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1.
Medicine (Baltimore) ; 103(7): e36436, 2024 Feb 16.
Artigo em Inglês | MEDLINE | ID: mdl-38363901

RESUMO

This study aimed to analyze the distribution of gout patients and the utilization of healthcare services in South Korea to provide valuable recommendations to clinicians and policymakers. A cross-sectional study was conducted. Claims data from the Health Insurance Review and Assessment Service spanning 2010 to 2019 were utilized, and a sample of 69,680 patients was included in the study. The incidence of gout was observed to be high in male patients over the age of 40, with most patients receiving outpatient care for gout management. Nonsteroidal anti-inflammatory drugs and urate-lowering agents were the most frequently prescribed medications, with prescriptions for colchicine and febuxostat increasing among urate-lowering agents. Musculoskeletal disorders were found to be the most common comorbidities among gout patients. Although the total costs of gout management increased, there was no significant increase in cost per patient. This study provides insights into the current state of healthcare utilization for gout patients in South Korea and trends in the disease burden and use of medications. The findings have crucial implications for clinicians and policymakers involved in decision-making regarding the management and treatment of gout.


Assuntos
Supressores da Gota , Gota , Humanos , Masculino , Supressores da Gota/uso terapêutico , Estudos Transversais , Ácido Úrico , Gota/tratamento farmacológico , Gota/epidemiologia , Febuxostat/uso terapêutico , Seguro Saúde , Custos de Cuidados de Saúde , Aceitação pelo Paciente de Cuidados de Saúde
2.
J Pharmacopuncture ; 24(4): 182-190, 2021 Dec 31.
Artigo em Inglês | MEDLINE | ID: mdl-35028169

RESUMO

OBJECTIVES: The purpose of this study was to analyze the microneedle therapy system (MTS) and its research methods for the past 10 years in Korea. METHODS: Data on microneedle therapy system were collected using NDSL, KISS, RISS, and OASIS electronic databases from January 2010 to August 2021. "microneedle," "derma stamp," "microneedle therapy system" were used as the keywords. The present study, however, excluded data that were 1) unrelated to the microneedle therapy system, 2) from review/meta/protocol studies, and 3) from overseas studies. Data selected through the primary screening process, animal studies, case reports, and clinical data were included in the analysis. However, information data not related to the microneedle therapy system were excluded from the study. RESULTS: Among the MTS-related papers published from January 2010 to August 2021, 7 animal research, 2 clinical trials, and 10 case studies were published. Based on the research topics, there were 8 papers on skin improvement and skin diseases, 7 papers on hair growth and hair loss, 3 papers on stability, and 1 paper on peripheral facial paralysis. CONCLUSION: Most of the studies related to MTS focused on skin, hair, and stability. The effect of MTS on hair growth and skin improvement has been confirmed, and it has been proven to have significant effects on the treatment of acne, acne scars, and hair loss in clinical practice. No serious side effects were observed during the MTS treatment, and the safety assessment confirmed that it was safe for use.

3.
J Pharmacopuncture ; 24(4): 173-181, 2021 Dec 31.
Artigo em Inglês | MEDLINE | ID: mdl-35028168

RESUMO

OBJECTIVES: The aim of this review was to appraise Korean studies published between 2010 and 2021 which examined the role of acupuncture in the treatment of obesity. METHODS: We performed a search of the NDSL, KISS, RISS, OASIS, PubMed, EMBASE electronic databases for relevant animal researches, case reports, and clinical trials, using the following search terms 'obesity', 'acupuncture', 'electroacupuncture', and 'pharmacopuncture'. We excluded previous reviews and meta-analyses, studies not related to obesity or acupuncture treatment, as well as studies conducted in countries other than Korea. We also excluded studies where relevant information on acupuncture treatment in obesity could not be obtained. RESULTS: Most studies were conducted in animals, followed by case reports and clinical trials. In animal researches and case reports, pharmacopuncture was the most used intervention. In case studies, electroacupuncture, thread-embedding therapy, manual acupuncture, acupotomy, and auricular acupuncture were also used. In animal researches, pharmacopuncture treatment was associated with improvement in obesity indices. In the case of local obesity, specific acupuncture techniques such as thread-embedding therapy and pharmacopuncture were associated with significant improvements in local obesity, even when diet and exercise were not controlled for. CONCLUSION: Acupuncture treatment showed significant benefit in the treatment of obesity, with a local effect evident for certain approaches, such thread-embedding therapy and acupotomy.

