• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.3
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• pp.797-807
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• 2004

This research investigates the effect of the Hibiscus syriacus(HSS) on Alzheimer's disease. The effects of the HSS extract on the behavior in the Morris water maze experiment; the expression of IL-1β, TNF-α, IL-1β mRNA, TNF-α mRNA, CD68/GFAP and RDS; the the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with M were investigated. The HSS extract group showed a significant inhibitory effect on the memory deficit on the mice with Alzheimer's disease induced by βA in the Morris water maze experiment. The HSS extract group suppressed the over-expression of IL-1β, TNF-α, IL-1β and TNF-α mRNA, CD68/GFAP, RDS in the mice with Alzheimer's disease induced by βA. The HSS extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by βA. This study suggest that HSS may be effective for the prevention and treatment of Alzheimer's disease

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1795-1804
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• 2004

This research investigated the effect of the Chaenomelis fructus(CMF) on Alzheimer's disease. The effects of the CMF extract on the behavior in the Morris water maze experiment; the expression of IL-1β, TNF-α, ROS on the microglial cell; IL-1β mRNA, TNF-α mRNA, CD68/GFAP and MDA on the brain tissue; the infarction area of the hippocampus, and brain tissue injury in the mice with Alzheimer's disease induced by βA were investigated. The CMF extract group showed a significant inhibitory effect on the memory deficit on the mice with Alzheimer's disease induced by βA in the Morris water maze experiment. The CMF extract group suppressed the over-expression of IL-1β, TNF-α, IL-1β and TNF-α mRNA, ROS, MDA, CD68/GFAP in the mice with Alzheimer's disease induced by βA. The CMF extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by [3A. This study suggest that CMF may be effective for the prevention and treatment of Alzheimer's disease.

• The Korean Journal of Food And Nutrition
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• v.34 no.5
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• pp.441-448
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• 2021

This study was designed to investigate the intracellular signaling pathways and immunoenhancing effect of macrophage activation by crude polysaccharides (CPP) extracted from citrus peels. CPP did not affect the cytotoxicity of RAW264.7 cells, but showed dose-dependent effects on cell viability. Also, CPP showed high production of chemokine (nitric oxide (NO)) and cytokines (interleukin (IL)-6 and tumor necrosis factor (TNF)-α). CPP increased IL-6, TNF-α, and inducible nitric oxide synthase (iNOS) mRNA expression dose-dependently. CPP also strongly induced the phosphorylation of the ERK, p38, and IκBα pathways in RAW 264.7 cells. In anti-pattern recognition receptors (PRRs) experiments, the effect of CPP on NO production was strongly suppressed by neutralizing toll-like receptor (TLR)2, TLR4, and Dectin1 antibodies, whereas IL-6 and TNF-α production by CPP was mainly suppressed by mannose receptor (MR). Therefore, these results suggest that CPP treatment-induced NO production was regulated by the ERK, p38, and NF-κB pathways through TLR2, TLR4, and Dectin1 receptors, whereas IL-6 and TNF-α production was primarily regulated by the ERK, p38, and NF-κB pathways through MR receptors.

• Korean Journal of Pharmacognosy
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• v.54 no.1
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• pp.1-8
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• 2023

The skin is an important barrier that protects the body from harmful environments such as UV rays. When the skin is repeatedly stimulated, such as UV rays, ROS and pro-inflammatory cytokines are overproduced. As a result, the proteins and nucleic acids that make up the skin are damaged, and aging occurs. Esculetin is known to have anti-inflammatory, antioxidant and UV-induced MMP-1 inhibitory effects. However, the inhibitory effect of MMP-1 on TNF-α-induced fibroblasts is not known. Therefore, in this study, the MMP-1 inhibitory effect of esculetin was confirmed in TNF-α-induced fibroblasts. As a result of confirming the cytotoxicity of esculetin in Hs68 cells by MTT assay, there was no significant toxicity up to 200 µM. As a result of real-time PCR and ELISA, it was confirmed that esculetin inhibited the expression of MMP-1. Esculetin did not inhibit MAPK (ERK, JNK, p38) phosphorylation, but inhibited phosphorylation of the mTOR-p70S6k signaling pathway. In addition, it was confirmed that the phosphorylation of the transcription factor NF-κB was inhibited. These results suggest that esculetin has potential as an anti-aging material.

