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[PMID]: 29441970 [Au] Autor: Ohkura N; Ohnishi K; Taniguchi M; Nakayama A; Usuba Y; Fujita M; Fujii A; Ishibashi K; Baba K; Atsumi G [Ti] Título: Anti-platelet effects of chalcones from Koidzumi (Ashitaba) . [So] Source: Pharmazie;71(11):651-654, 2016 Nov 02. [Is] ISSN: 0031-7144 [Cp] País de publicação: Germany [La] Idioma: eng [Ab] Resumo: Angelica keiskei Koidzumi (Ashitaba) is a traditional folk medicine that is also regarded in Japan as a health food with potential antithrombotic properties. The ability of the major chalcones, xanthoangelol (XA) and 4-hydroxyderricin (4-HD) extracted from Ashitaba roots to inhibit platelet aggregation activity in vitro was recently determined. However, the anti-platelet activities of Ashitaba chalcones in vivo have remained unclear. The present study examines the anti-platelet effects of Ashitaba exudate and its constituent chalcones using mouse tail-bleeding models that reflect platelet aggregation in vivo. Ashitaba exudate and the major chalcone subtype XA, suppressed the lipopolysaccharide (LPS)-induced shortening of mouse tail bleeding. However, trace amounts of other Ashitaba chalcone subtypes including xanthoangelols B (XB), D (XD), E (XE) and F (XF) did not affect tail bleeding. These results suggest that the major chalcone subtype in Ashitaba, XA, has anti-platelet-activities in vivo. [Mh] Termos MeSH primário: Angelica/química Chalconas/farmacologia Inibidores da Agregação de Plaquetas/farmacologia [Mh] Termos MeSH secundário: Animais Chalconas/química Hemorragia/tratamento farmacológico Lipopolissacarídeos/antagonistas & inibidores Lipopolissacarídeos/farmacologia Masculino Camundongos Camundongos Endogâmicos ICR Raízes de Plantas/química Agregação Plaquetária/efeitos dos fármacos Inibidores da Agregação de Plaquetas/química [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Chalcones); 0 (Lipopolysaccharides); 0 (Platelet Aggregation Inhibitors) [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.2016.6678

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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]: 29180018 [Au] Autor: Chen X; Cai X; Le R; Zhang M; Gu X; Shen F; Hong G; Chen Z [Ad] Endereço: Department of Endocrinology, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China. [Ti] Título: Isoliquiritigenin protects against sepsis-induced lung and liver injury by reducing inflammatory responses. [So] Source: Biochem Biophys Res Commun;496(2):245-252, 2018 02 05. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Sepsis, one of the most fatal diseases worldwide, often leads to multiple organ failure, mainly due to uncontrolled inflammatory responses. Despite accumulating knowledge obtained in recent years, effective drugs to treat sepsis in the clinic are still urgently needed. Isoliquiritigenin (ISL), a chalcone compound, has been reported to exert anti-inflammatory properties. However, little is known about the effects of ISL on sepsis and its related complications. In this study, we investigated the potential protective effects of ISL on lipopolysaccharide (LPS)-induced injuries and identified the mechanisms underlying these effects. ISL inhibited inflammatory cytokine expression in mouse primary peritoneal macrophages (MPMs) exposed to LPS. In an acute lung injury (ALI) mouse model, ISL prevented LPS-induced structural damage and inflammatory cell infiltration. Additionally, pretreatment with ISL attenuated sepsis-induced lung and liver injury, accompanied by a reduction in inflammatory responses. Moreover, these protective effects were mediated by the nuclear factor kappa B (NF-κB) pathway-mediated inhibition of inflammatory responses in vitro and in vivo. Our study suggests that ISL may be a potential therapeutic agent for sepsis-induced injuries. [Mh] Termos MeSH primário: Lesão Pulmonar Aguda/tratamento farmacológico