Objective To investigate the effects of Neuritin on the regeneration of the neural axons after acute spinal cord injury (SCI) in rats. Methods The model of acute SCI at T10 was establ ished in 54 adult healthy Wistar rats (half males and half females) weighing 250-300 g by using the improved Allen’s weight-drop method. The rats were randomly dividedinto 3 groups. 100 μL (6 μg) Neuritin and His protein was injected into group A (n=24) and group B (n=24), respectively,through subarachnoid catheter. Six rats from each group were killed 3, 7, 14, and 28 days after injury to receive Basso, Beattie and Bresnahan (BBB) locomotor rating scal ing, HE staining observation, and immunohistochemistry staining observation for neurofilament 200 (NF-200) and growth associated protein 43 (GAP-43). Group C (n=6) served as sham-operated group receiving laminectomy without spinal injury and with an empty catheter in the subarachnoid space and received the above observations 7 days after injury. Results BBB scale: after operation, the scale of groups A and B was increased over time; group A was significantly higher than group B from 14 days (P lt; 0.05); group C was higher than groups A and B at different time points after operation (P lt; 0.05). HE staining: in group C, the injured spinal tissue was normal after operation; from 7 days after operation, group A presented deeper-stained nissl body, less physal iferous cells, and more nerve synapses when compared with group B. NF-200 and GAP-43 immunohistochemistry observation: in group C, there was just l ittle positive expression; while in groups A and B, positive expression of NF-200 and GAP-43 was evident in the spinal cord from 7 days after operation. Mean density integral absorbency (IA) value of NF-200 and GAP-43: group A was higher than group B at each time point (P lt; 0.05) and group C was lower than groups A and B at each time point (P lt; 0.05). Conclusion Local application of exogenous Neuritin can promote the axonal regeneration after acute SCI in rats and the recovery of the locomotion function of hind-limbs in rats.
Objective To investigate a new composite matrix (BMSCs seeded on the denuded human amniotic membrane, BMSCs-DHAM) bridging the both stumps of spinal cord injury in rats to promote axon regeneration and improve motor function of hind l imbs. Methods The human amniotic membrane (HAM) was voluntarily donated by the healthy pregnant women after a caesarean section. The cells on the HAM were completely removed with a tryptic and mechanical approach to prepare DHAM. The BMSCs were separated and cultured from 4-week-old female rats (n=4), then the forth passage of BMSCs were labeled by PKH26 and seeded on DHAM (BMSCs-DHAM). The growing state of BMSCs was observed under themicroscopy. Moreover, 40 female rats (8-week-old, weighting 200-220 g) were made spinal cord injury models by transecting at T9 level, and were randomly divided into 4 groups (each group, n=10). The both stumps were respectively wrapped by BMSCs- DHAM or simple DHAM in groups A and C, and the same dose of BMSCs or physiological sal ine were also respectively injected the central lesion in groups B and D. At 12 weeks after surgery, the functional recovery of the hindl imbs was evaluated by the BBB locomotor rating score, and other indexes were tested including cortical motion evoked potential (MEP), anterograde biopinylated dextan amine (BDA) tracing, and immunofluorescence of neurofilament protein 200 (NF-200). Results HE staining proved that the DHAM was devoid of cellular components by this way, and BMSCs grew well on the substrate under the microscopy. At 12 weeks after operation, the BBB score (12.50 ± 1.26) in group A was significantly higher than those of other groups (P lt; 0.05), and the recovery in latency (3.52 ± 2.45) ms and ampl itude (480.68 ± 18.41) μV of MEP was also obviously improved in group A (P lt; 0.05) when compared with other groups. In addition, anterograde BDA tracing revealed that the rate of the positive BDA axons 54.12% ± 3.30% under the lesion level in group A was higher than those of other groups (P lt; 0.05), and lots of the regeneration axons (positive NF-200) were found to grow into the spinal cord under the composite matrix in group A. Conclusion The BMSCs-DHAM composite matrix can improve hindl imb motor function to some extent after spinal cord injury. It will be widely appl ied as the matrix material in the future.
The purpose of this experiment was to elucidate the influence of the low-energy He-Ne laser on the function of regeneration of peripheral nerve. Forty-four rabbits about 2.5 kg body weight were used in the experiment. The animals were divided into 4, 8, 12, 16 weeks groups according to the observation period. Six animals were used in each irradiated group and in the control group 5 rabbits were used in each observation period. Regeneration of the axon and myelinc sheath, the latent rate of the common peroneal nerve, the conditions of the anterior tibital muscle and the toe expansion test were all observed systematically in both groups. The experimental results was: A few thin regenerated axon was seen at 4 weeks in the irradiated group, while in the control group it might be seen at 8 weeks, the P value was lt; 0.01. A low amplitude latent rate of the common peroneal nerve is determined at the peroneal side of the anterior tibial muscle in a few animal at 4 weeks of the irradiated group, and it is not observed in the control group, from 12 to 16 weeks. THe latent rate of the common peroneal nerve was the irradiated group than in the controlled, the P value was lt; 0.01. The regeneration of the myeline sheath was evident in the irradiated group, and also the slstion of the musdle fibers anterior tibial muscle was clearly visible than the controlled. 16 weeks postoperatively, the toe expansion test was normal in the irradiated group, while in the control group it was the same as seen at 12 weeks after operation in the irradiated group. Now it was certain that the low-energy He-Ne laser could promole the function of the spinal motor nerve cells and accelerate the axonal regeneration.
Primary or secondary death of retinal ganglion cells (RGC) is a common outcome in various optic neuropathies, often resulting in severe visual damage. The inherent characteristics of RGC include the continuous upregulation of intracellular growth-inhibitory transcription factors and the downregulation of growth-inducing transcription factors during cell differentiation. Additionally, the external inhibitory microenvironment following RGC damage, including oxidative stress, chronic inflammation, lack of neurotrophic factors, high expression of myelin proteins, and the formation of glial scars, all restrict axonal regeneration. Both intrinsic and extrinsic factors lead to the death of damaged RGC and hinder axonal regeneration. Various neuroprotective agents and methods attempt to promote neuroprotection and axonal regeneration from both intrinsic and extrinsic aspects, and well knowledge of these neuroprotective strategies is of significant importance for promoting the neuroprotective experimental research and facilitating its translation into clinical practice.