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1.
Steroids ; 150: 108445, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31295461

RESUMO

Low vitamin D status has been associated with increased risks of renal cell carcinoma (RCC). This study aimed to analyze the link between low vitamin D status and interleukin (IL)-6/STAT3 hyper-activation in clear cell RCC (ccRCC) patients. Forty-three newly diagnosed ccRCC patients and 86 age- and sex-matched controls were recruited. The association between low vitamin D status and IL-6/STAT3 hyper-activation was analyzed. Proliferation makersand STAT3 signal were evaluated. As expected, serum IL-6 level was higher in ccRCC patients than in controls. Moreover, serum IL-6 level was reversely correlated with serum 25(OH)D in ccRCC patients but not in controls. In addition, STAT3 signaling was hyper-activated in cancerous tissue. CcRCC patients were divided into three groups according to serum 25(OH)D level: vitamin D sufficiency (VitD-S, ≥30 ng/ml), vitamin D insufficiency (VitD-I, ≥20 and <30 ng/ml) or vitamin D deficiency (VitD-D, <20 ng/ml). Serum IL-6 was higher in ccRCC patients with VitD-D than those with VitD-S/VitD-I. Cancerous pSTAT3 level was higher in ccRCC patients with VitD-D than those with VitD-S/VitD-I. The number of pSTAT3+ nuclei in cancerous tissue was more in ccRCC patients with VitD-D than those with VitD-S/VitD-I. The expressions of cancerous PCNA, cyclin D1 and Ki-67, three markers of proliferation, were higher in ccRCC patients with VitD-D than those with VitD-S/VitD-I. The in vitro experiments showed that active vitamin D3 inhibited LPS-induced STAT3 phosphorylation in ACHN cells. Our results provide evidence that low vitamin D status is correlated with hyper-activation of cancerous IL-6/STAT3 and proliferation in ccRCC patients.

2.
Oxid Med Cell Longev ; 2019: 1897316, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31019650

RESUMO

Background: Cellular stress is involved in ischemia/reperfusion- (I/R-) induced acute kidney injury (AKI). This study is aimed at investigating the effects of pretreatment with cholecalciferol on renal oxidative stress and endoplasmic reticulum (ER) stress during I/R-induced AKI. Methods: I/R-induced AKI was established by cross-clamping renal pedicles for 90 minutes and then reperfusion. In the Chol + I/R group, mice were orally administered with three doses of cholecalciferol (25 µg/kg) at 1, 24, and 48 h before ischemia. Renal cellular stress and kidney injury were measured at different time points after reperfusion. Results: I/R-induced AKI was alleviated in mice pretreated with cholecalciferol. In addition, I/R-induced renal cell apoptosis, as determined by TUNEL, was suppressed by cholecalciferol. Additional experiment showed that I/R-induced upregulation of renal GRP78 and CHOP was inhibited by cholecalciferol. I/R-induced renal IRE1α and eIF2α phosphorylation was attenuated by cholecalciferol. Moreover, I/R-induced renal GSH depletion, lipid peroxidation, and protein nitration were blocked in mice pretreated with cholecalciferol. I/R-induced upregulation of renal NADPH oxidases, such as p47phox, gp91phox, and nox4, was inhibited by cholecalciferol. I/R-induced upregulation of heme oxygenase- (HO-) 1, gshpx and gshrd, was attenuated in mice pretreated with cholecalciferol. Conclusions: Pretreatment with cholecalciferol protects against I/R-induced AKI partially through suppressing renal cellular stress response.


