RESUMO
We sought to investigate the effect of nerve growth factor (NGF) expression on the formation and prognosis of cerebral aneurysms. Forty-eight cases were selected following a diagnosis of cerebral aneurysm using computed tomography angiography and surgical confirmation. Thirty-four cases of healthy deaths were also chosen. The tissue was tested for NGF expression changes by reverse-transcription PCR, Western blot and histopathology, and NGF expression was compared between the cerebral aneurysm and healthy groups. The expression level of NGF in cerebral aneurysm tissue was significantly increased over that observed in control tissue. The abnormal expression of NGF is related to cerebral aneurysms. The elevated expression of NGF in cerebral aneurysms may be associated with a poor prognosis.
Assuntos
Angiografia Cerebral/métodos , Aneurisma Intracraniano/diagnóstico por imagem , Aneurisma Intracraniano/patologia , Fator de Crescimento Neural/metabolismo , Idoso , Feminino , Humanos , Aneurisma Intracraniano/mortalidade , Masculino , Pessoa de Meia-Idade , Fator de Crescimento Neural/biossíntese , Prognóstico , Tomografia Computadorizada por Raios XRESUMO
We sought to investigate the relationship between abnormal expression of nitric oxide synthase (NOS) and pathogenesis of cerebral aneurysm. Brain tissues were collected from 36 patients with cerebral aneurysm confirmed by computer tomography with angiography or neurosurgical therapy. The control group consisted of 25 patients of similar age who had no vascular diseases, as confirmed by magnetic resonance imaging. Samples of cortical arterioles were collected. The structure of the aneurysms was detected by hematoxylin and eosin staining, and the expression of inducible NOS was detected by immunohistochemistry. NOS expression was significantly higher in the patient group than in the control group (patients: 30/36 strongly positive; control: 0/25 strongly positive; P < 0.05). In conclusion, the pathogenesis underlying cerebral aneurysm may be due to abnormal expression of NOS, degradation of the extracellular matrix, aggravation of a pro-inflammatory reaction, or a deficiency in arterial elasticity layer synthesis. These changes may result in a deficiency in vascular remodeling.