Abstract:Objective: To observe the effect of electroacupuncture on the morphological change of the bladder tissue and the protein expression levels of NGF, TrkA, p-TrkA, AKT, and p-AKT in the bladder tissue of rats with neurogenic bladder after suprasacral spinal cord injury and to preliminarily explore its partial mechanism of action. Methods: Eighty female Sprague-Dawley rats were randomly divided into blank group, model group, electroacupuncture group, model/siNGF group, and electroacupuncture/siNGF group according … Show more
“…This result suggested successful modeling and indicated that NGF treatment had a certain recovery effect on neurons of spinal cord injury rats, which could further reduce the level of spinal cord injury in rats. The research conducted by the team of Zhang et al [20] shows that electroacupuncture can improve neurogenic bladder dysfunction by activating NGF/neurotrophin receptor (TrkA) signal transduction in rat model, which is similar to the results of this study. NGF is one of neurotrophic factors.…”
To explore the effect of nerve growth factor on neurons by establishing the animal model of spinal cord injury is the main objective. 40 Sprague Dawley rats were stochasticly divided into a model group and a control group of 20 rats. 5 rats in the model group were selected as model group A and the rest were model group B and 5 rats in the control group were selected as control group A and the rest were control group B. Model group A and control group A were treated with tail vein injection of nerve growth factor. The expression of nerve growth factor, vascular endothelial growth factor, glial fibrillary acidic protein and motor function in groups were observed, to observe the effect of nerve growth factor on proliferation and apoptosis of neuron cells. The expression of nerve growth factor in model group was significantly lower than that in control group (p<0.05) and the expression of nerve growth factor in model group A and control group A was higher than that in model group B and control group B group, respectively (p<0.05). Basso, Beattie and Bresnahan score in model group was lower than that in model group A (p<0.05). The expression of glial fibrillary acidic protein and vascular endothelial growth factor in model group A was higher than that of model group (p<0.05). The proliferation ability of control group was significantly higher than that of model group (p<0.05), the apoptosis rate of model group was higher than control group (p<0.05). Nerve growth factor participates in the occurrence and development of spinal cord injury and is bound up with the proliferation and apoptosis of neuronal cells.
“…This result suggested successful modeling and indicated that NGF treatment had a certain recovery effect on neurons of spinal cord injury rats, which could further reduce the level of spinal cord injury in rats. The research conducted by the team of Zhang et al [20] shows that electroacupuncture can improve neurogenic bladder dysfunction by activating NGF/neurotrophin receptor (TrkA) signal transduction in rat model, which is similar to the results of this study. NGF is one of neurotrophic factors.…”
To explore the effect of nerve growth factor on neurons by establishing the animal model of spinal cord injury is the main objective. 40 Sprague Dawley rats were stochasticly divided into a model group and a control group of 20 rats. 5 rats in the model group were selected as model group A and the rest were model group B and 5 rats in the control group were selected as control group A and the rest were control group B. Model group A and control group A were treated with tail vein injection of nerve growth factor. The expression of nerve growth factor, vascular endothelial growth factor, glial fibrillary acidic protein and motor function in groups were observed, to observe the effect of nerve growth factor on proliferation and apoptosis of neuron cells. The expression of nerve growth factor in model group was significantly lower than that in control group (p<0.05) and the expression of nerve growth factor in model group A and control group A was higher than that in model group B and control group B group, respectively (p<0.05). Basso, Beattie and Bresnahan score in model group was lower than that in model group A (p<0.05). The expression of glial fibrillary acidic protein and vascular endothelial growth factor in model group A was higher than that of model group (p<0.05). The proliferation ability of control group was significantly higher than that of model group (p<0.05), the apoptosis rate of model group was higher than control group (p<0.05). Nerve growth factor participates in the occurrence and development of spinal cord injury and is bound up with the proliferation and apoptosis of neuronal cells.