Assuntos
Lesão Renal Aguda/etiologia , Lesão Renal Aguda/patologia , Colecalciferol/farmacologia , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Rim/patologia , Estresse Oxidativo/efeitos dos fármacos , Traumatismo por Reperfusão/complicações , Animais , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Glutationa/metabolismo , Rim/efeitos dos fármacos , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Camundongos Endogâmicos ICR , NADPH Oxidases/metabolismo , Receptores de Calcitriol/metabolismo , Transdução de Sinais/efeitos dos fármacos , Regulação para Cima/efeitos dos fármacos
3.
Medicine (Baltimore) ; 98(12): e14788, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30896622

RESUMO

RATIONALE: Primary squamous cell carcinoma (SCC) of the seminal vesicle is extremely rare, and the clinical characteristics of this kind of malignancy are still unclear. PATIENT CONCERNS: A 62-year-old male patient presented with complaints of sensation of rectal tenesmus and dysuria. DIAGNOSIS: Ultrasonography suggested a hypoechoic mass behind the bladder, meanwhile, computerized tomography (CT) and magnetic resonance imaging (MRI) revealed a 40 mm × 45 mm × 48 mm mixed solid/cystic tumorous lesion in the right seminal vesicle. Postoperative histology confirmed the diagnosis of primary SCC in the seminal vesicle. INTERVENTION: The mass was surgically excised with a laparoscopic approach. Postoperatively, 6 cycles of chemotherapy and 50 Gy of external beam radiation were concurrently performed on this patient. OUTCOMES: No local recurrence or distant metastasis was detected within 2 years after the surgery. LESSONS: Primary SCC of the seminal vesicle is a rare neoplasm with a poor prognosis. Clinically, it is crucial to establish early precise diagnosis and apply multimodality treatment.


Assuntos
Carcinoma de Células Escamosas/patologia , Neoplasias dos Genitais Masculinos/patologia , Glândulas Seminais/patologia , Carcinoma de Células Escamosas/diagnóstico por imagem , Carcinoma de Células Escamosas/cirurgia , Quimioterapia Adjuvante/métodos , Neoplasias dos Genitais Masculinos/diagnóstico por imagem , Neoplasias dos Genitais Masculinos/cirurgia , Humanos , Laparoscopia/métodos , Masculino , Pessoa de Meia-Idade , Glândulas Seminais/diagnóstico por imagem , Glândulas Seminais/cirurgia
4.
Medicine (Baltimore) ; 97(39): e12459, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30278528

RESUMO

Benign prostatic hyperplasia (BPH) is a common disorder in the aging male population. Despite evidence that thyroid status impacts the prostate, the objective of this study was to examine whether patients with hyperthyroidism were at a greater risk for BPH.This study is a retrospective nationwide population-based cohort study of the Chinese population. Data for this study were retrieved from the Taiwan National Health Insurance Research Database (NHIRD). Overall, 1032 male patients aged 40 years or older with hyperthyroidism diagnosed between 2000 and 2006 were included in the hyperthyroidism group, and 4128 matched controls without hyperthyroidism were included in the non-hyperthyroidism group. Both groups were monitored until the end of 2011. A Cox proportional hazards regression model was used to compute and compare the risk of BPH between study participants with and those without hyperthyroidism.Patients with hyperthyroidism exhibited a greater incidence of BPH (18.51% vs 15.53%) than did the controls. Furthermore, the hazard ratio (HR) of the hyperthyroidism group was 1.24 times that of the control group [95% confidence interval (95% CI 1.05-1.46)] signifying that there is a significant 24% increase in the risk of BPH with the presence of hyperthyroidism. This increased risk of BPH with hyperthyroidism, however, failed to remain significant (adjusted HR = 1.11, 95% CI = 0.94-1.3) after adjusting for covariates of age (adjusted HR = 2.72, 95% CI = 2.32-3.2), diabetes (adjusted HR = 1.4, 95% CI = 1.17-1.68), hypertension (adjusted HR = 1.74, 95% CI = 1.49-2.03), hyperlipidemia (adjusted HR = 1.25, 95% CI = 1.03-1.53), neurogenic bladder, cystitis (adjusted HR = 1.23, 95% CI = 0.58-2.59), urethral stricture (adjusted HR = 2.01, 95% CI = 0.28-14.47), urethritis (adjusted HR = 1.52, 95% CI = 0.72-3.21), and urinary tract infection (adjusted HR = 1.77, 95% CI = 1.31-2.39).After adjustment for comorbidities and covariates, hyperthyroidism was not found to be a significant risk factor of BPH in our male study subjects. Further research is warranted to validate our results and elucidate the association of the pathophysiology of these 2 diseases.