Anti-Inflamatórios/farmacologia Chalconas/farmacologia Pulmão/efeitos dos fármacos Sepse/tratamento farmacológico [Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/induzido quimicamente Lesão Pulmonar Aguda/imunologia Lesão Pulmonar Aguda/patologia Animais Citocinas/genética Citocinas/imunologia Modelos Animais de Doenças Regulação da Expressão Gênica Células Hep G2 Seres Humanos Lipopolissacarídeos Fígado/efeitos dos fármacos Fígado/imunologia Fígado/patologia Pulmão/imunologia Pulmão/patologia Macrófagos Peritoneais/efeitos dos fármacos Macrófagos Peritoneais/imunologia Macrófagos Peritoneais/patologia Masculino Camundongos Camundongos Endogâmicos C57BL NF-kappa B/genética NF-kappa B/imunologia Cultura Primária de Células Sepse/induzido quimicamente Sepse/imunologia Sepse/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Anti-Inflammatory Agents); 0 (Chalcones); 0 (Cytokines); 0 (Lipopolysaccharides); 0 (NF-kappa B); B9CTI9GB8F (isoliquiritigenin) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180214 [Lr] Data última revisão: 180214 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171129 [St] Status: MEDLINE

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[PMID]: 27773742 [Au] Autor: Mahalingam S; Gao L; Eisner J; Helferich W; Flaws JA [Ad] Endereço: Department of Comparative Biosciences, College of Veterinary Medicine, University of Illinois, 2001 S. Lincoln Ave, Urbana, IL 61802, United States. Electronic address: mahalin2@illinois.edu. [Ti] Título: Effects of isoliquiritigenin on ovarian antral follicle growth and steroidogenesis. [So] Source: Reprod Toxicol;66:107-114, 2016 12. [Is] ISSN: 1873-1708 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Isoliquiritigenin is a botanical estrogen used as a dietary supplement. Previous studies show that other botanical estrogens affect ovarian estradiol synthesis, but isoliquiritigenin's effects on the ovary are unknown. Thus, this study tested the hypothesis that isoliquiritigenin inhibits ovarian antral follicle growth and steroidogenesis. Antral follicles from CD-1 mice were cultured with vehicle control (dimethyl sulfoxide; DMSO) or isoliquiritigenin (0.6µM, 6 µM, 36 µM, and 100 µM) for 48-96h. During culture, follicle diameters were measured daily to assess follicle growth. After culture, media were collected for hormone assays and follicles were collected for gene expression analysis of steroidogenic enzymes. Isoliquiritigenin inhibited antral follicle growth and altered estradiol, testosterone, and progesterone levels. Additionally, isoliquiritigenin altered the mRNA levels of cytochrome P450 steroid 17-α-hydroxylase 1, aromatase, 17ß-hydroxysteroid dehydrogenase 1, and steroidogenic acute regulatory protein. These data indicate that exposure to isoliquiritigenin inhibits growth and disrupts steroid production in antral follicles. [Mh] Termos MeSH primário: Chalconas/toxicidade Folículo Ovariano/efeitos dos fármacos [Mh] Termos MeSH secundário: 17-Hidroxiesteroide Desidrogenases/genética Animais Aromatase/genética Estradiol/metabolismo Feminino Camundongos Folículo Ovariano/crescimento & desenvolvimento Folículo Ovariano/metabolismo Fosfoproteínas/genética Progesterona/metabolismo RNA Mensageiro/metabolismo Esteroide 17-alfa-Hidroxilase/genética Testosterona/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL [Nm] Nome de substância: 0 (Chalcones); 0 (Phosphoproteins); 0 (RNA, Messenger); 0 (steroidogenic acute regulatory protein); 3XMK78S47O (Testosterone); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); B9CTI9GB8F (isoliquiritigenin); EC 1.1.- (17-Hydroxysteroid Dehydrogenases); EC 1.1.- (hydroxysteroid (17-beta) dehydrogenase 1, mouse); EC 1.14.14.1 (Aromatase); EC 1.14.14.19 (Steroid 17-alpha-Hydroxylase) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180113 [Lr] Data última revisão: 180113 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 161025 [St] Status: MEDLINE

