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| 1 | Green tea polyphenols inhibit testosterone production in rat Leydig cells显示文摘这研究调查了绿茶摘录(GTE ) 和它的多酚的尖锐效果成分,(-)-epigallocatechin-3-gallate (EGCG ) 和(-)-epicatechin (EC ) ,在由在 vitro 的老鼠 Leydig 房间的基础、刺激的睾丸激素生产上。在一个 Percoll 坡度净化的 Leydig 房间与 GTE, EGCG 或 EC 和睾丸激素先锋 androstenedione 为 3 h 被孵化,当面或任何一个蛋白质 kinase A (PKA ) 的缺席或蛋白质 kinase C (PKC ) 使活跃之物。效果的可逆性被 pretreating 房间与 GTE 或 EGCG 为 15 min 学习,允许他们为 1 h 恢复并且为有人的 chorionic 的 2 h 质问他们 gonadotropin (hCG ) , luteinizing 荷尔蒙释放荷尔蒙(LHRH ) , 22 (R)-hydroxycholesterol 或 androstenedione。GTE 和 EGCG,然而并非 EC,禁止了基础、刺激 kinase 的睾丸激素生产。在预告的处理条件下面, hCG/LHRH-stimulated 或 22 (R)-hydroxycholesterol-induced 睾丸激素生产上的 GTE/EGCG 的更高的集中的禁止的效果被维持,而支持 androstenedione 的睾丸激素生产回来了控制层次。在 GTE/EGCG 的更低的集中, 22 (R)-hydroxycholesterol-supported 睾丸激素生产上的这些多酚的禁止的效果被颠倒。GTE 的禁止的效果可以被它一个 gallate 组的主要部件, EGCG,和存在的行动在它的结构解释在禁止睾丸激素生产为它的高功效似乎重要。位于 GTE 和 EGCG 的效果下面的机制包含表明 P450 方面链劈开酶和 17-hydroxysteroid 脱氢酶功能的小径,以及抑制的 PKA/PKC 的抑制。 | Marina S. Figueiroa Juliany S. B. Cesar Vieira Disleide S. Leite Ruben C. O. Andrade Filho Fabiano Ferreira Patricia S. Gouveia Daniel P. Udrisar Maria I. Wanderley | 2009 | Asian Journal of Andrology2009，11，3： | 4 |
| 2 | Effectiveness ofcontraceptive counseling of women following an abortion : asystematic review and meta-analysis 显示文摘 | Ferreira AL Lemos A Figueiroa JN | 2009 | Eur J Contracept ReprodHealth Care2009，14，1： | 1 |
| 3 | Effect on infant illness of maternal supplementation with 400 000 IU vs 200 000 IU of vitamin A显示文摘 | Fernandes TF Figueiroa JN Grande de Arruda IK | 2012 | Pediatrics2012，129，4： | 1 |
| 4 | Years of potential life lost by children and adolescent victims of homicide,Recife,1997显示文摘 | Arnold MW Neto GH F Figueiroa JN | 2002 | J Trop Pediatr2002，48，2： | 1 |
| 5 | Hurst analysis applied to the study of single calcium-activated potassium channel kinetics显示文摘 | Liebovitch LS Figueiroa JN | 2000 | J Theor Biol2000，206，3： | 1 |
| 6 | Effectiveness of contraceptive counselling of women following an abortion:a systematic review and meta-analysis显示文摘 | Ferreira AL Lemos A Figueiroa JN | 2009 | Eur J Contracept Reprod Health Care2009，14，1： | 1 |
| 7 | Study of tumor necrosis factor receptor in the inflammatory bowel disease显示文摘Ulcerative colitis(UC)and Crohn’s disease(CD)are part of Inflammatory Bowel Diseases(IBD)and have pathophysiological processes such as bowel necrosis and enteric neurons and enteric glial cells.In addition,the main inflammatory mediator is related to the tumor necrosis factor-alpha(TNF-α).TNF-αis a mediator of the intestinal inflammatory processes,thus being one of the main cytokines involved in the pathogenesis of IBD,however,its levels,when measured,are present in the serum of patients with IBD.In addition,TNF-αplays an important role in promoting inflammation,such as the production of interleukins(IL),for instance IL-1βand IL-6.There are two receptors for TNF as following:The tumor necrosis factor 1 receptor(TNFR1);and the tumor necrosis factor 2 receptor(TNFR2).They are involved in the pathogenesis of IBD and their receptors have been detected in IBD and their expression is correlated with disease activity.The soluble TNF form binds to the TNFR1 receptor with,and its activation results in a signaling cascade effects such as apoptosis,cell proliferation and cytokine secretion.In contrast,the transmembrane TNF form can bind both to TNFR1 and TNFR2.Recent studies have suggested that TNF-αis one of the main pro-inflammatory cytokines involved in the pathogenesis of IBD,since TNF levels are present in the serum of both patients with UC and CD.Intravenous and subcutaneous biologics targeting TNF-αhave revolutionized the treatment of IBD,thus becoming the best available agents to induce and maintain IBD remission.The application