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[PMID]:29408309
[Au] Autor:Mohamed DI; Nabih ES; El-Waseef DAA; El-Kharashi OA; Abd El Samad AA
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
[Ti] Título:The protective effect of pentoxifylline versus silymarin on the pancreas through increasing adenosine by CD39 in a rat model of liver cirrhosis: Pharmacological, biochemical and histological study.
[So] Source:Gene;651:9-22, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Impaired glucose homoeostasis due to insulin resistance and decrease sensitivity of pancreatic ß-cells is a feature of liver disease and results into hepatogenous diabetes. Decrease expression of CD39 was linked to inflammation and occurrence of diabetes. Therefore, we performed this study to explore the protective effect of pentoxifylline (PTX) and silymarin administration on the ß-cells of the pancreas in a rat model of thioacetamide induced liver cirrhosis. Biochemical, histological and immunohistochemistry studies of the liver and pancreas were performed and provided an evidence on the protective effect of PTX to pancreatic ß-cells compared to silymarin. Also, silymarin induced a significant improvement of liver cirrhosis compared to PTX. In conclusion, the potential protective effect of PTX against ß-cells deterioration could be attributed to increasing pancreatic CD39 expression and the subsequent increase of adenosine.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Antígenos CD/metabolismo
Apirase/metabolismo
Cirrose Hepática Experimental/tratamento farmacológico
Pâncreas/efeitos dos fármacos
Pentoxifilina/uso terapêutico
Substâncias Protetoras/uso terapêutico
Silimarina/uso terapêutico
[Mh] Termos MeSH secundário: Amilases/sangue
Animais
Modelos Animais de Doenças
Células Secretoras de Insulina/efeitos dos fármacos
Fígado/patologia
Cirrose Hepática Experimental/metabolismo
Cirrose Hepática Experimental/patologia
Testes de Função Hepática
Masculino
Pâncreas/patologia
Ratos
Ratos Wistar
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Protective Agents); 0 (Silymarin); 0 (Transforming Growth Factor beta1); EC 3.2.1.- (Amylases); EC 3.6.1.5 (Apyrase); EC 3.6.1.5 (CD39 antigen); K72T3FS567 (Adenosine); SD6QCT3TSU (Pentoxifylline)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:29441915
[Au] Autor:Cao L-; Yan M; Ma YX; Zhang BK; Fang PF; Xiang DX; Li ZH; Gong H; Deng Y; Li HD
[Ti] Título:Isoliquiritigenin protects against triptolide-induced hepatotoxicity in mice through Nrf2 activation.
[So] Source:Pharmazie;71(7):394-397, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Isoliquiritigenin, a flavonoid found in licorice, has been considered as an antioxidive and hepato-protective agent. Recent studies have shown that a possible mechanism for triptolide-induced hepatotoxicity is related to oxidative damage induced by reactive oxygen species. This study was done to investigate the protection effect of isoliquiritigenin against triptolide-induced hepatotoxicity and the mechanism involved. An acute liver injury model was established by intraperitoneal injection of triptolide (1.0 mg · kg-1) in mice. Different doses of isoliquiritigenin (12.5, 25 and 50 mg · kg-1) were employed as protection. The activities of AST, ALT, ALP and LDH in serum and levels of GSH, GPx, SOD, CAT and MDA in liver tissue were detected. The histopathological changes of liver tissues were observed after HE staining. The protein expression of Nrf2 was detected by western blot. Pretreatment with isoliquiritigenin significantly prevented the triptolide-induced hepatotoxicity indicated by reduced activities of AST, ALT, ALP and LDH. Moreover, isoliquiritigenin pretreatment also prevented from triptolide-induced hepatotoxicity by inhibiting MDA and restoring the levels of GSH, GPx, SOD and CAT. In addition, isoliquiritigenin could attenuate histopathological changes induced by triptolide. Furthermore, the results indicated that isoliquiritigenin pretreatment caused an increase in the protein expression of Nrf2. These results indicated that isoliquiritigenin could protect against triptolide-induced hepatotoxicity via activation of the Nrf2 pathway.