Assuntos
Hipertireoidismo/complicações , Hipertireoidismo/epidemiologia , Próstata/patologia , Hiperplasia Prostática/epidemiologia , Hiperplasia Prostática/patologia , Adulto , Idoso , Idoso de 80 Anos ou mais , China/epidemiologia , Comorbidade/tendências , Fatores de Confusão (Epidemiologia) , Diabetes Mellitus/epidemiologia , Humanos , Hiperlipidemias/epidemiologia , Hipertireoidismo/diagnóstico , Incidência , Masculino , Pessoa de Meia-Idade , Avaliação de Resultados (Cuidados de Saúde) , Estudos Retrospectivos , Fatores de Risco , Taiwan/epidemiologia
5.
Eur J Pharmacol ; 838: 60-68, 2018 Nov 05.
Artigo em Inglês | MEDLINE | ID: mdl-30196109

RESUMO

It is increasingly recognized that farnesoid X receptor (FXR) has anti-inflammatory and antioxidant activities. The present study investigated the effects of obeticholic acid (OCA), a novel synthetic FXR agonist, on renal inflammation and oxidative stress in a model of sepsis-induced acute kidney injury. All mice except controls were intraperitoneally injected with lipopolysaccharide (LPS, 2.0 mg/kg). In the OCA + LPS group, mice were orally pretreated with three doses of OCA (5 mg/kg) at 48, 24 and 1 h before LPS injection. Interestingly, OCA pretreatment alleviated LPS-induced renal dysfunction and pathological damage. Moreover, OCA pretreatment repressed renal inflammatory cytokines and chemokines during LPS-induced acute kidney injury. In addition, OCA blocked nuclear translocation of nuclear factor kappa B (NF-κB) p65 and p50 subunits in tubular epithelial cells of renal cortex. Additional experiment showed that OCA pretreatment attenuated LPS-induced renal glutathione depletion, lipid peroxidation and protein nitration. Moreover, OCA pretreatment inhibited the upregulation of renal NADPH oxidase and inos genes during LPS-induced acute kidney injury. In conclusion, OCA pretreatment protects against sepsis-induced acute kidney injury through inhibiting renal inflammation and oxidative stress. These results provide evidence for roles of FXR as an important regulator of inflammation and oxidative stress in the kidney.

6.
J Steroid Biochem Mol Biol ; 182: 14-20, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-29684478

RESUMO

Vitamin D deficiency is especially prevalent in pregnant women and children. Our recent study demonstrated that vitamin D deficiency in early life disturbed testicular development. This study investigated the effects of vitamin D deficiency in early life on prostatic hyperplasia in middle-aged mice. In control group, dams and their male pups were fed with standard-chow diets. In VDD group, dams were fed with vitamin D deficient (VDD) diets throughout pregnancy and lactation. After weaning, male pups continued to be fed with VDD diets. As expected, prostate weight was elevated and prostatic hyperplasia was observed in VDD-fed mice. The number of prostatic Ki-67-positive epithelial cells, a proliferation marker, was increased in VDD-fed mice. Further analysis found that vitamin D deficiency promoted inflammatory infiltration and stromal fibrosis in prostate of middle-aged mice. Moreover, vitamin D deficiency activated NF-κB and up-regulated Il-6 mRNA in prostate of middle-aged mice. In addition, vitamin D deficiency activated prostatic STAT3, a proliferation pathway in middle-aged mice. Of interest, VDD-induced prostatic inflammation and hyperplasia were partially reversed when VDD diets was replaced with standard diets. These results provide evidence that vitamin D deficiency in early life promotes prostatic hyperplasia in middle-aged mice through exacerbating local inflammation.

