• Title/Summary/Keyword: Arthritis, Rheumatoid

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Beneficial Effect of Collagen Peptide Supplement on Anti-aging Against Photodamage (콜라겐 펩타이드의 피부 광노화 예방 효과)

  • Kim, Jeong-Kee;Lee, Ji-Hae;Yang, Mi-Sook;Seo, Dae-Bang;Lee, Sang-Jun
    • Korean Journal of Food Science and Technology
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    • v.41 no.4
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    • pp.441-445
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    • 2009
  • Recent research has revealed that hydrolyzed collagen peptides have beneficial effects in various diseases such as osteoarthritis and human rheumatoid arthritis and also play a protective role in skin by improving the activity of antioxidants. In this study, we investigated the effects of a novel mixture (AP-CPM01) containing collagen peptides and elastin peptides on photoaged hairless mice skin both in vivo and in vitro. To evaluate the effects of AP-CPM01 on UVBinduced skin wrinkle formation in vivo, the hairless mice were exposed to UVB irradiation and orally administered the AP-CPM01 at 333 mg/kg per day for 10 weeks. The effects on skin appearance and epidermal thickness were measured using bioengineering and histochemical methods. In addition, the influence of AP-CPM01 on collagen metabolism in human skin fibroblasts was also investigated. The skin of mice in the AP-CPM01 treated group had better appearance and less wrinkling than that of mice in the control group. In the human fibroblast cells, the amount of de novo procollagen synthesis was increased after AP-CPM01 treatment, reflecting that AP-CPM01 can induce de novo procollagen synthesis and reduce UVB-induced skin wrinkle formation. These results suggest that AP-CPM01 is a potent candidate for antiphotoaging functions.

Development of stimulator for peripheral disturbance therapy using A variable Micro-electromagnetic (미약 전자기장을 이용한 말초장애 치료시스템 개발)

  • Kim, Soo-Byung;Lee, Seung-Wook;Shim, Ta-Kyu;Lee, Na-Ra;Lee, Yong-Heum
    • Journal of the Korea Institute of Information and Communication Engineering
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    • v.14 no.5
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    • pp.1209-1216
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    • 2010
  • It has increased that peripheral disturbance(blood flow, nerve, Raynaud's phenomenon) and finger rheumatoid arthritis which is caused by the diabetic complications. To improve these pain issues, we proposed new method for the Finger Disease Therapy(FDT). In this paper, we manufactured solenoid cylindrical coil which was only for the FDT using a variable micro-electromagnetic. Also, we designed the Finger Disease Therapy System(FDTS) which could select three stimulation modes(N_pulse, S_pulse, N/S_pulse) and frequency(0.25hz, 0.5hz, 1hz). We used a Teslameter to measure magnetic flux inner solenoid, and measured magnetic flux as distance(0 ~ 3cm) inner solenoid with stimulation modes and frequency. In the results, magnetic flux was the highest in center of solenoid(0cm) for all stimulation modes. Also, the highest magnetic flux was measured as N_pulse(294.3mT), S_pulse(293.8mT) in 1Hz and N/S_pulse (275.4mT) in 0.25Hz, respectively. Therefore, we developed the FDTS using various pattern and intensity for finger diseases therapy, and checked therapy clinic application possibility of the FDTS as measuring magnetic flux inner solenoid.

Repurposing Auranofin, an Anti-Rheumatic Gold Compound, to Treat Acne Vulgaris by Targeting the NLRP3 Inflammasome

