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1.
Am J Physiol Renal Physiol ; 315(3): F460-F468, 2018 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-29717937

RESUMO

Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) is a chronic inflammatory disease without consistently effective treatment. We investigate the role of toll-like receptor 4 (TLR4) on voiding dysfunction and inflammation in the cyclophosphamide (CYP)-induced mouse cystitis. Male C57BL/6 [wild-type, (WT)] and/or TLR4 knockout (TLR4-/-) mice were treated with an injection of CYP (300 mg/kg, 24 h) or saline (10 ml/kg). The pharmacological blockade of the TLR4 by resatorvid (10 mg/kg) was also performed 1 h prior CYP-injection in WT mice. Urodynamic profiles were assessed by voiding stain on filter paper and filling cystometry. Contractile responses to carbachol were measured in isolated bladders. In CYP-exposed WT mice, mRNA for TLR4, myeloid differentiation primary response 88, and TIR-domain-containing adapter-inducing interferon-ß increased by 45%, 72%, and 38%, respectively ( P < 0.05). In free-moving mice, CYP-exposed mice exhibited a higher number of urinary spots and smaller urinary volumes. Increases of micturition frequency and nonvoiding contractions, concomitant with decreases of intercontraction intervals and capacity, were observed in the filling cystometry of WT mice ( P < 0.05). Carbachol-induced bladder contractions were significantly reduced in the CYP group, which was paralleled by reduced mRNA for M2 and M3 muscarinic receptors. These functional and molecular alterations induced by CYP were prevented in TLR4-/- and resatorvid-treated mice. Additionally, the increased levels of inflammatory markers induced by CYP exposure, myeloperoxidase activity, interleukin-6, and tumor necrosis factor-alpha were significantly reduced by resatorvid treatment. Our findings reveal a central role for the TLR4 signaling pathway in initiating CYP-induced bladder dysfunction and inflammation and thus emphasize that TLR4 receptor blockade may have clinical value for IC/BPS treatment.

2.
Neuroimmunomodulation ; 22(6): 373-84, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26088412

RESUMO

OBJECTIVE: intra-articular co-injection of kaolin with carrageenan (CGN) in rodents is widely used as an experimental model of arthritis. However, the ability of kaolin to cause arthritis and related immune responses when administered alone is unclear. We evaluated the contribution of prostanoids and sensory C-fibres (and their neuropeptide substance P) to kaolin-induced inflammation in the rat knee. METHODS: Wistar rats, 8-10 weeks old, received an intra-articular injection of kaolin (1-10 µg/joint) or saline into the knee joint. Knee inflammation, proinflammatory cytokines, pain behaviour and secondary tactile allodynia were assessed over 5 h, when synovial leukocyte counts, histopathological changes and proinflammatory cytokine levels were evaluated. RESULTS: The intra-articular injection of kaolin caused a dose- and time-dependent knee swelling and impairment of motion that were associated with secondary tactile allodynia, elevated concentrations of IL-1ß, IL-6 and TNFα, leukocyte infiltration, and histopathological changes in the ipsilateral hindpaw. The neurokinin-1 (NK1) receptor antagonist SR140333 or neonatal treatment with capsaicin markedly reduced the inflammatory parameters, cytokines and allodynia but failed to significantly inhibit the impaired motion. The cyclo-oxygenase inhibitor indomethacin partially inhibited knee oedema and allodynia but did not affect the leukocyte influx, myeloperoxidase activity or impaired motion in the kaolin-injected rat. CONCLUSIONS: We show the first evidence that intra-articular injection of kaolin without CGN produced severe acute monoarthritis. This was highly dependent on substance P (released from C-fibres) and NK1 receptor activation, which stimulated local production of proinflammatory cytokines. This model may be of critical importance for mechanistic studies and screening new anti-inflammatory/analgesic drugs.