4.
Eur J Pharmacol ; 582(1-3): 17-25, 2008 Mar 17.
Artigo em Inglês | MEDLINE | ID: mdl-18241858

RESUMO

Biphenolic components in Magnolia obovata including magnolol and honokiol have shown several pharmacological activities such as anti-tumor, anti-oxidant and anti-inflammatory effects. Previously in cultured macrophage Raw264.7 cells and fibroblast, we found that obovatol, an active compound isolated from M. obovata inhibited NF-kappaB activity which has been known to be a significant transcriptional factor to control of cancer cell growth. We investigated here whether obovatol could inhibit NF-kappaB activity, and thereby inhibit cancer cell growth in prostate (LNCaP and PC-3) and colon cancer (SW620 and HCT116) cells. Treatment of obovatol (10, 15, 20, 25 microM) inhibits cancer cell growth in the absence or the presence of tumor necrosis factor-alpha (TNF-alpha , 10 ng/ml) and tetradecanoyl phorbol acetate (TPA 10 or 50 nM) in a concentration-dependent manner through induction of apoptotic cell death. Cytotoxic activity was not observed in normal cells with up to 50 muM obovatol. It was also found that obovatol inhibited TNF-alpha and TPA-induced transcriptional and DNA binding activities of NF-kappaB. In further study, obovatol decreased translocation p65 and p50 into nucleus via decrease of phosphorylation of IkappaB. Correlated well with the induction of apoptosis, obovatol increased the expression of the apoptotic genes; Bax, caspase-3, caspase-9, whereas inhibited expression of anti-apoptotic genes; Bcl-2, inhibitor of apoptosis protein (IAP-1) and X chromosome IAP (XIAP) as well as the cell proliferation marker genes; Cox-2, c-Fos, c-Jun and cyclin D1. These results suggest that obovatol inhibits prostate and colon cancer cell growth via induction of apoptotic cell death, and that inhibition of NF-kappaB may be a significant as its action mechanism.


Assuntos
Apoptose , Compostos de Bifenilo/farmacologia , Neoplasias do Colo/patologia , NF-kappa B/antagonistas & inibidores , Éteres Fenílicos/farmacologia , Neoplasias da Próstata/patologia , Caspases/metabolismo , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Neoplasias do Colo/metabolismo , Relação Dose-Resposta a Droga , Humanos , Masculino , NF-kappa B/metabolismo , Fosforilação , Neoplasias da Próstata/metabolismo , Acetato de Tetradecanoilforbol/farmacologia , Transcrição Gênica , Fator de Necrose Tumoral alfa/farmacologia
5.
Cancer Biol Ther ; 12(4): 288-96, 2011 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-21613824

RESUMO

PPARγ ligands have been reported to reduce proliferation of human prostate cancer cells. However, the molecular mechanism of PPARγ agonist-induced cell growth inhibition of prostate cancer cells is not clear. GSK-3ß expression and NFκB activity have important roles in prostate cancer development. To investigate the mechanisms of the PPARγ agonist-induced prostate cancer cell growth inhibition, we examined the effect of troglitazone on the expression of PPARγ, GSK-3ß and activity of NFκB as well as on the prostate cancer cell growth. Troglitazone induced the expression of PPARγ in the nuclear of PC-3 cells, but not in LNCaP cells. Troglitazone (0-16 uM) inhibited cancer cell growth in a similar extend between both cells accompanied by the induction of cell cycle arrest in G(0)/G(1) phase and an increased in the similar extent of apoptotic cell death in concentration dependent manner. Troglitazone inhibited the constitutive expression of GSK-3ß and activation of NFκB. Co-treatment of troglitazone with a GSK-3ß inhibitor (AR-a014418) or GSK-3ß siRNA significantly augmented the inhibitory effect of troglitazone on the NFκB activity and on prostate cancer cell growth inhibition and apoptotic cell death. However, overexpression of GSK-3ß hindered troglitazone-induced cell growth inhibition and NFκB inactivation. These results suggest that PPARγ agonist, troglitazone, inhibits prostate cancer cell growth through inactivation of NFκB via suppression of GSK-3ß expression.