[Mh] Termos MeSH primário: Chalconas/farmacologia
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Diterpenos/antagonistas & inibidores
Diterpenos/toxicidade
Fator 2 Relacionado a NF-E2/metabolismo
Fenantrenos/antagonistas & inibidores
Fenantrenos/toxicidade
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/patologia
Compostos de Epóxi/antagonistas & inibidores
Compostos de Epóxi/toxicidade
Fígado/efeitos dos fármacos
Fígado/metabolismo
Testes de Função Hepática
Masculino
Malondialdeído/antagonistas & inibidores
Camundongos
Camundongos Endogâmicos ICR
Fator 2 Relacionado a NF-E2/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chalcones); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (Phenanthrenes); 0 (Protective Agents); 19ALD1S53J (triptolide); 4Y8F71G49Q (Malondialdehyde); B9CTI9GB8F (isoliquiritigenin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6535


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[PMID]:29267498
[Au] Autor:Ni XJ; Xu ZQ; Jin H; Zheng SL; Cai Y; Wang JJ
[Ad] Endereço:Transplantation Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
[Ti] Título:Ginsenoside Rg1 protects human renal tubular epithelial cells from lipopolysaccharide-induced apoptosis and inflammation damage.
[So] Source:Braz J Med Biol Res;51(2):e6611, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Ginsenoside Rg1, one of the most notable active components of Panax ginseng, has been widely reported to exert anti-inflammatory actions. This study aimed to reveal whether ginsenoside Rg1 also exhibits beneficial roles against lipopolysaccharide (LPS)-induced apoptosis and inflammation in human renal tubular epithelial cells, and to evaluate the potential role of the component on tubulointerstitial nephritis treatment. HK-2 cells were treated with various doses of ginsenoside Rg1 (0, 50, 100, 150, and 200 µM) in the absence or presence of 5 µg/mL LPS. Thereafter, CCK-8 assay, flow cytometry, western blot, migration assay, reactive oxygen species (ROS) assay, and ELISA were carried out to respectively assess cell viability, apoptosis, migration, ROS activity, and the release of inflammatory cytokines. As a result, ginsenoside Rg1 protected HK-2 cells from LPS-induced injury, as cell viability was increased, cell apoptosis was decreased, and the release of MCP-1, IL-1ß, IL-6, and TNF-α was reduced. Ginsenoside Rg1 functioned to HK-2 cells in a dose-dependent manner, and the 150 µM dose exhibited the most protective functions. Ginsenoside Rg1 had no significant impact on cell migration and ROS activity, while it alleviated LPS-induced ROS release and migration impairment. Furthermore, the down-regulations of p-PI3K, p-AKT, and up-regulations of PTEN, p-IκBα, p-p65, Bcl-3 induced by LPS were recovered to some extent after ginsenoside Rg1 treatment. In conclusion, ginsenoside Rg1 protects HK-2 cells against LPS-induced inflammation and apoptosis via activation of the PI3K/AKT pathway and suppression of NF-κB pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Apoptose/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Ginsenosídeos/farmacologia
Túbulos Renais/citologia
Lipopolissacarídeos
Nefrite/prevenção & controle
[Mh] Termos MeSH secundário: Análise de Variância
Western Blotting
Linhagem Celular
Ensaios de Migração Celular
Sobrevivência Celular/efeitos dos fármacos
Citocinas/análise
Citocinas/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Túbulos Renais/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/análise
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Proteínas Proto-Oncogênicas c-akt/análise
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Espécies Reativas de Oxigênio/análise
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Ginsenosides); 0 (Lipopolysaccharides); 0 (Protective Agents); 0 (Reactive Oxygen Species); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); PJ788634QY (ginsenoside Rg1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29267497
[Au] Autor:Caires A; Fernandes GS; Leme AM; Castino B; Pessoa EA; Fernandes SM; Fonseca CD; Vattimo MF; Schor N; Borges FT
[Ad] Endereço:Disciplina de Nefrologia, Departamento de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
[Ti] Título:Endothelin-1 receptor antagonists protect the kidney against the nephrotoxicity induced by cyclosporine-A in normotensive and hypertensive rats.