Assuntos
Antidiarreicos/toxicidade , Artrite/induzido quimicamente , Caulim/toxicidade , Receptores da Neurocinina-1/metabolismo , Animais , Animais Recém-Nascidos , Artrite/complicações , Artrite/tratamento farmacológico , Capsaicina/toxicidade , Citocinas/metabolismo , Modelos Animais de Doenças , Edema/etiologia , Inibidores Enzimáticos/uso terapêutico , Hiperalgesia/etiologia , Indometacina/uso terapêutico , Articulação do Joelho/patologia , Masculino , Medição da Dor , Peroxidase/metabolismo , Piperidinas/uso terapêutico , Quinuclidinas/uso terapêutico , Ratos , Ratos Wistar , Líquido Sinovial/metabolismo
3.
J Strength Cond Res ; 28(11): 3215-23, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-24832980

RESUMO

Concurrent training (CT) seems to impair training-induced muscle hypertrophy. This study compared the effects of CT, strength training (ST) and interval training (IT) on the muscle fiber cross-sectional area (CSA) response, and on the expression of selected genes involved in the myostatin (MSTN) signaling mRNA levels. Thirty-seven physically active men were randomly divided into 4 groups: CT (n = 11), ST (n = 11), IT (n = 8), and control group (C) (n = 7) and underwent an 8-week training period. Vastus lateralis biopsy muscle samples were obtained at baseline and 48 hours after the last training session. Muscle fiber CSA, selected genes expression, and maximum dynamic ST (1 repetition maximum) were evaluated before and after training. Type IIa and type I muscle fiber CSA increased from pre- to posttest only in the ST group (17.08 and 17.9%, respectively). The SMAD-7 gene expression significantly increased at the posttest in the ST (53.9%) and CT groups (39.3%). The MSTN and its regulatory genes ActIIb, FLST-3, FOXO-3a, and GASP-1 mRNA levels remained unchanged across time and groups. One repetition maximum increased from pre- to posttest in both the ST and CT groups (ST = 18.5%; CT = 17.6%). Our findings are suggestive that MSTN and their regulatory genes at transcript level cannot differentiate muscle fiber CSA responses between CT and ST regimens in humans.


Assuntos
Expressão Gênica , Miostatina/metabolismo , Músculo Quadríceps/metabolismo , Treinamento de Resistência , Corrida/fisiologia , Adolescente , Adulto , Teste de Esforço , Proteína Forkhead Box O3 , Fatores de Transcrição Forkhead/genética , Humanos , Masculino , Fibras Musculares de Contração Rápida/citologia , Fibras Musculares de Contração Lenta/citologia , Miostatina/genética , Consumo de Oxigênio , Condicionamento Físico Humano/métodos , Condicionamento Físico Humano/fisiologia , Proteínas/genética , Músculo Quadríceps/citologia , RNA Mensageiro/metabolismo , Transdução de Sinais/genética , Proteína Smad7/genética , Adulto Jovem
4.
Mol Endocrinol ; 27(12): 2055-65, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-24176915

RESUMO

Although it is well known that the thyroid hormone (T3) is an important positive regulator of cardiac function over a short term and that it also promotes deleterious effects over a long term, the molecular mechanisms for such effects are not yet well understood. Because most alterations in cardiac function are associated with changes in sarcomeric machinery, the present work was undertaken to find novel sarcomeric hot spots driven by T3 in the heart. A microarray analysis indicated that the M-band is a major hot spot, and the structural sarcomeric gene coding for the M-protein is severely down-regulated by T3. Real-time quantitative PCR-based measurements confirmed that T3 (1, 5, 50, and 100 physiological doses for 2 days) sharply decreased the M-protein gene and protein expression in vivo in a dose-dependent manner. Furthermore, the M-protein gene expression was elevated 3.4-fold in hypothyroid rats. Accordingly, T3 was able to rapidly and strongly reduce the M-protein gene expression in neonatal cardiomyocytes. Deletions at the M-protein promoter and bioinformatics approach suggested an area responsive to T3, which was confirmed by chromatin immunoprecipitation assay. Functional assays in cultured neonatal cardiomyocytes revealed that depletion of M-protein (by small interfering RNA) drives a severe decrease in speed of contraction. Interestingly, mRNA and protein levels of other M-band components, myomesin and embryonic-heart myomesin, were not altered by T3. We concluded that the M-protein expression is strongly and rapidly repressed by T3 in cardiomyocytes, which represents an important aspect for the basis of T3-dependent sarcomeric deleterious effects in the heart.