Assuntos
Proliferação de Células/efeitos dos fármacos , Cromanos/farmacologia , Quinase 3 da Glicogênio Sintase/metabolismo , NF-kappa B/metabolismo , PPAR gama/agonistas , Tiazolidinedionas/farmacologia , Apoptose/efeitos dos fármacos , Ciclo Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Núcleo Celular/efeitos dos fármacos , Núcleo Celular/metabolismo , Relação Dose-Resposta a Droga , Fase G1/efeitos dos fármacos , Quinase 3 da Glicogênio Sintase/antagonistas & inibidores , Quinase 3 da Glicogênio Sintase/genética , Glicogênio Sintase Quinase 3 beta , Humanos , Immunoblotting , Masculino , Microscopia de Fluorescência , Neoplasias da Próstata/genética , Neoplasias da Próstata/metabolismo , Neoplasias da Próstata/patologia , Interferência de RNA , Fase de Repouso do Ciclo Celular/efeitos dos fármacos , Tiazóis/farmacologia , Troglitazona , Ureia/análogos & derivados , Ureia/farmacologia
6.
Chem Biol Interact ; 188(1): 75-85, 2010 Oct 06.
Artigo em Inglês | MEDLINE | ID: mdl-20540935

RESUMO

Peroxisome proliferator-activated receptor (PPAR)-gamma agonists such as troglitazone, pioglitazone and thiazolidine have been shown to induce apoptosis in human colon cancer cells. The molecular mechanism of PPARgamma agonist-induced apoptosis of colon cancer cells, however, is not clear. Glycogen synthase kinase-3beta (GSK-3beta) is an indispensable element for the activation of nuclear factor-kappa B (NF-kappaB) which plays a critical role in the mediation of survival signals in cancer cells. To investigate the mechanisms of PPARgamma agonist-induced apoptosis of colon cancer cells, we examined the effect of troglitazone (0-16muM) on the activation of GSK-3beta and NF-kappaB. Our study showed that the inhibitory effect of troglitazone on colon cancer cell growth was associated with inhibition of NF-kappaB activity and GSK-3beta expression in a dose-dependent manner. Cells were arrested in G(0)/G(1) phase followed by the induction of apoptosis after treatment of troglitazone with concomitant decrease in the expression of the G(0)/G(1) phase regulatory proteins; Cdk2, Cdk4, cyclin B1, D1, and E as well as in the anti-apoptosis protein Bcl-2 along with an increase in the expression of the pro-apoptosis-associated proteins; Caspase-3, Caspase-9 and Bax. Transient transfection of GSK-3beta recovered troglitazone-induced cell growth inhibition and NF-kappaB inactivation. In contrast, co-treatment of troglitazone with a GSK-3beta inhibitor (AR-a014418) or siRNA against GSK-3beta, significantly augmented the inhibitory effect of troglitazone on the NF-kappaB activity, the cancer cell growth and on the expression of G(0)/G(1) phase regulatory proteins and pro-apoptosis regulatory proteins. These results suggest that the PPARgamma agonist, troglitazone, inhibits colon cancer cell growth via inactivation of NF-kappaB by suppressing GSK-3beta activity.