[So] Source:Braz J Med Biol Res;51(2):e6373, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Cyclosporin-A (CsA) is an immunosuppressant associated with acute kidney injury and chronic kidney disease. Nephrotoxicity associated with CsA involves the increase in afferent and efferent arteriole resistance, decreased renal blood flow (RBF) and glomerular filtration. The aim of this study was to evaluate the effect of Endothelin-1 (ET-1) receptor blockade with bosentan (BOS) and macitentan (MAC) antagonists on altered renal function induced by CsA in normotensive and hypertensive animals. Wistar and genetically hypertensive rats (SHR) were separated into control group, CsA group that received intraperitoneal injections of CsA (40 mg/kg) for 15 days, CsA+BOS and CsA+MAC that received CsA and BOS (5 mg/kg) or MAC (25 mg/kg) by gavage for 15 days. Plasma creatinine and urea, mean arterial pressure (MAP), RBF and renal vascular resistance (RVR), and immunohistochemistry for ET-1 in the kidney cortex were measured. CsA decreased renal function, as shown by increased creatinine and urea. There was a decrease in RBF and an increase in MAP and RVR in normotensive and hypertensive animals. These effects were partially reversed by ET-1 antagonists, especially in SHR where increased ET-1 production was observed in the kidney. Most MAC effects were similar to BOS, but BOS seemed to be better at reversing cyclosporine-induced changes in renal function in hypertensive animals. The results of this work suggested the direct participation of ET-1 in renal hemodynamics changes induced by cyclosporin in normotensive and hypertensive rats. The antagonists of ET-1 MAC and BOS reversed part of these effects.
[Mh] Termos MeSH primário: Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/prevenção & controle
Ciclosporina/toxicidade
Antagonistas do Receptor de Endotelina A/farmacologia
Imunossupressores/toxicidade
Pirimidinas/farmacologia
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/fisiopatologia
Animais
Creatinina/sangue
Antagonistas do Receptor de Endotelina A/uso terapêutico
Hemodinâmica
Immunoblotting
Imuno-Histoquímica
Rim/efeitos dos fármacos
Rim/fisiopatologia
Masculino
Estresse Oxidativo/fisiologia
Substâncias Protetoras/farmacologia
Substâncias Protetoras/uso terapêutico
Pirimidinas/uso terapêutico
Ratos Endogâmicos SHR
Ratos Wistar
Reprodutibilidade dos Testes
Sulfonamidas/uso terapêutico
Resultado do Tratamento
Ureia/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin A Receptor Antagonists); 0 (Immunosuppressive Agents); 0 (Protective Agents); 0 (Pyrimidines); 0 (Sulfonamides); 83HN0GTJ6D (Cyclosporine); 8W8T17847W (Urea); AYI8EX34EU (Creatinine); Q326023R30 (bosentan); Z9K9Y9WMVL (macitentan)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29378549
[Au] Autor:Li S; Pasquin S; Eid HM; Gauchat JF; Saleem A; Haddad PS
[Ad] Endereço:Department of Pharmacology and Physiology, Université de Montréal, P.O. Box 6128, Downtown Postal Station, Montreal, (Quebec), H3C 3J7, Canada.
[Ti] Título:Anti-apoptotic potential of several antidiabetic medicinal plants of the eastern James Bay Cree pharmacopeia in cultured kidney cells.
[So] Source:BMC Complement Altern Med;18(1):37, 2018 Jan 30.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Our team has identified 17 Boreal forest species from the traditional pharmacopeia of the Eastern James Bay Cree that presented promising in vitro and in vivo biological activities in the context of type 2 diabetes (T2D). We now screened the 17 plants extracts for potential anti-apoptotic activity in cultured kidney cells and investigated the underlying mechanisms. METHODS: MDCK (Madin-Darnby Canine Kidney) cell damage was induced by hypertonic medium (700 mOsm/L) in the presence or absence of maximal nontoxic concentrations of each of the 17 plant extracts. After 18 h' treatment, cells were stained with Annexin V (AnnV) and Propidium iodide (PI) and subjected to flow cytometry to assess the cytoprotective (AnnV /PI ) and anti-apoptotic (AnnV /PI ) potential of the 17 plant extracts. We then selected a representative subset of species (most cytoprotective, moderately so or neutral) to measure the activity of caspases 3, 8 and 9. RESULTS: Gaultheria hispidula and Abies balsamea are amongst the most powerful cytoprotective and anti-apoptotic plants and appear to exert their modulatory effect primarily by inhibiting caspase 9 in the mitochondrial apoptotic signaling pathway. CONCLUSION: We conclude that several Cree antidiabetic plants exert anti-apoptotic activity that may be relevant in the context of diabetic nephropathy (DN) that affects a significant proportion of Cree diabetics.