  • Yang, Gabsik;Lee, Seon Joo;Kang, Han Chang;Cho, Yong-Yeon;Lee, Hye Suk;Zouboulis, Christos C.;Han, Sin-Hee;Ma, Kyung-Ho;Jang, Jae-Ki;Lee, Joo Young
    • Biomolecules & Therapeutics
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    • v.28 no.5
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    • pp.437-442
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    • 2020
  • Activation of the NLRP3 inflammasome is critical for host defense as well as the progression of inflammatory diseases through the production of the proinflammatory cytokine IL-1β, which is cleaved by active caspase-1. It has been reported that overactivation of the NLRP3 inflammasome contributes to the development and pathology of acne vulgaris. Therefore, inhibiting activation of the NLRP3 inflammasome may provide a new therapeutic strategy for acne vulgaris. In this study, we investigated whether auranofin, an anti-rheumatoid arthritis agent, inhibited NLRP3 inflammasome activation, thereby effectively treating acne vulgaris. Auranofin suppressed NLRP3 inflammasome activation induced by Propionibacterium acnes, reducing the production of IL-1β in primary mouse macrophages and human sebocytes. In a P. acnes-induced acne mouse model, injection of P. acnes into the ears of mice induced acne symptoms such as redness, swelling, and neutrophil infiltration. Topical application of auranofin (0.5 or 1%) to mouse ears significantly reduced the inflammatory symptoms of acne vulgaris induced by P. acnes injection. Topical application of auranofin led to the downregulation of the NLRP3 inflammasome activated by P. acnes in mouse ear skin. These results show that auranofin inhibits the NLRP3 inflammasome, the activation of which is associated with acne symptoms. The results further suggest that topical application of auranofin could be a new therapeutic strategy for treating acne vulgaris by targeting the NLRP3 inflammasome.

Development of a Food Frequency Questionnaire for the Korea National Health and Nutrition Examination Survey: Data from the Fourth Korea National Health and Nutrition Examination Survey (KNHANES IV) (국민건강영양조사 식품섭취빈도조사지 개발: 국민건강영양조사 제4기 (2007-2009) 자료 이용)

  • Yun, Sung Ha;Shim, Jee-Seon;Kweon, Sanghui;Oh, Kyungwon
    • Journal of Nutrition and Health
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    • v.46 no.2
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    • pp.186-196
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    • 2013
  • The objective of this study was to develop a semi-quantitative food frequency questionnaire (FFQ) for an adult population for use in the Korea National Health and Nutrition Examination Survey (KNHANES). The 24-hour recall data for 2,939 subjects aged 19 years and over from the fourth KNHANES first year (2007) were used to extract the items included in the questionnaire. The FFQ items were developed by selection of major dishes based on the cumulative contribution rate, between-person variability based on the cumulative R2 of energy and 14 nutrients (carbohydrate, protein, fat, crude fiber, calcium, phosphorous, iron, sodium, potassium, vitamin A, thiamin, riboflavin, niacin, and vitamin C) and the number of consumers of each dish. In addition, the FFQ items were revised with analysis of 24-hour recall data of the fourth KNHANES second and third year (2008, 2009). Finally, 112 items were included in the FFQ and grouped as follows: rice (5 items), noodles and dumplings (6), breads and rice cakes (8), soups and stews (12), soybeans, eggs, meat and fish (23), vegetables, seaweed and potatoes (27), milk and dairy products (4), fruits (13), beverages (5), snacks (6) and alcoholic beverages (3). The food items of FFQ accounted for an average of 87.0% of energy and 14 nutrient intakes and also accounted for 81.7% of the between-person variability. The frequency range of the FFQ items was classified into nine categories (never or seldom, once per month, 2-3 times per month, once per week, 2-4 times per week, 5-6 times per week, once per day, twice per day and three times per day) and the portion size was divided into three categories (small, medium and large). We expect that this developed dish-based FFQ could be used in assessment of longterm dietary intakes of Korean adults.