Assuntos
Cromanos/farmacologia , Neoplasias do Colo/patologia , Quinase 3 da Glicogênio Sintase/antagonistas & inibidores , NF-kappa B/antagonistas & inibidores , PPAR gama/agonistas , Tiazolidinedionas/farmacologia , Ciclo Celular/efeitos dos fármacos , Divisão Celular , Ensaio de Desvio de Mobilidade Eletroforética , Citometria de Fluxo , Glicogênio Sintase Quinase 3 beta , Humanos , Troglitazona
7.
Biochemistry ; 44(23): 8326-36, 2005 Jun 14.
Artigo em Inglês | MEDLINE | ID: mdl-15938622

RESUMO

Cobrotoxin is known to bind with cysteine residues of biological molecules such as nicotine acetylcholine receptor. Cobrotoxin may modify IKKs and p50 through protein-protein interaction since cysteine residues are present in the kinase domains of IKKalpha and IKKbeta and in the p50 of NF-kappaB. Our surface plasmon resonance analysis showed that cobrotoxin directly binds to p50 (K(d) = 1.54 x 10(-)(5) M), IKKalpha (K(d) = 3.94 x 10(-)(9) M) and IKKbeta (K(d) = 3.4 x 10(-)(8) M) with high binding affinity. Moreover, these protein-protein interactions suppressed the lipopolysaccharide (LPS, 1 microg/mL)- and the sodium nitroprusside (SNP, 200 microM)-induced DNA binding activity of NF-kappaB and NF-kappaB-dependent luciferase activity in astrocytes and Raw 264.7 macrophages. These inhibitory effects were correlated with the inhibition of IkappaB release and p50 translocation. Inhibition of NF-kappaB by cobrotoxin resulted in reductions in the LPS-induced expressions of COX-2, iNOS, cPLA(2), IL-4, and TNF-alpha in astrocytes and in COX-2 expression induced by SNP, LPS, and TNF-alpha in astrocytes. Moreover, these inhibitory effects of cobrotoxin were reversed by adding reducing agents, dithiothreitol and glutathione. In addition, cobrotoxin did not have any inhibitory effect on NF-kappaB activity in cells carrying mutant p50 (C62S), IKKalpha (C178A), and IKKbeta (C179A), with the exception of IKKbeta (K44A) mutant plasmid. Confocal microscopic analysis showed that cobrotoxin is uptaken into the nucleus of cells. These results demonstrate that cobrotoxin directly binds to the sulfhydryl groups of p50 and IKKs, and that this results in reduced IkappaB release and the translocation of p50, thereby inhibiting the activation of NF-kappaB.


Assuntos
Proteínas Neurotóxicas de Elapídeos/química , Regulação da Expressão Gênica/efeitos dos fármacos , Inativação Gênica/efeitos dos fármacos , NF-kappa B/antagonistas & inibidores , NF-kappa B/metabolismo , Precursores de Proteínas/antagonistas & inibidores , Precursores de Proteínas/metabolismo , Transdução de Sinais/genética , Animais , Astrócitos/efeitos dos fármacos , Astrócitos/enzimologia , Astrócitos/metabolismo , Ligação Competitiva/efeitos dos fármacos , Linhagem Celular , Células Cultivadas , Proteínas Neurotóxicas de Elapídeos/metabolismo , Cisteína/química , Cisteína/metabolismo , Proteínas de Ligação a DNA/antagonistas & inibidores , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Proteínas de Ligação a DNA/fisiologia , Inibidores Enzimáticos/química , Inibidores Enzimáticos/metabolismo , Regulação da Expressão Gênica/fisiologia , Quinase I-kappa B , Luciferases/antagonistas & inibidores , Luciferases/metabolismo , Camundongos , NF-kappa B/fisiologia , Subunidade p50 de NF-kappa B , Ligação Proteica/efeitos dos fármacos , Precursores de Proteínas/fisiologia , Proteínas Serina-Treonina Quinases/antagonistas & inibidores , Proteínas Serina-Treonina Quinases/metabolismo , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia
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