7.
Asian J Androl ; 20(3): 265-269, 2018 May-Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29286007

RESUMO

The present study aimed to investigate the relationship between histopathological subtype and the probability of inguinal lymph node metastasis (ILNM) in patients with penile squamous cell carcinoma (PSCC). The clinical records of 198 consecutive patients with PSCC were analyzed retrospectively. Primary lesions were reevaluated according to the 2016 World Health Organization (WHO) histopathological classification. We retrieved the clinicopathological factors from the medical records including age, clinical lymph node stage, pathological tumor stage, lymphatic invasion, and nerve invasion. Uni- and multivariate logistic regression analyses were used to explore the risk factors of ILNM. Multivariate analyses identified clinical lymph node stage (P = 0.000), pathological tumor stage (P = 0.016), histologic grade (P = 0.000), and risk group of histological subtypes (P = 0.029) as independent predictors for ILNM. Compared with the low-risk group of PSCC subtypes, the intermediate- (HR: 3.66, 95% CI: 1.30-10.37, P = 0.021) and high-risk groups (HR: 28.74, 95% CI: 2.37-348.54, P = 0.008) were significantly associated with ILNM. In conclusion, the histopathological subtype of the primary lesion is a significant predictor for ILNM in patients with PSCC.

8.
PLoS One ; 12(8): e0182584, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28783760

RESUMO

Previous studies demonstrated that inflammatory microenvironment promoted prostate cancer progression. This study investigated whether total glucosides of paeony (TGP), the active constituents extracted from the root of Paeonia Lactiflora Pall, suppressed lipopolysaccharide (LPS)-stimulated proliferation, migration and invasion in androgen insensitive prostate cancer cells. PC-3 cells were incubated with LPS (2.0 µg/mL) in the absence or presence of TGP (312.5 µg /mL). As expected, cells at S phase and nuclear CyclinD1, the markers of cell proliferation, were increased in LPS-stimulated PC-3 cells. Migration activity, as determined by wound-healing assay and transwell migration assay, and invasion activity, as determined by transwell invasion assay, were elevated in LPS-stimulated PC-3 cells. Interestingly, TGP suppressed LPS-stimulated PC-3 cells proliferation. Moreover, TGP inhibited LPS-stimulated migration and invasion of PC-3 cells. Additional experiment showed that TGP inhibited activation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK)/p38 in LPS-stimulated PC-3 cells. Correspondingly, TGP attenuated upregulation of interleukin (IL)-6 and IL-8 in LPS-stimulated PC-3 cells. In addition, TGP inhibited nuclear translocation of signal transducer and activator of transcription 3 (STAT3) in LPS-stimulated PC-3 cells. These results suggest that TGP inhibits inflammation-associated STAT3 activation and proliferation, migration and invasion in androgen insensitive prostate cancer cells.


Assuntos
Movimento Celular/efeitos dos fármacos , Glucosídeos/farmacologia , Lipopolissacarídeos/farmacologia , Paeonia/química , Neoplasias de Próstata Resistentes à Castração/patologia , Transporte Ativo do Núcleo Celular/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral , Núcleo Celular/efeitos dos fármacos , Núcleo Celular/metabolismo , Proliferação de Células/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Humanos , Interleucina-6/metabolismo , Interleucina-8/metabolismo , Masculino , NF-kappa B/metabolismo , Invasividade Neoplásica , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais/efeitos dos fármacos , Regulação para Cima/efeitos dos fármacos , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
9.
Oncotarget ; 8(13): 22076-22085, 2017 Mar 28.
Artigo em Inglês | MEDLINE | ID: mdl-28423553

RESUMO

Vitamin D deficiency has been associated with increased risks of prostate cancer. Nevertheless, the mechanisms remain unclear. The aim of this study was to analyze the association among prostate cancer, vitamin D status and inflammation. Sixty patients with newly diagnosed prostate cancer and 120 age-matched controls were recruited for this study. Vitamin D status was evaluated and serum inflammatory molecules were measured. Serum 25-(OH)D was lower in patients with prostate cancer. Moreover, serum 25(OH)D was lower in patients with severe prostate cancer than patients with mild and moderate prostate cancer. By contrast, serum C-reactive protein (CRP) and interleukin (IL)-8, two inflammatory molecules, were elevated in patients with prostate cancer. Serum 25-(OH)D was negatively correlated with serum CRP and IL-8 in patients with prostate cancer. Additional analysis showed that the percentage of vitamin D receptor positive nucleus in the prostate was reduced in patients with prostate cancer. By contrast, the percentage of nuclear factor kappa B p65-positive nucleus was elevated in patients with prostate cancer. Our results provide evidence that there is an association among prostate cancer, vitamin D deficiency and inflammatory signaling. Inflammation may be an important mediator for prostate cancer progression in patients with low vitamin D status.