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[PMID]: 29207336 [Au] Autor: Mohamed MF; Hassaneen HM; Abdelhamid IA [Ad] Endereço: Department of Chemistry (Biochemistry Branch), Faculty of Science, Cairo University, Giza, Egypt. Electronic address: magdafikry85@yahoo.com. [Ti] Título: Cytotoxicity, molecular modeling, cell cycle arrest, and apoptotic induction induced by novel tetrahydro-[1,2,4]triazolo[3,4-a]isoquinoline chalcones. [So] Source: Eur J Med Chem;143:532-541, 2018 Jan 01. [Is] ISSN: 1768-3254 [Cp] País de publicação: France [La] Idioma: eng [Ab] Resumo: Novel tetrahydro-[1,2,4]triazolo[3,4-a]isoquinolin-3-yl)-3-arylprop-2-en-1-one derivatives were synthesized and their structures were confirmed by different spectral tools. Cytotoxicity test revealed that some compounds exhibited strong to moderate effect, while others showed weak action against different cancer cell lines (MCF7, A549, HCT116, and Hepg2). Breast carcinoma revealed higher sensitivity toward all derivatives especially compounds 5 and 8 which offered the lowest IC values (50.05, and 27.15 µg/ml) respectively, relative to the positive control 5-fluorouracil (5-FU) (IC = 178 µg/ml). In addition, the two compounds exhibited less toxic effect toward normal melanocytes (HFB4). Several theoretical and experimental studies were done to reveal the molecular mechanisms that control breast carcinoma metastasis using the two promising novels 5 and 8. Docking simulation studies against the two proteins EGFR and DHFR demonstrate that compound 8 showed higher binding affinity toward the two proteins more than compound 5, suggesting that trimethoxy groups may be responsible for this higher activity through the formation of five hydrogen bonding with the active domain (4r3r) and other four interactions with the active domain (1dls). Real time PCR assay illustrates that the two compounds up regulated BAX, p53, caspase-3 genes and down regulated BCL2, MMP1, CDK4 ones. In addition, it was noted that compound 8 was more effective in gene regulation and apoptotic induction than compound 5. Also, flow cytometer analysis demonstrates that both compounds 5 and 8 induced cell growth arrest at G1 phase and thus, inhibit G1/S transition and cell cycle progression. In addition, both compounds stimulate apoptotic death of breast cells significantly to reach 8.72%, and 17.28% respectively, compared to their control (0.55%). Apoptotic induction of breast cells was enhanced effectively through activation of caspase-3 by compound 8 using Elisa assay. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Apoptose/efeitos dos fármacos Chalconas/farmacologia Isoquinolinas/farmacologia Triazóis/farmacologia [Mh] Termos MeSH secundário: Antineoplásicos/síntese química Antineoplásicos/química Pontos de Checagem do Ciclo Celular/efeitos dos fármacos Linhagem Celular Tumoral Proliferação Celular/efeitos dos fármacos Sobrevivência Celular/efeitos dos fármacos Chalconas/síntese química Chalconas/química Relação Dose-Resposta a Droga Ensaios de Seleção de Medicamentos Antitumorais Seres Humanos Isoquinolinas/síntese química Isoquinolinas/química Modelos Moleculares Estrutura Molecular Relação Estrutura-Atividade Triazóis/síntese química Triazóis/química [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Chalcones); 0 (Isoquinolines); 0 (Triazoles); 0 (tetrahydro-(1,2,4)triazolo(3,4-a)isoquinoline) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180110 [Lr] Data última revisão: 180110 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171206 [St] Status: MEDLINE