Assuntos
Cardiomegalia/genética , Conectina/genética , Regulação para Baixo/genética , Hormônios Tireóideos/farmacologia , Animais , Animais Recém-Nascidos , Sequência de Bases , Cardiomegalia/etiologia , Cardiomegalia/fisiopatologia , Linhagem Celular , Células Cultivadas , Conectina/metabolismo , Regulação para Baixo/efeitos dos fármacos , Hipotireoidismo/genética , Masculino , Camundongos , Dados de Sequência Molecular , Contração Miocárdica/efeitos dos fármacos , Contração Miocárdica/genética , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Análise de Sequência com Séries de Oligonucleotídeos , Regiões Promotoras Genéticas/genética , Ligação Proteica/efeitos dos fármacos , Ligação Proteica/genética , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , Receptores dos Hormônios Tireóideos/metabolismo , Sarcômeros/metabolismo , Tireotoxicose/complicações , Tri-Iodotironina/farmacologia , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/genética
5.
Vet Parasitol ; 177(1-2): 97-103, 2011 Apr 19.
Artigo em Inglês | MEDLINE | ID: mdl-21273000

RESUMO

The Rio Grande do Sul state, in Southern Brazil, is one of the foci of human cystic echinococcosis (CE). The sheep strain (G1) of Echinococcus granulosus and Echinococcus ortleppi (also known as cattle strain G5) have been reported before to infect livestock. However, up to the present, no molecular data are available on isolates of the E. granulosus complex from humans and dogs. The present study analyzed hydatid cysts from 6 CE patients and adult worms from 12 dogs. Sequencing of the mitochondrial cox1 and 12S rRNA genes detected the E. granulosus G1 genotype from four human cases, the G3 genotype (or buffalo strain) from one human case and E. ortleppi from another human case, respectively. Ten of the twelve dogs were found infected with the G1 genotype, and one dog each harbored worms of the G3 genotype and E. ortleppi. Obvious morphological differences were recognized between the G1 and E. ortleppi adult worms from dogs in this region. The buffalo strain (G3) is for the first time reported from South America.


Assuntos
Equinococose/parasitologia , Echinococcus/classificação , Animais , Sequência de Bases , Brasil/epidemiologia , DNA Mitocondrial/genética , Equinococose/epidemiologia , Echinococcus/genética , Genótipo , Humanos , Dados de Sequência Molecular , Especificidade da Espécie
6.
Muscle Nerve ; 40(6): 992-9, 2009 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-19705480

RESUMO

In this study we investigated the gene expression of proteins related to myostatin (MSTN) signaling during skeletal muscle longitudinal growth. To promote muscle growth, Wistar male rats were submitted to a stretching protocol for different durations (12, 24, 48, and 96 hours). Following this protocol, soleus weight and length and sarcomere number were determined. In addition, expression levels of the genes that encode MSTN, follistatin isoforms 288 and 315 (FLST288 and FLST315), follistatin-like 3 protein (FLST-L3), growth and differentiation factor-associated protein-1 (GASP-1), activin IIB receptor (ActIIB), and SMAD-7 were determined by real-time polymerase chain reaction. Prolonged stretching increased soleus weight, length, and sarcomere number. In addition, MSTN gene expression was increased at 12-24 hours, followed by a decrease at 96 hours when compared with baseline values. FLST isoforms, FLST-L3, and GASP-1 mRNA levels increased significantly over all time-points. ActIIB gene expression decreased quickly at 12-24 hours. SMAD-7 mRNA levels showed a late increase at 48 hours, which peaked at 96 hours. The gene expression pattern of inhibitory proteins related to MSTN signaling suggests a strong downregulation of this pathway in response to prolonged stretching.


Assuntos
Regulação da Expressão Gênica , Exercícios de Alongamento Muscular , Músculo Esquelético/crescimento & desenvolvimento , Miostatina/antagonistas & inibidores , Animais , Regulação para Baixo , Masculino , Músculo Esquelético/metabolismo , Miostatina/metabolismo , Ratos , Ratos Wistar , Sarcômeros/metabolismo , Transdução de Sinais
7.
Eur J Pharmacol ; 589(1-3): 206-14, 2008 Jul 28.
Artigo em Inglês | MEDLINE | ID: mdl-18554582

