RESUMEN
Alzheimer's disease (AD) is one of the most prevalent neurodegenerative disorder. It is characterized by the formation of amyloid plaques and neurofibrillary tangles in the brain, the degeneration of cholinergic neurons and neuronal cell death. The present study aimed to investigate the effect of luteolin, a flavonoid compound, on memory impairment in a streptozotocin (STZ)induced Alzheimer's rat model. Morris water maze and probe tests were performed to examine the effect of luteolin treatment on cognition and memory. The effect of luteolin on CA1 pyramidal layer thickness was also examined. The results demonstrated that luteolin significantly ameliorated the spatial learning and memory impairment induced by STZ treatment. STZ significantly reduced the thickness of CA1 pyramidal layer and treatment of luteolin completely abolished the inhibitory effect of STZ. Our results suggest that luteolin has a potentially protective effect on learning defects and hippocampal structures in AD.
Asunto(s)
Enfermedad de Alzheimer/tratamiento farmacológico , Enfermedad de Alzheimer/fisiopatología , Región CA1 Hipocampal/fisiopatología , Luteolina/farmacología , Aprendizaje por Laberinto/efectos de los fármacos , Memoria/efectos de los fármacos , Enfermedad de Alzheimer/inducido químicamente , Enfermedad de Alzheimer/patología , Animales , Región CA1 Hipocampal/patología , Modelos Animales de Enfermedad , Masculino , Ratas , Ratas Wistar , Estreptozocina/toxicidadRESUMEN
The non-steroidal anti-inflammatory agent, sulindac, has shown strong effects on cancer prevention in colorectal cancers, however, its anticancer activities on prostate cancer remain unclear. In the current study, human prostate cancer cell lines, LNCaP and PC-3, were treated with various concentrations of sulindac and it was found that sulindac significantly inhibits prostate cancer cell proliferation and promotes cell apoptosis in a dose- and time-dependent manner. Further studies revealed that sulindac significantly induces c-Jun NH2-terminal kinase (JNK) 1 phosphorylation and inhibits ß-catenin at the transcriptional and post-transcriptional levels. In conclusion, by targeting the JNK1/ß-catenin signaling pathway, sulindac may present a potential preventive or therapeutic agent for treatment of patients with prostate cancer.