Assuntos
Biomarcadores Tumorais/sangue , Inflamação/sangue , Neoplasias da Próstata/complicações , Deficiência de Vitamina D/sangue , Vitamina D/sangue , Idoso , Proteína C-Reativa/metabolismo , Estudos de Casos e Controles , Seguimentos , Humanos , Inflamação/etiologia , Masculino , Gradação de Tumores , Prognóstico , Receptores de Calcitriol/sangue , Fatores de Risco , Deficiência de Vitamina D/etiologia
10.
Exp Toxicol Pathol ; 68(4): 215-22, 2016 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-26776764

RESUMO

Bladder cancer is one of the leading causes of cancer-related death in the world. Prolonged exposure to benzidine is a known cause of bladder cancer. Curcumin has been clinically used in chemoprevention and treatment of cancer. However, it remains unknown whether mitogen-activated protein kinase (MAPK) pathways are involved in curcumin-mediated protection from benzidine-associated promotive effects on bladder cancer. In our study, we found that benzidine increased the proliferation of human bladder cancer T24 cells, triggered transition of the cells from G1 to S phase, elevated the expression of cyclin D1 and proliferating cell nuclear antigen (PCNA) and decreased p21 expression. Meanwhile, exposure of T24 cells to benzidine resulted in activation of extracellular regulated protein kinases 1 and 2 (ERK1/2) pathway as well as activator protein 1 (AP-1) proteins. Treatment with ERK1/2 inhibitor U0126 or curcumin effectively abrogated benzidine-triggered cell proliferation and ERK1/2/AP-1 activation. These results suggested for the first time that curcumin in low concentrations played a protective role in benzidine-induced ERK1/2/AP-1 activation and proliferation of bladder cancer cells, therefore providing new insights into the pathogenesis and chemoprevention of benzidine-associated bladder cancer.


Assuntos
Antineoplásicos/farmacologia , Benzidinas/toxicidade , Proliferação de Células/efeitos dos fármacos , Curcumina/farmacologia , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Neoplasias da Bexiga Urinária , Técnicas de Cultura de Células , Ciclo Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Humanos , Neoplasias da Bexiga Urinária/enzimologia , Neoplasias da Bexiga Urinária/patologia
11.
Sci Rep ; 5: 18687, 2015 Dec 22.
Artigo em Inglês | MEDLINE | ID: mdl-26691774

RESUMO

Vitamin D receptor (VDR) is highly expressed in human and mouse kidneys. Nevertheless, its functions remain obscure. This study investigated the effects of vitamin D3 (VitD3) pretreatment on renal inflammation during lipopolysaccharide (LPS)-induced acute kidney injury. Mice were intraperitoneally injected with LPS. In VitD3 + LPS group, mice were pretreated with VitD3 (25 µg/kg) at 48, 24 and 1 h before LPS injection. As expected, an obvious reduction of renal function and pathological damage was observed in LPS-treated mice. VitD3 pretreatment significantly alleviated LPS-induced reduction of renal function and pathological damage. Moreover, VitD3 pretreatment attenuated LPS-induced renal inflammatory cytokines, chemokines and adhesion molecules. In addition, pretreatment with 1,25(OH)2D3, the active form of VitD3, alleviated LPS-induced up-regulation of inflammatory cytokines and chemokines in human HK-2 cells, a renal tubular epithelial cell line, in a VDR-dependent manner. Further analysis showed that VitD3, which activated renal VDR, specifically repressed LPS-induced nuclear translocation of nuclear factor kappa B (NF-κB) p65 subunit in the renal tubules. LPS, which activated renal NF-κB, reciprocally suppressed renal VDR and its target gene. Moreover, VitD3 reinforced the physical interaction between renal VDR and NF-κB p65 subunit. These results provide a mechanistic explanation for VitD3-mediated anti-inflammatory activity during LPS-induced acute kidney injury.


