TLR4/Myd88/NF-κB의 활성을 확인한 결과, LRE 처리에 따라 농도 의존적으로 억제되는 것을 확인하였다. 또한 산화 환원 효소로 항염증효과를 나타내는 것으로 알려진2상 효소 중 하나인 NQO-1과 이의 전사인자인 Nrf2를 분석 한 결과 LRE 처리에 의해 효소의 활성이 높아지는 것을 확인할 수 있었다. 결론적으로 LRE는 TLR4/Myd88/NF-κB 신호전달 경로를 억제하고 NQO1/Nrf2 활성을 유도함으로써 HGF-1 세포에서 LPS-PG에 의해 유도된 염증을 억제하는 것으로 사료되며, 향후 LRE는 식·의약품 소재 개발에서 치주질환 개선의 가능성이 있는 후보물질이 될 수 있을 것으로 사료된다.