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[PMID]: 29198636 [Au] Autor: de Almeida CLB; Cechinel-Filho V; Boeing T; Mariano LNB; Silva LMD; Andrade SF; de Souza P [Ad] Endereço: Programa de Pós-Graduação em Ciências Farmacêuticas, Núcleo de Investigações Químico-Farmacêuticas (NIQFAR), Universidade do Vale do Itajaí (UNIVALI), Itajaí, SC 88302-901, Brazil. [Ti] Título: Prolonged diuretic and saluretic effect of nothofagin isolated from Leandra dasytricha (A. Gray) Cogn. leaves in normotensive and hypertensive rats: Role of antioxidant system and renal protection. [So] Source: Chem Biol Interact;279:227-233, 2018 Jan 05. [Is] ISSN: 1872-7786 [Cp] País de publicação: Ireland [La] Idioma: eng [Ab] Resumo: Although the acute diuretic effect of nothofagin has been recently demonstrated, its effects after dose-repeated treatment have not yet been explored. For that, male Wistar normotensive (NTR) and spontaneously hypertensive rats (SHR) were orally treated, once a day, with vehicle (VEH: distilled water; 1 ml/kg), hydrochlorothiazide (HCTZ; 10 mg/kg) or nothofagin (NOT; 1 mg/kg). The cumulative diuretic index and urinary electrolytes excretion were measured each 24 h. On the last day of the experiment (7th day), urine, blood and kidney samples were collected for biochemical and molecular analyzes. The urinary volume of both NTR and SHR were significantly increased with the treatment with NOT (from the second to the seventh day of treatment), with final values reaching an increase of 56% and 82%, respectively, when compared with VEH-treated group. This effect was associated with increased levels of urinary excretion of Na and Cl , without any changes on K excretion. None of the treatments modified urinary pH or density values. Importantly, neither the NOT nor the HCTZ caused any change in body weight following the dose-repeated treatment, and also did not provoke an electrolytic disturbance. Regarding the renal analyzes, when compared with the vehicle-treated NTR group, the activity of superoxide dismutase (SOD) and the reduced glutathione (GSH) levels in kidney homogenates of the SHR group were decreased, while the generation of lipid hydroperoxides were significantly increased. The daily treatment with NOT was able to restore the GSH levels and SOD activity, as well as reduced the lipoperoxidation in the kidney homogenates obtained from SHR animals. Finally, NOT significantly augmented the levels of nitrite, a marker of nitric oxide production, in the plasma obtained from SHR group when compared with the vehicle-treated only NTR. This study revealed the prolonged diuretic and saluretic effect of nothofagin in normotensive and hypertensive rats. Our data also showed the renal protective effects of nothofagin by the improvement of antioxidative capacity, as well as by the augmented bioavailability of plasma nitric oxide in the hypertensive group. [Mh] Termos MeSH primário: Antioxidantes/farmacologia Chalconas/farmacologia Hipertensão/tratamento farmacológico Rim/efeitos dos fármacos Melastomataceae/química Folhas de Planta/química [Mh] Termos MeSH secundário: Animais Chalconas/uso terapêutico Diuréticos/farmacologia Hidroclorotiazida/farmacologia Masculino Ratos Ratos Wistar [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antioxidants); 0 (Chalcones); 0 (Diuretics); 0 (nothofagin); 0J48LPH2TH (Hydrochlorothiazide) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180103 [Lr] Data última revisão: 180103 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171205 [St] Status: MEDLINE

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[PMID]: 29111459 [Au] Autor: Chen H; Song Z; Ying S; Yang X; Wu W; Tan Q; Ju X; Wu W; Zhang X; Qu J; Wang Y [Ad] Endereço: Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China; The Eye Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. [Ti] Título: Myeloid differentiation protein 2 induced retinal ischemia reperfusion injury via upregulation of ROS through a TLR4-NOX4 pathway. [So] Source: Toxicol Lett;282:109-120, 2018 Jan 05. [Is] ISSN: 1879-3169 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: Retinal ischemia reperfusion (I/R) injury is common in many ophthalmic diseases. Recent studies have shown that toll-like receptor 4 (TLR4) is involved