of antibodies aimed at neutralizing TNF-αin patients with IBD that induce a satisfactory clinical response in up to 60%of patients,and also induced long-term maintenance of disease remission in most patients.It has been suggested that anti-TNF-αagents inactivate the pro-inflammatory cytokine TNF-αby direct neutralization,i.e.,resulting in suppression of inflammation.However,anti-TNF-αantibodies perform more complex functions than a simple blockade. | Roberta Figueiroa Souza Marcos Antônio Ferreira Caetano Henrique Inhauser Riceti Magalhães Patricia Castelucci | 2023 | World Journal of Gastroenterology2023，29，18： | 1 |
| 8 | Postpartum dexamethasone for women with hemolysis,elevated liver enzymes,and low platelets (HELLP) syndrome:a doubleblind,placebo-controlled,randomized clinical trial显示文摘 | Katz L Amorim MM Figueiroa JN | | 0，，03： | 1 |
| 9 | Gestational vitamin D deft- ciency:long-term effects on the brain显示文摘 | Levenson CW Figueiroa SM | 2008 | Nutr Rev2008，66，12： | 1 |
| 10 | Postpartum dexamethasone for women with hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome: a double-blind, placebo-controlled, randomized clinical trial 显示文摘 | Katz L de Amorim MM Figueiroa JN | 2008 | Am J Obstet Gynecol2008，198，3： | 1 |
| 11 | Years of potential life lost by children and adolescent victims of homicide, Recife,1997 显示文摘 | Arnold MW Neto GH F Figueiroa JN | 2002 | J Trop Pediatr2002，48，2： | 1 |
| 12 | P2X7 receptor antagonist recovers ileum myenteric neurons after experimental ulcerative colitis显示文摘BACKGROUND The P2X7 receptor is expressed by enteric neurons and enteric glial cells.Studies have demonstrated that administration of a P2X7 receptor antagonist,brilliant blue G(BBG),prevents neuronal loss.AIM To report the effects of BBG in ileum enteric neurons immunoreactive(ir)following experimental ulcerative colitis in Rattus norvegicus albinus.METHODS 2,4,6-trinitrobenzene sulfonic acid(TNBS group,n=5)was injected into the distal colon.BBG(50 mg/kg,BBG group,n=5)or vehicle(sham group,n=5)was given subcutaneously 1 h after TNBS.The animals were euthanized after 24 h,and the ileum was removed.Immunohistochemistry was performed on the myenteric plexus to evaluate immunoreactivity for P2X7 receptor,neuronal nitric oxide synthase(nNOS),choline acetyltransferase(ChAT),HuC/D and glial fibrillary acidic protein.RESULTS The numbers of nNOS-,ChAT-,HuC/D-ir neurons and glial fibrillary acidic protein-ir glial cells were decreased in the TNBS group and recovered in the BBG group.The neuronal profile area(μm^2)demonstrated that nNOS-ir neurons decreased in the TNBS group and recovered in the BBG group.There were no differences in the profile areas of ChAT-and HuC/D-ir neurons.CONCLUSION Our data conclude that ileum myenteric neurons and glial cells were affected by ulcerative colitis and that treatment with BBG had a neuroprotective effect.Thus,these results demonstrate that the P2X7 receptor may be an important target in therapeutic strategies. | Roberta Figueiroa Souza Mariá Munhoz Evangelinellis Cristina Eusébio Mendes Marta Righetti Múcio Cevulla Silva Lourenco Patricia Castelucci | 2020 | World Journal of Gastrointestinal Pathophysiology2020，11，4： | 1 |
| 13 | Chronic caloric restriction reduces tissue damage and improves spatial memory in a rat model of traumatic brain injury显示文摘 | Rich N J Van Landingham J W Figueiroa S | 2010 | J Neurosci Res2010，88，13： | 1 |
| 14 | Years of potential life lost by children and adolescent victims of homicide,Recife,1997显示文摘 | Arnold MW Neto GH F Figueiroa JN | 2002 | J Trop Pediatr2002，48，2： | 1 |
| 15 | Papain-induced experimental pulmonary emphysema in male and female mice显示文摘 | Machado MN Figueiroa SF Mazzoli-Rocha F | 2014 | Respir Physiol Neurobiol2014，200，15： | 1 |