RESUMO

In addition to reducing blood pressure, hydralazine can reduce the production of inflammatory cytokines and reduce the expression of leukocyte adhesion molecules. Differences in leukocyte behavior and leukocyte adhesion molecule expression in spontaneously hypertensive rats (SHR) compared to normotensive rats have been reported. However, whether hydralazine can reduce leukocyte migration in vivo in hypertension and in normotension remains unknown. To address this question, male SHR and Wistar rats were treated for 15 days with hydralazine at a dose of ~3.5 mg/kg or ~14 mg/kg in their drinking water. The numbers of rollers and adherent and migrated cells were determined by direct vital microscopy, and blood pressure was assessed by tail plethysmography. In addition, following treatment with the higher dose, immunohistochemistry was used to measure the expression of intercellular adhesion molecule-1 (ICAM-1), P-selectin, and platelet-endothelial cell adhesion molecule-1 (PECAM-1) in endothelial cells, while flow cytometry was used to evaluate the expression of leukocyte CD18 and L-selectin. Hydralazine reduced leukocyte adherence and migration in SHR either at the higher, that reduced blood pressure levels, or lower dose, which did not reduce it. Reduced ICAM-1 expression might be involved in the reduced migration observed in SHR. In Wistar rats, only at the higher dose hydralazine reduced blood pressure levels and leukocyte migration. Reduced P-selectin expression might be involved. We therefore conclude that hydralazine reduces leukocyte migration by different mechanisms in SHR and Wistar rats, specifically by reducing ICAM-1 expression in the former and P-selectin expression in the latter.


Assuntos
Anti-Inflamatórios/farmacologia , Anti-Hipertensivos/farmacologia , Moléculas de Adesão Celular/metabolismo , Quimiotaxia de Leucócito/efeitos dos fármacos , Hidralazina/farmacologia , Hipertensão/tratamento farmacológico , Leucócitos/efeitos dos fármacos , Animais , Velocidade do Fluxo Sanguíneo/efeitos dos fármacos , Pressão Sanguínea/efeitos dos fármacos , Peso Corporal/efeitos dos fármacos , Antígenos CD18/metabolismo , Adesão Celular/efeitos dos fármacos , Moléculas de Adesão Celular/genética , Modelos Animais de Doenças , Endotélio Vascular/efeitos dos fármacos , Endotélio Vascular/imunologia , Citometria de Fluxo , Hipertensão/imunologia , Hipertensão/fisiopatologia , Imuno-Histoquímica , Molécula 1 de Adesão Intercelular/metabolismo , Selectina L/metabolismo , Contagem de Leucócitos , Migração e Rolagem de Leucócitos/efeitos dos fármacos , Leucócitos/imunologia , Masculino , Microscopia de Vídeo , Selectina-P/metabolismo , Molécula-1 de Adesão Celular Endotelial a Plaquetas/metabolismo , Pletismografia , RNA Mensageiro/metabolismo , Ratos , Ratos Endogâmicos SHR , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa
8.
Arch Phys Med Rehabil ; 87(2): 241-6, 2006 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-16442979

RESUMO

UNLABELLED: The effect of 30 minutes of passive stretch of the rat soleus muscle on the myogenic differentiation, myostatin, and atrogin-1 gene expressions. OBJECTIVE: To evaluate the effect of passive stretch, applied for 30 minutes to the rat soleus muscle, on the myogenic differentiation (myoD), myostatin, and atrogin-1 gene expressions. DESIGN: Case-controlled study. SETTING: University laboratory. ANIMALS: Fifty 12-week-old male Wistar rats. INTERVENTIONS: Six groups of animals were given a single stretch bout and were evaluated immediately and 8, 24, 48, 72, and 168 hours later. Another 3 groups were evaluated immediately after 2, 3, and 7 stretches. An intact control group was also analyzed. MAIN OUTCOME MEASURES: The messenger ribonucleic acid (mRNA) levels of myoD, myostatin, and atrogin-1 were assessed by real-time polymerase chain reaction. RESULTS: Twenty-four hours after a single session of stretch only, the myoD mRNA levels had increased compared with the control group, whereas an increase in the atrogin-1 expression was observed after 2, 3, and 7 stretches. CONCLUSIONS: A single session of passive stretch increased the myoD gene expression, a factor related to muscle growth. Interestingly, daily stretches increased the atrogin-1 gene expression, a gene primarily associated with muscle atrophy. The results indicated that gene expression was responsive to the number of stretch sessions.