in ischemic retinal injury. Activation of TLRs requires specific accessory proteins such as myeloid differentiation protein 2 (MD2), which facilitate in ligand responsiveness. Therefore, inhibiting MD2 may be a novel approach to modulate TLR4 signaling and deleterious downstream effects in ischemic retinal injury. We used human Müller MIO-M1 cells treated with tert-butyl hydroperoxide (TBHP) to establish an in vitro I/R model of oxidative injury and tested the therapeutic effect of inhibiting MD2. Furthermore, we inhibited MD2 in a mouse model of retinal I/R injury and confirmed the results using MD2 knockout mice. Our studies show that pharmacological inhibition of MD2 prevented TBHP-induced reactive oxygen species (ROS) generation, inflammation and subsequent apoptosis in Müller cells. We also show that retinal I/R injury in mice induced functional deficits, increased ROS levels, inflammation and apoptosis. These pathological changes were not observed in MD2 knockout mice and attenuated when MD2 was inhibited in wildtype mice. In addition, we discovered that the mechanism of these therapeutic effects involved regulation of NADPH oxidase 4 (NOX4)-MD2-TLR4 complex formation. This study provides evidence that MD2 plays a key role in the pathogenesis of retinal I/R damage by participating in TLR4-NOX4 complex formation and elaboration of oxidative and inflammatory damage. Hence, inhibition of MD2 may reduce TLR-dependent damage during retinal I/R injury. [Mh] Termos MeSH primário: Antígeno 96 de Linfócito/antagonistas & inibidores NADPH Oxidase 4/metabolismo Espécies Reativas de Oxigênio/metabolismo Traumatismo por Reperfusão/metabolismo Doenças Retinianas/metabolismo Receptor 4 Toll-Like/metabolismo [Mh] Termos MeSH secundário: Animais Apoptose/efeitos dos fármacos Sobrevivência Celular/efeitos dos fármacos Chalconas/farmacologia Modelos Animais de Doenças Células Ependimogliais Seres Humanos Antígeno 96 de Linfócito/genética Camundongos Endogâmicos C57BL Camundongos Knockout Estresse Oxidativo/efeitos dos fármacos Transdução de Sinais terc-Butil Hidroperóxido/farmacologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (1-(3,4-dihydroxyphenyl)-3-(2-methoxyphenyl)prop-2-en-1-one); 0 (Chalcones); 0 (Ly96 protein, mouse); 0 (Lymphocyte Antigen 96); 0 (Reactive Oxygen Species); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 955VYL842B (tert-Butylhydroperoxide); EC 1.6.3.- (NADPH Oxidase 4); EC 1.6.3.- (Nox4 protein, mouse) [Em] Mês de entrada: 1712 [Cu] Atualização por classe: 171201 [Lr] Data última revisão: 171201 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171108 [St] Status: MEDLINE

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[PMID]: 28964928 [Au] Autor: Keiler AM; Macejova D; Dietz BM; Bolton JL; Pauli GF; Chen SN; van Breemen RB; Nikolic D; Goerl F; Muders MH; Zierau O; Vollmer G [Ad] Endereço: Chair for Molecular Cell Physiology & Endocrinology, Department of Biology, Technische Universität Dresden, 01062 Dresden, Germany; Institute for Doping Analytics and Sports Biochemistry Dresden (IDAS), Dresdner Str. 12, 01731 Kreischa, Germany. [Ti] Título: Evaluation of estrogenic potency of a standardized hops extract on mammary gland biology and on MNU-induced mammary tumor growth in rats. [So] Source: J Steroid Biochem Mol Biol;174:234-241, 2017 Nov. [Is] ISSN: 1879-1220 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Supplements with estrogenic activities are intensively investigated as potential alternatives for the treatment of menopausal symptoms. These investigations include studies on their safety regarding potential breast cancer risks. Therefore, the aim of this study was to assess whether or not a standardized hops (Humulus lupulus) extract, containing 0.42% of the estrogenic flavanone, 8-prenylnaringenin, would stimulate growth of methyl-nitrosourea (MNU) induced mammary cancer in ovariectomized (OVX) Sprague-Dawley (SD) rats or would impact on the proliferative activity within the normal mammary gland of Wistar rats. To induce tumorigenesis SD-rats received an intraperitoneal injection of 50mg/kg body weight of MNU on postnatal days PND 50 and 52. 