• BMB Reports
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• v.49 no.3
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• pp.185-190
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• 2016

Crotamine is a peptide toxin found in the venom of the rattlesnake Crotalus durissus terrificus and has antiproliferative, antimicrobial, and antifungal activities. Herein, we show that crotamine dose-dependently induced macrophage phagocytic and cytostatic activity by the induction of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-α). Moreover, the crotamineinduced expression of iNOS and TNF-α is mediated through the phosphorylation of p38 and the NF-κB signaling cascade in macrophages. Notably, pretreatment with SB203580 (a p38-specific inhibitor) or BAY 11-7082 (an NF-κB inhibitor) inhibited crotamine-induced NO production and macrophage phagocytic and cytotoxic activity. Our results show for the first time that crotamine stimulates macrophage phagocytic and cytostatic activity by induction of NO and TNF-α via the p38 and NF-κB signaling pathways and suggest that crotamine may be a useful therapeutic agent for the treatment of inflammatory disease.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.4
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• pp.707-713
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• 2002

Astragali radix (AR) is one of the oldest and mast frequently used crude drug for traditional medicine in many Asian countries. This study designed to investigate the hepatoprotective effects of the aqueous extracted AR (ARE) against acetaminophen (APAP)-induced hepatic damage in ICR mice. APAP at the dose of 450 mg/kg i.p produced liver damage in ICR mice. Serum enzyme activities of alanine aminotransferase, aspartate aminotransferase and sorbitol dehydrogenese was dramatically decreased up to control level by pretreatment of ARE. However, hepatic glutathione level did not show a significant change between the tested groups. We also investigated TNF α mRNA gene expression on APAP-induced liver damage by RT-PCR. APAP dramatically induced TNF α mRNA gene expression in ICR mice. Pretreatment of mice with ARE led to a marked decrease of TNF α mRNA gene expression. These data indicate that 1) ARE has clearly revealed a hepatoprotective effect against APAP-induced hepatic damage in ICR mice, and 2) the protective effect of ARE may be, in part, associated with the regulation of TNF α mRNA gene expression.

• The Journal of Korean Obstetrics and Gynecology
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• v.34 no.2
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• pp.1-15
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• 2021

Objectives: This study was designed to examine immuno-modulatory effects of Evodia Rutaecarpine by activating innate immune system and inhibiting inflammation. Methods: First, Cell cytotoxicity was examined with 4T1 breast carcinoma and TG-induced macrophage. To investigate activating innate immune system of Evodiamine Rutacarpine Extract (ERE) on macrophage, we tested tumor necrosis factor-alpha (TNF-α), interleukin-12 (IL-12), and interleukin-6 (IL-6). In addition, TNF-α and nitric oxide (NO) induced by lipopolysaccharide (LPS) were measured after treating with ERE to observe innate immune modulating effect of ERE on RAW 264.7 cell. Also, mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) were examined by western blot analysis. Results: In cytotoxicity analysis, ERE significantly affected tumor cell growth above specific concentration. Also, ERE significantly affected macrophage growth above specific concetration. As compared with the control group, the production of TNF-α, IL-12 and IL-6 were increased in TG-induced macrophage. As compared with the control group, TNF-α and IL-6 were significantly up-regulated in RAW 264.7 cell. The expression of TNF-α and NO induced by LPS after treating ERE was significantly decreased compared with control group. In addition, We observed ERE inhibited the phosphorylation levels of p-extracellular signal-regulated kinase (p-ERK), p-Jun N-terminal kinase (p-JNK), and p-p38 in western blotting by treating ERE on RAW 264.7 cell. Conclusions: ERE seems to have considerable impact on the anti-cancer effect by activation of innate immune system and inflammation control.

• The Korea Journal of Herbology
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• v.37 no.3
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• pp.41-47
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• 2022

Objectives : Terminalia chebula (TC) has been used as a traditional remedy to treat gastrointestinal infectious and inflammatory diseases. However, its protective effects and mechanisms against skin inflammation have not been well-elucidated. Thus, the aim of this study is to evaluate the protective effects of the TC water extract and also to suggest a putative mechanism of TC against skin injury on human keratinocytes, HaCaT cells. Methods : HaCaT cells were pre-treated with TC for 1 h and then stimulated with tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) (10 ng/mL each) to induce skin inflammation and injury. After 24 h, the cells were harvested to evaluate the expression of Th2 chemokines, such as C-C motif chemokine ligand 5 (CCL5, also known as RANTES), C-C chemokine ligand 17 (CCL17, also known as TARC) and C-C chemokine ligand 22 (CCL22, also known as MDC). To investigate the regulatory mechanisms of TC, we also assessed the phosphorylation of signal transducer and activator of transcription 1 (STAT1) signaling pathways in HaCaT cells. Results : Treatment of TC decreased the mRNA levels of RANTES, TARC and MDC with a concentration dependent manner against co-stimulation of TNF-α and IFN-γ. In addition, TC significantly reduced TNF-α and IFN-γ induced phosphorylation of STAT1. Conclusions : In summary, we propose that TC may be a promising candidate for anti-inflammatory skin protector through the inhibition of chemokines via STAT1 deactivation.