| 16 | 500 years of mining in Brazil: a brief review 显示文摘 | IRAN F MACHADO SILVIA F DE M FIGUEIROA | 2001 | Resources Policy2001，，： | 1 |
| 17 | Study of the roles of caspase-3 and nuclear factor kappa B in myenteric neurons in a P2X7 receptor knockout mouse model of ulcerative colitis显示文摘BACKGROUND The literature indicates that the enteric nervous system is affected in inflammatory bowel diseases(IBDs)and that the P2X7 receptor triggers neuronal death.However,the mechanism by which enteric neurons are lost in IBDs is unknown.AIM To study the role of the caspase-3 and nuclear factor kappa B(NF-κB)pathways in myenteric neurons in a P2X7 receptor knockout(KO)mouse model of IBDs.METHODS Forty male wild-type(WT)C57BL/6 and P2X7 receptor KO mice were euthanized 24 h or 4 d after colitis induction by 2,4,6-trinitrobenzene sulfonic acid(colitis group).Mice in the sham groups were injected with vehicle.The mice were divided into eight groups(n=5):The WT sham 24 h and 4 d groups,the WT colitis 24 h and 4 d groups,the KO sham 24 h and 4 d groups,and the KO colitis 24 h and 4 d groups.The disease activity index(DAI)was analyzed,the distal colon was collected for immunohistochemistry analyses,and immunofluorescence was performed to identify neurons immunoreactive(ir)for calretinin,P2X7 receptor,cleaved caspase-3,total caspase-3,phospho-NF-κB,and total NF-κB.We analyzed the number of calretinin-ir and P2X7 receptor-ir neurons per ganglion,the neuronal profile area(μm^(2)),and corrected total cell fluorescence(CTCF).RESULTS Cells double labeled for calretinin and P2X7 receptor,cleaved caspase-3,total caspase-3,phospho-NF-κB,or total NF-κB were observed in the WT colitis 24 h and 4 d groups.The number of calretinin-ir neurons per ganglion was decreased in the WT colitis 24 h and 4 d groups compared to the WT sham 24 h and 4 d groups,respectively(2.10±0.13 vs 3.33±0.17,P<0.001;2.92±0.12 vs 3.70±0.11,P<0.05),but was not significantly different between the KO groups.The calretinin-ir neuronal profile area was increased in the WT colitis 24 h group compared to the WT sham 24 h group(312.60±7.85 vs 278.41±6.65,P<0.05),and the nuclear profile area was decreased in the WT colitis 4 d group compared to the WT sham 4 d group(104.63±2.49 vs 117.41±1.14,P<0.01).The number of P2X7 receptor-ir neurons per ganglion was decreased in the WT colitis 24 h and 4 d groups compared to the WT sham 24 h and 4 d groups,respectively(19.49±0.35 vs 22.21±0.18,P<0.001;20.35±0.14 vs 22.75±0.51,P<0.001),and no P2X7 receptor-ir neurons were observed in the KO groups.Myenteric neurons showed ultrastructural changes in the WT colitis 24 h and 4 d groups and in the KO colitis 24 h group.The cleaved caspase-3 CTCF was increased in the WT colitis 24 h and 4 d groups compared to the WT sham 24 h and 4 d groups,respectively(485949±14140 vs 371371±16426,P<0.001;480381±11336 vs 378365±4053,P<0.001),but was not significantly different between the KO groups.The total caspase-3 CTCF,phospho-NF-κB CTCF,and total NF-κB CTCF were not significantly different among the groups.The DAI was recovered in the KO groups.Furthermore,we demonstrated that the absence of the P2X7 receptor attenuated inflammatory infiltration,tissue damage,collagen deposition,and the decrease in the number of goblet cells in the distal colon.CONCLUSION Ulcerative colitis affects myenteric neurons in WT mice but has a weaker effect in P2X7 receptor KO mice,and neuronal death may be associated with P2X7 receptor-mediated caspase-3 activation.The P2X7 receptor can be a therapeutic target for IBDs. | Henrique Inhauser Riceti Magalhães Felipe Alexandre Machado Roberta Figueiroa Souza Marcos Antônio Ferreira Caetano Vanessa Ribeiro Figliuolo Robson Coutinho-Silva Patricia Castelucci | 2023 | World Journal of Gastroenterology2023，29，22： | 0 |
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