Anti-tuberculosis effects of frankincense through immune responses of Mycobacterium tuberculosis-infected macrophages (결핵균이 감염된 대식세포의 면역반응을 통한 유향(Frankincense)의 항결핵효과)

  • Son, Eun-Soon;Lee, Sun Kyoung;Cho, Sang-Nae;Park, Hae-Ryoung;Lee, Jong Seok
    • Korean Journal of Food Science and Technology
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    • v.53 no.6
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    • pp.756-760
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    • 2021
  • Frankincense has been used as a traditional medicine for treating rheumatoid arthritis, dermatitis, and muscle pain. In this study, the anti-tuberculosis effects of Frankincense were evaluated in immune responses of macrophages. Frankincense methanol extract was not cytotoxic to the host. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction assay using human macrophage (THP-1) cells did not show cytotoxic effects or morphological changes with treatments of 31.3, 62.5, and 125 ㎍/mL Frankincense methanol extract (FRM). Inhibitory effects of Frankincense methanol extract on the growth of Mycobacterium tuberculosis in human macrophages were investigated. The immune response was measured by monitoring the levels of TNF-α and IL-1β in THP-1 cells with or without M. tuberculosis infection under Frankincense methanol extract treatment. Inflammatory cytokine levels and M. tuberculosis numbers were reduced in THP-1 cells treated with Frankincense methanol extract. Therefore, Frankincense methanol extract could be used as a potential anti-tuberculosis agent.

Triptolide Inhibits Lipopolysaccharide-Induced MUC5AC/5B Expression via Nuclear Factor-Kappa B in Human Airway Epithelial Cells (사람 호흡기 상피세포에서 Triptolide의 Nuclear Factor-Kappa B를 통한 Lipopolysaccharide로 유도된 MUC5AC/5B 발현 억제 효과)

  • Seo, Bo Hyeon;Choi, Tae Yeong;Choi, Yoon Seok;Bae, Chang Hoon;Na, Hyung Gyun;Song, Si-Youn;Kim, Yong-Dae
    • Korean Journal of Otorhinolaryngology-Head and Neck Surgery
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    • v.61 no.12
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    • pp.674-680
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    • 2018
  • Background and Objectives The representative mucin genes in the human airway are MUC5AC and MUC5B, which are regulated by several inflammatory and anti-inflammatory substances. Triptolide (TPL), udenafil, betulinic acid, changkil saponin, and glucosteroid are some of the many anti-inflammatory substances that exist. TPL is a diterpenoid compound from the thunder god vine, which is used in traditional Chinese medicine for treatment of immune inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosus, nephritis and asthma. However, the effects of TPL on mucin expression of human airway epithelial cells have yet to be reported. Hence, this study investigated the effect of TPL on lipopolysaccharide (LPS)-induced MUC5AC and MUC5B expression in human airway epithelial cells. Subjects and Method The NCI-H292 cells and the primary cultures of human nasal epithelial cells were used to investigate the effects of TPL on LPS-induced MUC5AC and MUC5B expression using real-time polymerase chain reaction, enzyme immunoassay, and Western blot. Results TPL significantly decreased the LPS-induced MUC5AC and MUC5B mRNA expression and protein production. TPL also significantly decreased the nuclear factor-kappa B (NF-kB) phosphorylation. Conclusion These results suggest that TPL down regulates MUC5AC and MUC5B expression via inhibition of NF-kB activation in human airway epithelial cells. This study may provide important information about the biological role of triptolide on mucus-secretion in airway inflammatory diseases and the development of novel therapeutic agents for controlling such diseases.

Effects of Tumor Necrosis Factor-alpha Inhibitors on the Incidence of Tuberculosis (Tumor Necrosis Factor-alpha 저해제가 결핵 발생에 미치는 영향)