28days later animals were OVX or were SHAM operated (positive control) and randomly allocated and maintained for 140days on either a phytoestrogen-free placebo diet (SHAM and negative control) or on the hops fortified diet. For the investigations in the normal mammary gland young adult Wistar rats were bilaterally OVX and randomly allocated to a control group fed to a phytoestrogen-free diet, or to a diet supplemented either with E -benzoate or the hops extract. As a major result, the tumor incidence was 15% (3 tumors totally) in OVX controls, whereas it was 85% (39 tumors totally) in SHAM operated positive controls. No tumors were detectable in the hops group. In addition, no estrogenic activity of the hops extract was detectable in uterus and liver of these animals. In investigations on the normal mammary gland, no impact of hops extract on the expression of estrogen dependent proliferation markers or of progesterone receptor became apparent. In conclusion, the lack of growth stimulation of MNU-induced breast cancer in OVX SD-rats and the lack of stimulation proliferative events in the normal mammary gland of OVX Wistar rats by standardized hops extracts provides an important piece of evidence regarding the safety of these extracts in the management of menopausal symptoms. [Mh] Termos MeSH primário: Humulus Glândulas Mamárias Animais/efeitos dos fármacos Extratos Vegetais/farmacologia [Mh] Termos MeSH secundário: Alquilantes Animais Proliferação Celular/efeitos dos fármacos Chalconas/sangue Chalconas/metabolismo Feminino Flavanonas/sangue Flavanonas/metabolismo Fígado/efeitos dos fármacos Fígado/crescimento & desenvolvimento Fígado/metabolismo Neoplasias Mamárias Experimentais/induzido quimicamente Metilnitrosoureia Tamanho do Órgão/efeitos dos fármacos Ovariectomia Ratos Sprague-Dawley Ratos Wistar Útero/efeitos dos fármacos Útero/crescimento & desenvolvimento [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Alkylating Agents); 0 (Chalcones); 0 (Flavanones); 0 (Plant Extracts); 684-93-5 (Methylnitrosourea) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171113 [Lr] Data última revisão: 171113 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171002 [St] Status: MEDLINE

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[PMID]: 28867710 [Au] Autor: Suthar SK; Bansal S; Narkhede N; Guleria M; Alex AT; Joseph A [Ad] Endereço: Department of Pharmaceutical Chemistry, Manipal College of Pharmaceutical Sciences. [Ti] Título: Design, Synthesis and Biological Evaluation of Oxindole-Based Chalcones as Small-Molecule Inhibitors of Melanogenic Tyrosinase. [So] Source: Chem Pharm Bull (Tokyo);65(9):833-839, 2017. [Is] ISSN: 1347-5223 [Cp] País de publicação: Japan [La] Idioma: eng [Ab] Resumo: The enzyme tyrosinase regulates melanogenesis and skin hyperpigmentation by converting L-3,4-dihydroxyphenylalanine (L-DOPA) into dopaquinone, a key step in the melanin biosynthesis. The present work deals with design and synthesis of various oxindole-based chalcones as monophenolase and diphenolase activity inhibitors of tyrosinase. Among the screened compounds, 4-hydroxy-3-methoxybenzylidene moiety bearing chalcone (7) prepared by one pot reaction of oxindole and vanillin displayed the highest activity against tyrosinase with IC s of 63.37 and 59.71 µM in monophenolase and diphenolase activity assays, respectively. In molecular docking studies, chalcone 7 also showed the highest binding affinity towards the enzyme tyrosinase while exhibiting the lowest estimated free energy of binding, among all the ligands docked. [Mh] Termos MeSH primário: Chalconas/química Desenho de Drogas Inibidores Enzimáticos/síntese química Monofenol