“…The maturation, plasticity, and survival of cholinergic neurons are inseparable from the nutritional support of NGF. NGF exerts physiological effects by binding to the TrkA or p75NTR receptor, while TrkA signaling inhibits apoptosis and promotes neuronal survival [49]; in contrast, the intracellular domain of p75NTR contains a "death domain, " and p75NTR overexpression facilitates neuronal apoptosis [2,14]. Therefore, we explored the effects of IHG and CHG on NGF receptors due to the close relationship between NGF receptors and neuronal apoptosis, and found that both IHG and CHG decreased TrkA level.…”
Background
Glucose fluctuation promotes neuronal apoptosis, which plays a central role in diabetic encephalopathy (DE). Nerve growth factor (NGF), and its interaction with high-affinity (TrkA) and low-affinity (p75NTR) receptors, are involved in neuronal survival. NGF/TrkA contributes to the activation of the PI3K/AKT pathway, which is beneficial for neuronal survival, and α-Lipoic acid (ALA) exerts clinically favorable neuroprotective effects in the periphery. Whether NGF receptors and the PI3K/AKT pathway are involved in glucose fluctuation-induced neuronal damage, as well as the potential molecular mechanism of ALA in protecting glucose fluctuation-induced neuronal damage, remain unclear.
Results
The results indicated that constant high glucose (CHG) and intermittent high glucose (IHG) significantly increased the expression of Bax and caspase-3, and decreased the expression of TrkA/p75NTR and p-AKT/AKT, while ALA stimulation reversed the above proteins in PC12 cells. IHG stimulates apoptosis more effectively than CHG in PC12 cells, which is related to the PI3K/AKT pathway but not to the TrkA/p75NTR. Furthermore, neuronal apoptosis induced by IHG was aggravated by the TrkA inhibitor K252a or the PI3K/AKT inhibitor LY294002, but this effect was alleviated by the p75NTR inhibitor TAT-pep5.
Conclusion
Glucose fluctuation induced cell apoptosis by regulating the TrkA/p75NTR and PI3K/AKT pathway, meanwhile ALA exhibited neuroprotective effects in response to IHG and CHG. These observations indicated that the PI3K/AKT pathway and the balance of TrkA/p75NTR are likely to serve as potential therapeutic targets for DE. In addition, ALA could be a possible therapeutic drug for DE.
“…Electroacupuncture (EA), which is a traditional Chinese medicinal therapy, has been widely used and applied during clinical practice and in animal models for the treatment of SCI 9â14 . The application of EA has been demonstrated to have neural protective and antiâinflammatory effects, which would improve the suitability of the damaged areas for axonal regeneration after SCI.…”
Aims
This study was aimed to investigate whether electroacupuncture (EA) would increase the secretion of neurotrophinâ3 (NTâ3) from injured spinal cord tissue, and, if so, whether the increased NTâ3 would promote the survival, differentiation, and migration of grafted tyrosine kinase C (TrkC)âmodified mesenchymal stem cell (MSC)âderived neural network cells. We next sought to determine if the latter would integrate with the host spinal cord neural circuit to improve the neurological function of injured spinal cord.
Methods
After NTâ3âmodified Schwann cells (SCs) and TrkCâmodified MSCs were coâcultured in a gelatin sponge scaffold for 14Â days, the MSCs differentiated into neuronâlike cells that formed a MSCâderived neural network (MN) implant. On this basis, we combined the MN implantation with EA in a rat model of spinal cord injury (SCI) and performed immunohistochemical staining, neural tracing, electrophysiology, and behavioral testing after 8Â weeks.
Results
Electroacupuncture application enhanced the production of endogenous NTâ3 in damaged spinal cord tissues. The increase in local NTâ3 production promoted the survival, migration, and maintenance of the grafted MN, which expressed NTâ3 highâaffinity TrkC. The combination of MN implantation and EA application improved cortical motorâevoked potential relay and facilitated the locomotor performance of the paralyzed hindlimb compared with those of controls. These results suggest that the MN was better integrated into the host spinal cord neural network after EA treatment compared with control treatment.
Conclusions
Electroacupuncture as an adjuvant therapy for TrkCâmodified MSCâderived MN, acted by increasing the local production of NTâ3, which accelerated neural network reconstruction and restoration of spinal cord function following SCI.
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