  • Park, Hyun Jin;Choi, Bo Yoon;Sohn, Minji;Han, Na Young;Kim, In-Wha;Oh, Jung Mi
    • Korean Journal of Clinical Pharmacy
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    • v.28 no.4
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    • pp.333-341
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    • 2018
  • Objective: Tumor necrosis factor-alpha (TNF-alpha) inhibitors are used as a treatment in various immune-mediated inflammatory diseases (IMIDs). Tuberculosis (TB) risk is reported in several meta-analyses in patients treated with TNF-alpha inhibitors. The purpose of this study is to collect, review, and evaluate the TB risk in TNF-alpha inhibitors according to IMIDs indications and between soluble-receptor TNF-alpha inhibitor and monoclonal-antibody TNF-alpha inhibitors. Methods: A systematic literature search on systematic reviews and meta-analyses was performed in PubMed, MEDLINE, Cochrane library, and EMBASE. We identified meta-analyses that evaluated TB infection risk of TNF-alpha inhibitors in IMIDs patients. Results: Thirteen meta-analyses including 41 study results were included in this umbrella review. IMIDs patients treated with TNF-alpha inhibitors had an increased risk of TB than control group (placebo with or without standard therapy patients) (relative risk ratio (RR) 2.057, 95% confidence interval (CI) 1.697 to 2.495). Among them, RA patients with TNF-alpha inhibitors had a higher risk of TB than control group (RR 1.847, 95% CI 1.385 to 2.464), and non-RA patients with TNF-alpha inhibitors had an increased risk of TB (RR 2.236, 95% CI 1.284 to 3.894). In subgroup analysis on TB risk between soluble-receptor TNF-alpha inhibitor and monoclonal-antibody TNF-alpha inhibitors in RA patients, the analysis indicated that monoclonal-antibody TNF-alpha inhibitors had higher risk of TB than soluble-receptor TNF-alpha inhibitor (RR 2.880, 95% CI 1.730 to 4.792). Conclusion: This umbrella review confirms that the risk of TB is significantly increased in TNF-alpha inhibitor treated patients compared to control group.

Impact of NR1I2, adenosine triphosphate-binding cassette transporters genetic polymorphisms on the pharmacokinetics of ginsenoside compound K in healthy Chinese volunteers

  • Zhou, Luping;Chen, Lulu;Wang, Yaqin;Huang, Jie;Yang, Guoping;Tan, Zhirong;Wang, Yicheng;Liao, Jianwei;Zhou, Gan;Hu, Kai;Li, Zhenyu;Ouyang, Dongsheng
    • Journal of Ginseng Research
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    • v.43 no.3
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    • pp.460-474
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    • 2019
  • Background: Ginsenoside compound K (CK) is a promising drug candidate for rheumatoid arthritis. This study examined the impact of polymorphisms in NR1I2, adenosine triphosphate-binding cassette (ABC) transporter genes on the pharmacokinetics of CK in healthy Chinese individuals. Methods: Forty-two targeted variants in seven genes were genotyped in 54 participants using Sequenom MassARRAY system to investigate their association with major pharmacokinetic parameters of CK and its metabolite 20(S)-protopanaxadiol (PPD). Subsequently, molecular docking was simulated using the AutoDock Vina program. Results: ABCC4 rs1751034 TT and rs1189437 TT were associated with increased exposure of CK and decreased exposure of 20(S)-PPD, whereas CFTR rs4148688 heterozygous carriers had the lowest maximum concentration ($C_{max}$) of CK. The area under the curve from zero to the time of the last quantifiable concentration ($AUC_{last}$) of CK was decreased in NR1I2 rs1464602 and rs2472682 homozygous carriers, while $C_{max}$ was significantly reduced only in rs2472682. ABCC4 rs1151471 and CFTR rs2283054 influenced the pharmacokinetics of 20(S)-PPD. In addition, several variations in ABCC2, ABCC4, CFTR, and NR1I2 had minor effects on the pharmacokinetics of CK. Quality of the best homology model of multidrug resistance protein 4 (MRP4) was assessed, and the ligand interaction plot showed the mode of interaction of CK with different MRP4 residues. Conlusion: ABCC4 rs1751034 and rs1189437 affected the pharmacokinetics of both CK and 20(S)-PPD. NR1I2 rs1464602 and rs2472682 were only associated with the pharmacokinetics of CK. Thus, these hereditary variances could partly explain the interindividual differences in the pharmacokinetics of CK.