Assuntos
Proteínas Musculares/biossíntese , Músculo Esquelético/metabolismo , Proteína MyoD/biossíntese , Proteínas Ligases SKP Culina F-Box/biossíntese , Estresse Mecânico , Fator de Crescimento Transformador beta/biossíntese , Animais , Diferenciação Celular , Expressão Gênica , Masculino , Proteínas Musculares/genética , Proteína MyoD/genética , Miostatina , Reação em Cadeia da Polimerase , RNA Mensageiro/biossíntese , Ratos , Ratos Wistar , Proteínas Ligases SKP Culina F-Box/genética , Fator de Crescimento Transformador beta/genética
9.
Cell Tissue Res ; 321(2): 233-41, 2005 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-15947969

RESUMO

Triiodothyronine (T3) is known to play a key role in the function of several tissues/organs via the thyroid hormone receptor isoforms alpha (TRalpha) and beta (TRbeta). We have investigated the effects of GC-24, a novel synthetic TRbeta-selective compound, on skeletal muscle fiber-type determination, cross-sectional area, and gene expression in rat skeletal muscles. For fiber typing, cross sections of soleus and extensor digitorum longus (EDL) muscles were stained for myosin ATPase activity at various pHs. Serum T3, T4, and cholesterol levels were also determined. Analysis of highly T3-responsive genes, viz., myosin heavy chain IIa (MHCIIa) and sarcoendoplasmic reticulum adenosine triphosphatase (SERCA1), was performed by quantitative real-time polymerase chain reaction. Equimolar doses of T3 and GC-24 had a similar cholesterol-lowering effect. T3, but not GC-24, decreased fiber type I and increased fiber type II abundance in soleus and EDL muscles. Conversely, in EDL, both T3 and GC-24 decreased the mean cross-sectional area of type I fibers. MHCIIa gene expression was reduced (approximately 50%) by T3 and unchanged by GC-24. SERCA1 gene expression was strongly induced by T3 (approximately 20-fold) and mildly induced by GC-24 (approximately two-fold). These results show that GC-24 does not significantly alter the composition of skeletal muscle fiber type and further strengthens the putative use of GC compounds as therapeutic agents.


Assuntos
Acetatos/farmacologia , Compostos Benzidrílicos/farmacologia , Fibras Musculares de Contração Rápida/efeitos dos fármacos , Fibras Musculares de Contração Lenta/efeitos dos fármacos , Músculo Esquelético/efeitos dos fármacos , Receptores beta dos Hormônios Tireóideos/agonistas , Acetatos/uso terapêutico , Animais , Compostos Benzidrílicos/uso terapêutico , ATPases Transportadoras de Cálcio/genética , Diferenciação Celular/efeitos dos fármacos , Diferenciação Celular/fisiologia , Tamanho Celular/efeitos dos fármacos , Colesterol/metabolismo , Expressão Gênica/efeitos dos fármacos , Expressão Gênica/fisiologia , Fibras Musculares de Contração Rápida/metabolismo , Fibras Musculares de Contração Lenta/metabolismo , Músculo Esquelético/citologia , Músculo Esquelético/metabolismo , Cadeias Pesadas de Miosina/genética , Fenótipo , RNA Mensageiro/efeitos dos fármacos , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático , Receptores beta dos Hormônios Tireóideos/metabolismo , Tri-Iodotironina/efeitos adversos
10.
Cell Tissue Res ; 319(3): 479-89, 2005 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-15726428