Assuntos
Lesão Renal Aguda/induzido quimicamente , Lesão Renal Aguda/patologia , Colecalciferol/uso terapêutico , Inflamação/tratamento farmacológico , Rim/patologia , Lesão Renal Aguda/tratamento farmacológico , Lesão Renal Aguda/enzimologia , Animais , Linhagem Celular , Quimiocinas/metabolismo , Colecalciferol/farmacologia , Ciclo-Oxigenase 2/metabolismo , Humanos , Inflamação/complicações , Molécula 1 de Adesão Intercelular/metabolismo , Rim/efeitos dos fármacos , Lipopolissacarídeos , Masculino , Camundongos , Fosfatidilinositol 3-Quinases/metabolismo , Ligação Proteica/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-akt/metabolismo , RNA Interferente Pequeno/metabolismo , Receptores de Calcitriol/metabolismo , Transdução de Sinais/efeitos dos fármacos , Fator de Transcrição RelA/metabolismo , Transfecção , Molécula 1 de Adesão de Célula Vascular/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
12.
J Steroid Biochem Mol Biol ; 152: 133-41, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-26013770

RESUMO

Increasing evidence demonstrates that reactive oxygen species plays important roles in sepsis-induced acute kidney injury. This study investigated the effects of VitD3 pretreatment on renal oxidative stress in sepsis-induced acute kidney injury. Mice were intraperitoneally injected with lipopolysaccharide (LPS, 2.0mg/kg) to establish an animal model of sepsis-induced acute kidney injury. In VitD3+LPS group, mice were orally pretreated with three doses of VitD3 (25 µg/kg) at 1, 24 and 48 h before LPS injection. As expected, oral pretreatment with three daily recommended doses of VitD3 markedly elevated serum 25(OH)D concentration and efficiently activated renal VDR signaling. Interestingly, LPS-induced renal GSH depletion and lipid peroxidation were markedly alleviated in VitD3-pretreated mice. LPS-induced serum and renal nitric oxide (NO) production was obviously suppressed by VitD3 pretreatment. In addition, LPS-induced renal protein nitration, as determined by 3-nitrotyrosine residue, was obviously attenuated by VitD3 pretreatment. Further analysis showed that LPS-induced up-regulation of renal inducible nitric oxide synthase (inos) was repressed in VitD3-pretreated mice. LPS-induced up-regulation of renal p47phox and gp91phox, two NADPH oxidase subunits, were normalized by VitD3 pretreatment. In addition, LPS-induced down-regulation of renal superoxide dismutase (sod) 1 and sod2, two antioxidant enzyme genes, was reversed in VitD3-pretreated mice. Finally, LPS-induced tubular epithelial cell apoptosis, as determined by TUNEL, was alleviated by VitD3 pretreatment. Taken together, these results suggest that VitD3 pretreatment alleviates LPS-induced renal oxidative stress through regulating oxidant and antioxidant enzyme genes.


Assuntos
Lesão Renal Aguda/tratamento farmacológico , Colecalciferol/uso terapêutico , Rim/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , 25-Hidroxivitamina D 2/sangue , Lesão Renal Aguda/induzido quimicamente , Animais , Apoptose/efeitos dos fármacos , Glutationa/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Lipopolissacarídeos , Masculino , Glicoproteínas de Membrana/biossíntese , Camundongos , NADPH Oxidase 2 , NADPH Oxidases/biossíntese , Óxido Nítrico/biossíntese , Óxido Nítrico Sintase Tipo II/biossíntese , Receptores de Calcitriol/metabolismo , Superóxido Dismutase/biossíntese , Superóxido Dismutase-1 , Tirosina/análogos & derivados , Tirosina/análise
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