Mono-Oxigenase/antagonistas & inibidores [Mh] Termos MeSH secundário: Animais Benzaldeídos/química Sítios de Ligação Domínio Catalítico Chalconas/síntese química Chalconas/metabolismo Inibidores Enzimáticos/química Inibidores Enzimáticos/metabolismo Indóis/química Concentração Inibidora 50 Melaninas/metabolismo Simulação de Acoplamento Molecular Monofenol Mono-Oxigenase/metabolismo Ratos [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Benzaldehydes); 0 (Chalcones); 0 (Enzyme Inhibitors); 0 (Indoles); 0 (Melanins); 0S9338U62H (2-oxindole); CHI530446X (vanillin); EC 1.14.18.1 (Monophenol Monooxygenase) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171019 [Lr] Data última revisão: 171019 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170905 [St] Status: MEDLINE [do] DOI: 10.1248/cpb.c17-00301

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MEDLINE

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[PMID]: 28803046 [Au] Autor: Shaik AB; Rao GK; Kumar GB; Patel N; Reddy VS; Khan I; Routhu SR; Kumar CG; Veena I; Chandra Shekar K; Barkume M; Jadhav S; Juvekar A; Kode J; Pal-Bhadra M; Kamal A [Ad] Endereço: Medicinal Chemistry and Pharmacology, CSIR - Indian Institute of Chemical Technology, Hyderabad 500007, India. [Ti] Título: Design, synthesis and biological evaluation of novel pyrazolochalcones as potential modulators of PI3K/Akt/mTOR pathway and inducers of apoptosis in breast cancer cells. [So] Source: Eur J Med Chem;139:305-324, 2017 Oct 20. [Is] ISSN: 1768-3254 [Cp] País de publicação: France [La] Idioma: eng [Ab] Resumo: Cancer has been established as the "Emperor of all maladies". In recent years, medicinal chemistry has focused on identifying novel anti-cancer compounds; though discovery of these compounds appears to be a herculean task. In present study, we synthesized forty pyrazolochalcone conjugates and explored their cytotoxic activity against a panel of sixty cancer cell lines. Fifteen conjugates of the series showed excellent growth inhibition (13b-e, 13h-j, 14c-d, 15 a, 15 c-d, 16b, 16d and 18f; GI for MCF-7: 0.4-20 µM). Conjugates 13b, 13c, 13d, 16b and 14d were also evaluated for their cytotoxic activity in human breast cancer cell line (MCF-7). The promising candidates induced cell cycle arrest, mitochondrial membrane depolarization and apoptosis in MCF-7 cells at a 2 µM concentration. Furthermore, inhibition of PI3K/Akt/mTOR pathway-regulators such as PI3K, p-PI3K, p-AKT, and mTOR were observed; as well as upregulation of p-GSK3ß and tumor-suppressor protein, PTEN. Our study indicates that pyrazolochalcone conjugates could serve as potential leads in the development of tailored cancer therapeutics. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Apoptose/efeitos dos fármacos Neoplasias da Mama/tratamento farmacológico Chalconas/farmacologia Desenho de Drogas Inibidores de Proteínas Quinases/farmacologia Pirazóis/farmacologia [Mh] Termos MeSH secundário: Antineoplásicos/síntese química Antineoplásicos/química Neoplasias da Mama/metabolismo Neoplasias da Mama/patologia Chalconas/síntese química Chalconas/química Relação Dose-Resposta a Droga Feminino Seres Humanos Células MCF-7 Estrutura Molecular Fosfatidilinositol 3-Quinases/antagonistas & inibidores Fosfatidilinositol 3-Quinases/metabolismo Inibidores de Proteínas Quinases/síntese química Inibidores de Proteínas Quinases/química Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores Proteínas Proto-Oncogênicas c-akt/metabolismo Pirazóis/síntese química Pirazóis/química Relação Estrutura-Atividade Serina-Treonina Quinases TOR/antagonistas & inibidores Serina-Treonina Quinases TOR/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Chalcones); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171018 [Lr] Data última revisão: 171018 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170814 [St] Status: MEDLINE

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