RESUMO

This work was undertaken to provide further insights into the expression of tropism-related genes in regenerating skeletal muscle of adult rats treated with cyclosporin-A (CsA), a calcineurin inhibitor. Rats were treated with CsA for 5 days and, on the 6th day, were submitted to cryolesion of the soleus muscles. CsA treatment continued for 1, 10, and 21 days after cryolesion. Muscles were removed, frozen, and stored in liquid nitrogen. Body and muscle weights, histological sections stained with toluidine blue, and gene expression of the regeneration molecular markers, viz., desmin and neonatal myosin heavy chain, were assessed to confirm that cryolesion and CsA treatment were effective during the allowed regeneration time. Quantitative reverse transcription/polymerase chain reaction demonstrated that myostatin gene expression was not altered by either cryolesion or CsA treatment combined with cryolesion. Calpain-3 gene expression decreased at 1 day after cryolesion and also following CsA treatment combined with cryolesion. However, calpain-3 gene expression was strongly up-regulated (approximately five-fold) 10 days after cryolesion and returned to control levels at day 21. CsA treatment blocked calpain-3 gene expression rise induced by 10 days of cryolesion. Atrogin-1 gene expression was decreased at 1 day after cryolesion and following cryolesion combined with CsA treatment, returning to control levels at day 10. These results suggest that (1) calpain-3 has a differential role in the early and late stages of regeneration in a calcineurin-dependent manner, and (2) atrogin-1 is involved in the early stages of regeneration independently of calcineurin.


Assuntos
Calpaína/genética , Ciclosporina/farmacologia , Inibidores Enzimáticos/farmacologia , Expressão Gênica/efeitos dos fármacos , Isoenzimas/genética , Proteínas Musculares/genética , Músculo Esquelético/efeitos dos fármacos , Proteínas Ligases SKP Culina F-Box/genética , Fator de Crescimento Transformador beta/genética , Animais , Peso Corporal/efeitos dos fármacos , Calpaína/metabolismo , Temperatura Baixa/efeitos adversos , Criocirurgia , Primers do DNA/química , Modelos Animais de Doenças , Injeções Intraperitoneais , Isoenzimas/metabolismo , Masculino , Proteínas Musculares/metabolismo , Músculo Esquelético/lesões , Músculo Esquelético/metabolismo , Miostatina , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , Regeneração/fisiologia , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Proteínas Ligases SKP Culina F-Box/metabolismo , Fator de Crescimento Transformador beta/metabolismo
11.
Am J Physiol Endocrinol Metab ; 285(5): E1135-41, 2003 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-12965872

RESUMO

Thyrotoxicosis is frequently associated with increased bone turnover and decreased bone mass. To investigate the role of thyroid hormone receptor-beta (TR beta) in mediating the osteopenic effects of triiodothyronine (T3), female adult rats were treated daily (64 days) with GC-1 (1.5 microg/100 g body wt), a TR beta-selective thyromimetic compound. Bone mass was studied by dual-energy X-ray absorptiometry of several skeletal sites and histomorphometry of distal femur, and the results were compared with T3-treated (3 microg/100 g body wt) or control animals. As expected, treatment with T3 significantly reduced bone mineral density (BMD) in the lumbar vertebrae (L2-L5), femur, and tibia by 10-15%. In contrast, GC-1 treatment did not affect the BMD in any of the skeletal sites studied. The efficacy of GC-1 treatment was verified by a reduction in serum TSH (-52% vs. control, P < 0.05) and cholesterol (-21% vs. control, P < 0.05). The histomorphometric analysis of the distal femur indicated that T3 but not GC-1 treatment reduced the trabecular volume, thickness, and number. We conclude that chronic, selective activation of the TR beta isoform does not result in bone loss typical of T3-induced thyrotoxicosis, suggesting that the TR beta isoform is not critical in this process. In addition, our findings suggest that the development of TR-selective T3 analogs that spare bone mass represents a significant improvement toward long-term TSH-suppressive therapy.


Assuntos
Doenças Ósseas Metabólicas/prevenção & controle , Receptores dos Hormônios Tireóideos/agonistas , Tri-Iodotironina/análogos & derivados , Tri-Iodotironina/efeitos adversos , Animais , Peso Corporal/efeitos dos fármacos , Densidade Óssea/efeitos dos fármacos , Doenças Ósseas Metabólicas/induzido quimicamente , Colesterol/sangue , Feminino , Fêmur , Ratos , Ratos Wistar , Receptores dos Hormônios Tireóideos/efeitos dos fármacos , Receptores dos Hormônios Tireóideos/metabolismo , Receptores beta dos Hormônios Tireóideos , Tireotoxicose/induzido quimicamente , Tireotoxicose/complicações , Tireotropina/sangue , Tiroxina/sangue , Tri-Iodotironina/administração & dosagem
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