[Mh] Termos MeSH primário: Hipoglicemiantes/farmacologia
Medicina Tradicional
Extratos Vegetais/farmacologia
Plantas Medicinais/química
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Anexina A5/química
Apoptose/efeitos dos fármacos
Canadá
Caspases/metabolismo
Nefropatias Diabéticas/metabolismo
Cães
Hipoglicemiantes/química
Células Madin Darby de Rim Canino
Extratos Vegetais/química
Propídio/química
Substâncias Protetoras/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Hypoglycemic Agents); 0 (Plant Extracts); 0 (Protective Agents); 36015-30-2 (Propidium); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2104-1


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[PMID]:29302038
[Au] Autor:Lucas S; Omata Y; Hofmann J; Böttcher M; Iljazovic A; Sarter K; Albrecht O; Schulz O; Krishnacoumar B; Krönke G; Herrmann M; Mougiakakos D; Strowig T; Schett G; Zaiss MM
[Ad] Endereço:Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054, Erlangen, Germany.
[Ti] Título:Short-chain fatty acids regulate systemic bone mass and protect from pathological bone loss.
[So] Source:Nat Commun;9(1):55, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Microbial metabolites are known to modulate immune responses of the host. The main metabolites derived from microbial fermentation of dietary fibers in the intestine, short-chain fatty acids (SCFA), affect local and systemic immune functions. Here we show that SCFA are regulators of osteoclast metabolism and bone mass in vivo. Treatment of mice with SCFA as well as feeding with a high-fiber diet significantly increases bone mass and prevents postmenopausal and inflammation-induced bone loss. The protective effects of SCFA on bone mass are associated with inhibition of osteoclast differentiation and bone resorption in vitro and in vivo, while bone formation is not affected. Mechanistically, propionate (C3) and butyrate (C4) induce metabolic reprogramming of osteoclasts resulting in enhanced glycolysis at the expense of oxidative phosphorylation, thereby downregulating essential osteoclast genes such as TRAF6 and NFATc1. In summary, these data identify SCFA as potent regulators of osteoclast metabolism and bone homeostasis.
[Mh] Termos MeSH primário: Reabsorção Óssea/metabolismo
Osso e Ossos/metabolismo
Ácidos Graxos Voláteis/metabolismo
Osteoclastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Densidade Óssea/efeitos dos fármacos
Reabsorção Óssea/prevenção & controle
Osso e Ossos/efeitos dos fármacos
Butiratos/metabolismo
Butiratos/farmacologia
Fibras na Dieta/administração & dosagem
Ácidos Graxos Voláteis/farmacologia
Feminino
Expressão Gênica/efeitos dos fármacos
Glicólise/efeitos dos fármacos
Seres Humanos
Camundongos Endogâmicos C57BL
Osteoclastos/efeitos dos fármacos
Propionatos/metabolismo
Propionatos/farmacologia
Substâncias Protetoras/metabolismo
Substâncias Protetoras/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Butyrates); 0 (Dietary Fiber); 0 (Fatty Acids, Volatile); 0 (Propionates); 0 (Protective Agents)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02490-4


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[PMID]:29353722
[Au] Autor:Xu GB; Xiao YH; Zhang QY; Zhou M; Liao SG
[Ad] Endereço:School of Pharmacy/State Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang 550004, Guizhou, China; National Engineering Research Center of Miao's Medicines & Engineering Research Center for the Development and Application of Ethnic Medicine and
[Ti] Título:Hepatoprotective natural triterpenoids.
[So] Source:Eur J Med Chem;145:691-716, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Liver diseases are one of the leading causes of death in the world. In spite of tremendous advances in modern drug research, effective and safe hepatoprotective agents are still in urgent demand. Natural products are undoubtedly valuable sources for drug leads. A number of natural triterpenoids were reported to possess pronounced hepatoprotective effects, and triterpenoids have become one of the most important classes of natural products for hepatoprotective agents. However, the significance of natural triterpenoids has been underestimated in the hepatoprotective drug discovery, with only very limited triterpenoids being covered in the reviews of hepatoprotective natural products. In this paper, ca 350 natural triterpenoids with reported hepatoprotective effects in ca 120 references between 1975 and 2016 will be reviewed, and the structure-activity relationships of certain types of natural triterpenoids, if available, will be discussed. Patents are not included.
