RESUMO
AIM: Investigate how AT1/2R affected the proliferation and apoptosis of chondrocytes induced by oxygen-glucose deprivation. METHODS: The proliferation and apoptosis of ATDC5 cells was detected by CCK-8 assay and flow cytometry analysis. The expression of Bax, Bcl-2, caspase-3, cleaved-caspase-3, AT1R, AT2R and HIF-1 was determined by Western blot analysis. The collagen II expression was detected by ELISA assay. RESULTS: Increased ratio of AT1R to AT2R induced by Ang II suppressed the proliferation of oxygen-glucose deprivation ATDC5 cells. Telmisartan, as AT1R inhibitor, promoted the proliferation and inhibited the apoptosis of ATDC5 cells and oxygen-glucose deprivation ATDC5 cells. The collagen II expression either intracellular or cellular supernatant was decreased after Ang II treatment, which was reversed by telmisartan. And, telmisartan reduced the AT1R expression while increased the AT2R expression in ATDC5 cells and oxygen-glucose deprivation ATDC5 cells. CONCLUSIONS: Ang II caused an increased ratio of AT1R to AT2R, which suppressed the proliferation of oxygen-glucose deprivation ATDC5 cells. Furthermore, telmisartan caused a decrease of AT1R and increase of AT2R, which promoted the proliferation and inhibited the apoptosis of oxygen-glucose deprivation ATDC5 cells. This new finding could provide a new insight into the treatment of osteoarthritis (Fig. 4, Ref. 19).
Assuntos
Apoptose , Condrócitos , Receptor Tipo 1 de Angiotensina , Receptor Tipo 2 de Angiotensina , Angiotensina II , Animais , Proliferação de Células , Glucose , Camundongos , Proteínas do Tecido Nervoso , Oxigênio , Proteínas RepressorasRESUMO
Metal prostheses of artificial joints undergo wear, producing numerous metal particles and ions, such as Cr3+ . Cr3+ is considered a key factor leading to aseptic loosening. Many studies focus on the effect of Cr3+ on osteoblasts; however, little is known about the effect of Cr3+ on the B-cell maturation antigen (BCMA) in the osteoblasts. In this study, we first demonstrated the BCMA expressed in human SaOS-2 osteoblasts through reverse transcriptase-PCR, Western blot, and immunocytochemical analyses. Cr3+ decreased alkaline phosphatase (ALP), osteocalcin (OC), cell mineralization, and collagen type I mRNA and protein expression. Moreover, Cr3+ has an inhibitive effect on the expression of the BCMA in human SaOS-2 osteoblasts. However, after we upregulated the expression of the BCMA, ALP, OC, cell mineralization, and collagen type I mRNA and protein expression were increased. Overall, this study demonstrates that the BCMA is involved in human SaOS-2 osteoblast osteogenetic metabolism and plays a regulatory role on the toxic effect of chromium ions on human SaOS-2 osteoblasts.
Assuntos
Antígeno de Maturação de Linfócitos B/metabolismo , Cromo/toxicidade , Regulação da Expressão Gênica/efeitos dos fármacos , Osteoblastos/efeitos dos fármacos , Osteogênese/efeitos dos fármacos , Fosfatase Alcalina/metabolismo , Antígeno de Maturação de Linfócitos B/genética , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Humanos , Osteoblastos/citologia , Osteoblastos/fisiologia , Osteogênese/genéticaRESUMO
Glucocorticoids (GC), the basic function of which is modulating carbohydrates metabolism, play a critical role in stress response by enhancing the organism's resistance. It is widely believed that they could promote glycogen synthesis. However, it is doubtful whether GC can still stimulate glycogen deposition in stress response, as it is known that glucose is imperatively needed at that time. Here, we used primary cultured rat hepatocytes to investigate the effects of GC on glycogen metabolism in vitro to exclude other influences in stress. The results showed that dexamethasone (Dex) played biphasic effects on hepatocytes glycogen metabolism depending on its dosage and the duration of stimulation. Dex could decrease glycogen content of hepatocytes in the higher concentration within a relatively shorter period of time, which could not be blocked by cycloheximide. Therefore, dual roles in hepatic glycogen metabolism played by GC were demonstrated, and a non-genomic mechanism might be involved in the glycogenolytic action of GC. We postulated that the biphasic effects of GC on hepatic glycogen metabolism might be of important significance in stress response.
Assuntos
Dexametasona/farmacologia , Glucocorticoides/farmacologia , Hepatócitos/efeitos dos fármacos , Glicogênio Hepático/metabolismo , Animais , Células Cultivadas , Cicloeximida/farmacologia , Hepatócitos/metabolismo , Masculino , Ratos , Ratos Sprague-DawleyRESUMO
Using succinate as a substrate, the activities of ATP synthase and adenylate kinase in liver mitochondria of male Sprague-Dawley rats 30 min after 20 per cent full skin thickness burns were increased in comparison with the sham burn rats, suggesting that these two enzymes might contribute to the increased rates of ATP formation and oxidative phosphorylation coupling during the early phase after burn injury.
Assuntos
Adenilato Quinase/metabolismo , Queimaduras/enzimologia , Mitocôndrias Hepáticas/enzimologia , ATPases Translocadoras de Prótons/metabolismo , Animais , Masculino , Fosforilação Oxidativa , Ratos , Ratos Sprague-Dawley , Fatores de TempoRESUMO
The modulation mechanism of IL-1 in relation to endotoxin (ET) was investigated in hemorrhangic shock rat. It was found that within 4 h after hemorrhagic shock, SD rat showed a significant increase in both ET and IL-1, the latter taking place earlier than the former. While SD rat reared in germ free condition showed an obvious increas in IL-1 but without marked change in ET, no matter whether the rats reared in different condition were pretreated with lactuolsc or anti-ET. Within 5 d after reinfusion of lost blood to the ordinary shock rat, IL-1 and ET changed in a parallel manner. When shock rats were treated with lactulose or anti-ET, both IL-1 and ET showed significant decrease as compared with the control. It is suggested from the above observation that ET is not an important factor in enhancing IL-1 activity in the early stage of hemorrhagic shock, but does contribute to the increased IL-1 activity in the later phase of hemorrhagic shock. The ET comes mainly from the gut in hemorrhagic state.
Assuntos
Endotoxinas/sangue , Interleucina-1/sangue , Choque Hemorrágico/sangue , Animais , Feminino , Vida Livre de Germes/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Ratos , Ratos WistarRESUMO
Hashimoto's encephalopathy may present with a variety of neurological symptoms and signs, including myoclonus, epileptic seizures, disturbance of consciousness, psychosis, ataxia, and presenile dementia. This report is of a 57-year-old woman with a history of thyroid disease who was investigated for generalised seizures, rapid decline in cognitive function, increasing dependency, and gradual change in personality. High thyroid autoantibody titres confirmed the diagnosis of Hashimoto's encephalopathy and her symptoms improved with treatment with prednisolone. The differential diagnosis of presenile dementia, aetiology and pathogenesis of Hashimoto's encephalomyelitis, and treatment options are discussed. Hashimoto's encephalomyelitis should be considered in the differential diagnosis of presenile dementia, particularly in patients with a history of thyroid disease.