RESUMO
Increasing evidence suggests that the cerebrospinal fluid-contacting nucleus (CSF-contacting nucleus) mediates the transduction and regulation of pain signals. However, the precise molecular mechanisms remain unclear. Studies show that release of fractalkine (FKN) from neurons plays a critical role in nerve injury-related pain. We tested the hypothesis that release of FKN from the CSF-contacting nucleus regulates neuropathic pain, in a chronic constriction injury rat model. The results show that FKN is expressed by neurons, via expression of its only receptor CX3CR1 in the microglia. The levels of soluble FKN (sFKN) were markedly upregulated along with the increase in FKN mRNA level in rats subjected to chronic constriction injury. In addition, injection of FKN-neutralizing antibody into the lateral ventricle alleviated neuropathic pain-related behavior followed by reduction in microglial activation in the CSF-contacting nucleus. The results indicate that inhibition of FKN release by the CSF-contacting nucleus may ameliorate neuropathic pain clinically.
Assuntos
Animais , Masculino , Ratos , Núcleo Celular/metabolismo , Líquido Cefalorraquidiano/metabolismo , Limiar da Dor/fisiologia , Quimiocina CX3CL1/metabolismo , Dor Crônica/metabolismo , Neuralgia/metabolismo , Regulação para Cima , Ratos Sprague-Dawley , Modelos Animais de Doenças , Injeções IntraventricularesRESUMO
The aim of this study was to investigate the repair effect of human acellular amniotic membrane (HAAM) loading bone marrow mesenchymal stem cells (BMSCs) on articular cartilage defect in rabbits. Rabbit BMSCs were isolated and cultured, and they were then inoculated on HAAM to prepare the complex of HAAM and BMSCs. Twenty-four rabbits were randomly divided into groups A and B, with 12 animals in each group. The left and right sides were used as the experimental and control sides, respectively. The models of bilateral articular cartilage defect were established. The defect areas on the experimental side in groups A and B were implanted with the complex of HAAM and BMSCs and HAAM alone, respectively. The control sides of the two groups were not implanted with any material. In the 8th and 12th week after surgery, gross observation, histological examination and cartilage defect scoring were performed. In the 8th and 12th postoperative week, gross observation and histological observation showed that dense cartilage-like cells appeared in group A but not in group B, indicating preferable cartilage repair. The cartilage defect score on the experimental side in group A was 5.31 ± 0.68 in the 8th week and 3.23 ± 0.52 in the 12th week, and that in group A was significantly lower than in group B (P < 0.05). HAAM loading BMSCs has a good repair effect on articular cartilage defect under an in vitro environment.