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Objective To study the endogenous glucocorticoid on rat femoral head microenvironment of 11 hydroxysteroid dehydrogenase expression ,and to discuss the influence of combined with femoral head pathological changes of the corresponding mechanism .Methods Sixty SD rats were divided into control group ,1‐month group ,3‐months group ,each 20 rats in group .1‐month group and 3‐months group inject cortisone acetate in the abdominal cavity intraperitoneal for 1‐month or 3‐months each .Im‐munohistochemical ,immunofluorescence ,Real‐time qPCR ,HE staining were employed in this study .Results From immunohisto‐chemical ,immunofluorescence ,Real‐time qPCR ,the 11 hydroxysteroid dehydrogenase content of 1‐month group and 3‐months group were higher than that of the control group(P<0 .05) .From HE staining we detected 1‐month group in the bone marrow cavity in‐creased in fat cells ,3‐months group subchondral trabecular bone density decreased ,compared with the control group(P< 0 .05) . Conclusion Supplement of corticosterone could promote rat femoral head microenvironment 11 hydroxysteroid dehydrogenase ex‐pression and subchondral trabecular bone density decrease .
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<p><b>OBJECTIVE</b>To observe the effect of Sam68 gene silencing on proliferation of nasopharyngeal carcinoma (NPC) cell line 5-8F and explore its possible molecular mechanism.</p><p><b>METHODS</b>The NPC cell line 5-8F was transfected with a small interfering RNA (siRNA) targeting Sam68 and the cell proliferation changes were observed. Quantitative RT-PCR and Western blotting were used to examine the changes in the expressions of Sam68, cell cycle-related proteins, and some up-stream proteins in the transfected cells.</p><p><b>RESULTS</b>Transfection of 5-8F cells with Sam68-specific siRNA significantly lowered the mRNA and proteins levels of Sam68, suppressed cell proliferation, decreased the expression of Cyclin D1, and increased the expression of p27. The transfected cells showed obviously decreased expressions of p-FOXO3a, p-Akt and p-GSK-3β, but the expressions of FOXO3a, Akt and GSK-3β were not obviously affected.</p><p><b>CONCLUSIONS</b>Sam68 modulates the proliferation of NPC cells probably by activating Akt/FOXO3a pathway and regulating the cell proliferation-related molecules.</p>
Assuntos
Humanos , Proteínas Adaptadoras de Transdução de Sinal , Genética , Metabolismo , Carcinoma , Linhagem Celular Tumoral , Proliferação de Células , Proteínas de Ligação a DNA , Genética , Metabolismo , Proteína Forkhead Box O3 , Fatores de Transcrição Forkhead , Metabolismo , Inativação Gênica , Quinase 3 da Glicogênio Sintase , Metabolismo , Glicogênio Sintase Quinase 3 beta , Neoplasias Nasofaríngeas , Genética , Patologia , Proteínas Proto-Oncogênicas c-akt , Metabolismo , RNA Mensageiro , Genética , Metabolismo , RNA Interferente Pequeno , Genética , Proteínas de Ligação a RNA , Genética , MetabolismoRESUMO
Objective To explore the relations between UA and serum hs-CRP, the effects of early intervention with atovastatin on serum hs-CRP in patients with UA and its clinical significance in the early management of UA. Methods T 60 patients with UA (UA group),53 patients with stable angina (SA group) and 50 healthy controls (control group) were enrolled to the study. The serum hs-CRP levels were measured by particle enhanced immunoturbidimetric assay. UA group were randomly assigned to the atovastatin group and the routine group for a 4-week treatment immediately after admission. Selected coronary artery angiography was performed in 78 patients and 29 healthy controls with Judkin's technique. Results Baseline of hs-CRP in patients with UA was significantly higher than those in SA group and control group ( P