Anthocyanins from Hibiscus syriacus L. Attenuate LPS-Induced Inflammation by Inhibiting the TLR4-Mediated NF-κB Signaling Pathway

  • Karunarathne, Wisurumuni Arachchilage Hasitha Maduranga;Molagoda, Ilandarage Menu Neelaka;Lee, Kyoung Tae;Choi, Yung Hyun;Kang, Chang-Hee;Jeong, Jin-Woo;Kim, Gi-Young
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2019.10a
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    • pp.92-92
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    • 2019
  • Excessive or chronic inflammation contributes to the pathogenesis of many inflammatory diseases such as sepsis, rheumatoid arthritis, and ulcerative colitis. Hibiscus syriacus L. has been used as a medicinal plant in many Asian countries, even though its anti-inflammatory activity has been unclear. Therefore, we investigated the anti-inflammatory effect of anthocyanin fractions from the H. syriacus L. varieties Pulsae (PS) on the lipopolysaccharide (LPS)-induced expression of proinflammatory mediators and cytokines in RAW264.7 macrophages. PS suppressed LPS-induced nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) secretion concomitant with downregulation of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Furthermore, PS inhibited the production of proinflammatory cytokines such as tumor necrosis factor-alpha ($TNF-{\alpha}$), interleukin-6 (IL-6), and IL-12 in LPS-stimulated RAW264.7 macrophages. Further study showed that PS significantly decreased LPS-induced nuclear translocation of the nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) subunits, p65 and p50. Molecular docking data showed that many anthocyanins from PS fit into the hydrophobic pocket of MD2 and bound to Toll-like receptor 4 (TLR4), indicating that PS inhibits the TLR4-MD2-mediated inflammatory signaling pathway. Especially, apigenin-7-O-glucoside most powerfully bound to MD2 and TLR4 through LYS122, LYS122, and SER127 at a distance of $2.205{\AA}$, $3.098{\AA}$, and $2.844{\AA}$ and SER441 at a distance of $2.873{\AA}$ (docking score: -8.4) through hydrogen bonding, respectively. Additionally, PS inhibited LPS-induced TLR4 dimerization/expression on the cell surface, which consequently decreased MyD88 recruitment and IRAK4 phosphorylation. PS completely blocked LPS-mediated mortality in zebrafish larvae by diminishing the recruitment of neutrophil and macrophages accompanied by low levels of proinflammatory cytokines. Taken together, our results indicate that PS attenuates LPS-mediated inflammation in both in vitro and in vivo by blocking the TLR4/MD2-MyD88/IRAK4-$NF-{\kappa}B$ axis. Therefore, PS might be used as a novel modulatory candidate for effective treatment of LPS-mediated inflammatory diseases.

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Mechanism of Human Endogenous Retrovirus (HERV) in Inflammatory Response (인간 내생 레트로바이러스(Human Endogenous Retrovirus, HERV)의 염증반응 조절 기작)

  • Ko, Eun-Ji;Cha, Hee-Jae
    • Journal of Life Science
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    • v.31 no.8
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    • pp.771-777
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    • 2021
  • Human endogenous retroviruses (HERVs) were inserted into the human genome millions of years ago but they are currently inactive and non-infectious due to recombinations, deletions, and mutations after insertion into the host genome. Nonetheless, recent studies have shown that HERV-derived elements are actually involved in physiological phenomena and certain diseases including cancers. Among the various physiological phenomena related to HERV-derived elements, it is necessary to focus on inflammatory response. HERV-derived elements have been reported to be directly involved in various inflammatory diseases, including autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, amyotrophic lateral sclerosis, and Sjogren's syndrome. As a mechanism for regulating inflammation through HERV-derived elements, the possibility that HERV-derived elements may cause nonspecific innate immune processes and that HERV-derived RNA or proteins may cause selective signaling mechanisms through specific receptors can be considered. However, the mechanism through which HERV-derived elements regulate inflammatory response, such as how silent HERV elements are activated in inflammatory response and what factors and signaling mechanisms are involved in HERV-derived elements, have not been identified to date, making it difficult to study the onset of HERV-related inflammatory disease. In this review, we introduce HERV-related autoimmune diseases and propose the mechanisms of HERV-derived elements at the molecular level of HERV in inflammatory response.