[Mh] Termos MeSH primário: Produtos Biológicos/farmacologia
Hepatopatias/tratamento farmacológico
Fígado/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Triterpenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Produtos Biológicos/química
Relação Dose-Resposta a Droga
Seres Humanos
Fígado/patologia
Estrutura Molecular
Substâncias Protetoras/química
Relação Estrutura-Atividade
Triterpenos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biological Products); 0 (Protective Agents); 0 (Triterpenes)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


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[PMID]:29442003
[Au] Autor:Li Z; Shu J; Yang B; Xu C; Zou Y; Sun W
[Ti] Título:Evaluating the relationship between cell viability and volatile organic compound production following DMSO treatment of cultured human cells.
[So] Source:Pharmazie;71(12):727-732, 2016 12 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Methylsulfinylmethane (dimethyl sulfoxide; DMSO) is widely used in clinical treatment and bioresearch. Moreover, there is bioconversion between methylsulfanylmethane (dimethyl sulfide; DMS), DMSO, and methylsulfonylmethane (DMSO2) in mammalian metabolism. Due to the real-time detection limits for volatile compounds, most research has focused on DMSO2 as a stable byproduct of DMSO. Therefore, details about the production of DMS as a byproduct of DMSO metabolism remain to be elucidated. Here, we report the characterization of trace-level volatile organic compounds (VOCs) produced following DMSO treatment of cultured human cells using an ultrasensitive vacuum ultraviolet photoionization mass spectrometer (VUV-PIMS). Using this approach, 24 h after DMSO treatment we detected 16.9 and 21 parts per billion by volume (ppbv) DMS in the atmosphere above the cells (headspace) within HeLa and 293T tissue culture flasks, respectively. When simultaneously exposed to 50 nM paclitaxel (PTX), 17.6 and 22.3 ppbv DMS were detected in the headspace of HeLa and 293T culture flasks, respectively. Nevertheless, at doses of PTX more or less than 50 nM, the detectable levels of DMS were reduced to as low as 8.4 ppbv. Our experimental results demonstrate that by co-administering 5 to 10 nM PTX with DMSO, it is possible to moderate the production of DMS considerably. However, at higher doses of PTX, increased apoptosis was observed that likely contributed to higher DMS production by cells.
[Mh] Termos MeSH primário: Sobrevivência Celular/efeitos dos fármacos
Dimetil Sulfóxido/farmacologia
Substâncias Protetoras/farmacologia
Compostos Orgânicos Voláteis/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos Fitogênicos/antagonistas & inibidores
Antineoplásicos Fitogênicos/toxicidade
Células Cultivadas
Células HEK293
Células HeLa
Seres Humanos
Paclitaxel/antagonistas & inibidores
Paclitaxel/toxicidade
Sulfonas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Protective Agents); 0 (Sulfones); 0 (Volatile Organic Compounds); 9H4PO4Z4FT (dimethyl sulfone); P88XT4IS4D (Paclitaxel); YOW8V9698H (Dimethyl Sulfoxide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6075


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[PMID]:29342206
[Au] Autor:Papackova Z; Heczkova M; Dankova H; Sticova E; Lodererova A; Bartonova L; Poruba M; Cahova M
[Ad] Endereço:Department of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
[Ti] Título:Silymarin prevents acetaminophen-induced hepatotoxicity in mice.