• Journal of The Korean Society of Integrative Medicine
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• v.11 no.1
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• pp.63-70
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• 2023

Purpose : Excessive alcohol causes damage to skeletal muscles, leading to the development of a specific disease entity called alcoholic myopathy. Chronic inflammation is related as an underlying mechanism for the loss of muscle mass induced by alcohol. Pro-inflammatory cytokines such as TNF-α (tumor necrosis factor-α) and IL-6 (interleukin-6) play a role in this process. The acupuncture point Feng Shi (GB 31) is located on the midline of the lateral aspect of the thigh, above the transverse popliteal crease. This acupoint is used for the treatment of weakness, atrophy, numbness, and post-stroke symptoms of lower limbs. The purpose of this study was to investigate the effect of Feng Shi stimulation on muscle atrophy caused by chronic alcohol administration. Method : Young male Sprague-Dawley rats were randomly divided into three groups of eight each: Normal, Control, and GB31. The rats in the Control and GB31 groups were orally given 25 % ethanol (5 ㎖/kg, body weight) daily for 4 weeks. The Normal group was similarly administered saline. The acupressure at Feng Shi was treated to rats in the GB31 group. After 4 weeks, the body weight, muscle weight and cross-sectional area of gastrocnemius were assessed and the histological changes in gastrocnemius muscle fiber were observed by hematoxylin and eosin staining. Moreover, TNF-α and IL-6 expressions were immunohistochemistrically evaluated. Results : Acupressure stimulation at Feng Shi had a protective effect on the weight reduction of the gastrocnemius muscle caused by alcohol intake, and had an effect of suppressing anatomical change in muscle fiber and decreasing the average cross-sectional area. Also, the immunoreactivities of TNF-α and IL-6 in the GB31 group were decreased. Conclusion : These results suggest that acupressure at Feng Shi has protective effects on chronic alcohol-induced muscle atrophy by inhibiting pre-inflammatory proteins such as TNF-α and IL-6.

• Journal of Veterinary Science
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• v.23 no.2
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• pp.27.1-27.16
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• 2022

Background: The role of Toll-like receptors (TLRs) in a feline infectious peritonitis virus (FIPV) infection is not completely understood. Objectives: This study examined the expression of TLR3, TLR7, TLR9, tumor necrosis factor-alpha (TNF-α), interferon (IFN)-β, and interleukin (IL)-10 upon an FIPV infection in Crandell-Reese feline kidney (CRFK) cells and feline monocytes. Methods: CRFK cells and monocytes from feline coronavirus (FCoV)-seronegative cats and FCoV-seropositive cats were infected with type II FIPV-79-1146. At four, 12, and 24 hours post-infection (hpi), the expression of TLR3, TLR7, TLR9, TNF-α, IFN-β, and IL-10, and the viral load were measured using reverse transcription quantitative polymerase chain reaction. Viral protein production was confirmed using immunofluorescence. Results: FIPV-infected CRFK showed the upregulation of TLR9, TNF-α, and IFN-β expression between 4 and 24 hpi. Uninfected monocytes from FCoV-seropositive cats showed lower TLR3 and TLR9 expression but higher TLR7 expression compared to uninfected monocytes from FCoV-seronegative cats. FIPV-infected monocytes from FCoV-seropositive cats downregulated TLR7 and TNF-α expression between 4 and 24 hpi, and 4 and 12 hpi, respectively. IFN-β was upregulated early in FIPV-infected monocytes from FCoV-seropositive cats, with a significant difference observed at 12 hpi compared to FCoV-seronegative cats. The viral load in the CRFK and FIPV-infected monocytes in both cohorts of cats was similar over time.ConclusionTLR7 may be the key TLR involved in evading the innate response against inhibiting TNF-α production. Distinct TLR expression profiles between FCoV-seronegative and FCoV-seropositive cats were observed. The associated TLR that plays a role in the induction of IFN-β needs to be explored further.