[So] Source:PLoS One;13(1):e0191353, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acetaminophen or paracetamol (APAP) overdose is a common cause of liver injury. Silymarin (SLM) is a hepatoprotective agent widely used for treating liver injury of different origin. In order to evaluate the possible beneficial effects of SLM, Balb/c mice were pretreated with SLM (100 mg/kg b.wt. per os) once daily for three days. Two hours after the last SLM dose, the mice were administered APAP (300 mg/kg b.wt. i.p.) and killed 6 (T6), 12 (T12) and 24 (T24) hours later. SLM-treated mice exhibited a significant reduction in APAP-induced liver injury, assessed according to AST and ALT release and histological examination. SLM treatment significantly reduced superoxide production, as indicated by lower GSSG content, lower HO-1 induction, alleviated nitrosative stress, decreased p-JNK activation and direct measurement of mitochondrial superoxide production in vitro. SLM did not affect the APAP-induced decrease in CYP2E1 activity and expression during the first 12 hrs. Neutrophil infiltration and enhanced expression of inflammatory markers were first detected at T12 in both groups. Inflammation progressed in the APAP group at T24 but became attenuated in SLM-treated animals. Histological examination suggests that necrosis the dominant cell death pathway in APAP intoxication, which is partially preventable by SLM pretreatment. We demonstrate that SLM significantly protects against APAP-induced liver damage through the scavenger activity of SLM and the reduction of superoxide and peroxynitrite content. Neutrophil-induced damage is probably secondary to necrosis development.
[Mh] Termos MeSH primário: Acetaminofen/efeitos adversos
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Silimarina/farmacologia
[Mh] Termos MeSH secundário: Acetaminofen/farmacologia
Animais
Overdose de Drogas/patologia
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Necrose/patologia
Substâncias Protetoras/farmacologia
Silimarina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Protective Agents); 0 (Silymarin); 362O9ITL9D (Acetaminophen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191353


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[PMID]:29367149
[Au] Autor:Shanuja SK; Iswarya S; Gnanamani A
[Ad] Endereço:Microbiology Division, CSIR-CLRI, Adyar, Chennai 20, India.
[Ti] Título:Marine fungal DHICA as a UVB protectant: Assessment under in vitro and in vivo conditions.
[So] Source:J Photochem Photobiol B;179:139-148, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The present study explores UVB protective role of a melanin precursor namely DHICA (5,6- Dihydroxyindole-2-carboxylic acid) expressed by the marine imperfect fungus Aspergillus nidulans. In brief, A. nidulans grown in a modified growth medium for the period of 5 days at 25 °C under shaking conditions and the extracellular medium free from fungal biomass used for the extraction of DHICA. The extracted DHICA further exposed to partial purification and subjected to UVB protection studies using HaCaT cells and Balb/c mice independently. DHICA obtained in the present study found soluble in water. Experiments on HaCaT cell compatibility revealed nil cell death up to 500 µM concentration of DHICA. UVB protection studies under in vitro conditions emphasizes DHICA significantly protect HaCaT cells from UVB exposure by quenching the generated ROS, reducing cell apoptosis, maintain the cellular integrity and sequentially down regulating the LPO (Lipid peroxidation) and up-regulating the antioxidant enzyme (SOD (Superoxide Dismutase), Catalase, GPx (Glutathione peroxidase)) respectively. Further, experiments on cell cycle arrest analysis, gelatin zymography, and western blot analysis on COX-2 and TNF-alpha, IHC (Immunohistochemistry) on apoptotic markers (Bax, Bcl2) substantiate the protective role of DHICA. Furthermore, in vivo studies on BALB/c mice carried out and compared with the sunscreen cream with sun protective factor (SPF) of 20. Analysis of skin sections of experimental samples revealed that an appreciable reduction in the epidermal thickness of the skin samples of mice pre-exposed to DHICA followed by UVB exposure compared to UVB exposure alone. RT-PCR results on various inflammatory apoptotic markers also suggested that DHICA has UVB protective potential. The observations made in the present study explore the possible application of DHICA alone as a sun-protective agent for skin care.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Aspergillus nidulans/metabolismo
Indóis/farmacologia
Pele/efeitos dos fármacos
Raios Ultravioleta
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Catalase/metabolismo
Linhagem Celular
Dano ao DNA/efeitos dos fármacos
Feminino
Glutationa Peroxidase/metabolismo
Seres Humanos
Indóis/química
Peroxidação de Lipídeos/efeitos dos fármacos
Melaninas/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Estresse Oxidativo/efeitos dos fármacos
Substâncias Protetoras/química
Substâncias Protetoras/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Pele/patologia
Pele/efeitos da radiação
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Indoles); 0 (Melanins); 0 (Protective Agents); 0 (Reactive Oxygen Species); 4790-08-3 (5,6-dihydroxy-2-indolylcarboxylic acid); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE



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