Tibial transverse transport induces mobilization of endothelial progenitor cells to accelerate angiogenesis and ulcer wound healing through the VEGFA/CXCL12 pathway.

BACKGROUND: Tibial transverse transport (TTT) can promote the healing of chronic foot ulcers, but the specific cellular and molecular mechanisms by which TTT promotes wound healing remain unclear. METHODS: New Zealand White rabbits were selected to induce foot ulcer models. The treatment included unilateral TTT surgery and bilateral TTT surgery. Observation of tissue neovascularization structure by HE staining and CD31 immunofluorescence detection. Collagen fiber formation was detected through the Masson staining. The mobilization of endothelial progenitor cell (EPCs) were analyzed by VEGFR2 immunofluorescence detection and flow cytometry detection of the number of VEGFR2/Tie-2-positive cells in peripheral blood. ELISA and qPCR assay were performed to detect VEGFA and CXCL12 levels. RESULTS: The complete healing time of ulcer surfaces in sham, unilateral and bilateral TTT groups was about 22 days, 17 days and 13 days, respectively. TTT treatment significantly increased the deposition of granulation tissue and epithelialization of wounds. It also led to an increase in collagen fiber content and the level of the microvascular marker CD31. Furthermore, TTT treatment upregulated the levels of VEGFA and CXCL12 in peripheral blood and wound tissues, as well as increased the expression of VEGFR2 in wound tissues and the proportion of VEGFR2/Tie-2 in peripheral blood. Moreover, these effects of TTT treatment in the bilateral group was more significant than that in the unilateral group. CONCLUSIONS: TTT may facilitate wound fibroblasts to release VEGFA and CXCL12, causing EPC mobilization, thus promoting angiogenesis and ulcer wound healing.

Effect of combination of nerve fragments with nerve growth factor in autologous epineurium small gap coaptation on peripheral nerve injury repair.

The aim of this study was to explore the effect of the combination of nerve fragments with nerve growth factor (NGF) on the repair of peripheral nerve injury through autologous epineurium small gap coaptation. A total of 150 male Sprague-Dawley rats weighing 200-250 g were divided into five groups randomly with 30 rats per group, including the following: a control group that was subjected to traditional end-to-end neuroanastomosis; an autologous epineurium small gap group that received autologous epineurium small gap coaptation suture; a nerve fragments group in which nerve fragments were added to the small gap; an NGF group in which NGF was added to the small gap; and an NGF combined with nerve fragments group in which both NGF and nerve fragments were added to the small gap. All groups were examined at 4, 6, and 8 weeks after the operation, respectively; furthermore, electroneurophysiological detection and histological observation were performed at 8 weeks. Autonomic activities and root ulcers recovered sooner in rats in the NGF combined with nerve fragments group than the other groups. Moreover, the numbers of regenerated nerve fibers were greater and nerve conduction velocity was faster in the NGF combined with nerve fragments group than the other groups. Therefore, the combination of NGF with nerve fragments plays a significant role in the repair of peripheral nerve injury through autologous epineurium small gap coaptation. Therefore, compared with the other four methods, the combination of nerve fragments with NGF on the repair of peripheral nerve injury through autologous epineurium small gap coaptation has a better effect.

Atherosclerosis, inflammatory factor changes, cognitive disorder and vascular endothelial functions in patients with different grades of leukoaraiosis.

OBJECTIVE: To study the atherosclerosis (AS), inflammatory factor level, cognitive disorder and vascular endothelial functions in patients with different grades of leukoaraiosis (LA), and to explore the correlations of different grades of LA with cognitive disorder. METHODS: A total of 180 patients with cerebral infarction admitted and treated in the Department of Neurology of our hospital were selected, and they were graded according to the Tarvonen-shcolder standard, with 45 patients in each group. The atherosclerotic plaques of the patients were detected via a color Doppler ultrasound system and magnetic resonance imaging (MRI). Their inflammatory factor levels were determined using enzyme-linked immunosorbent assay (ELISA). The cognitive function was scored based on the mini-mental state examination (MMSE), and the levels of malondialdehyde (MDA), superoxide dismutase (SOD), endothelin (ET) and nitric oxide (NO) were measured to evaluate vascular endothelial functions. RESULTS: According to the comparisons among four groups of the patients, the incidence rate of AS was gradually increased among patients with different grades of LA (p < 0.05). With the aggravation of LA, the levels of inflammatory factors in patients were obviously increased (p < 0.05). LA patients had evidently lowered MMSE scores and levels of SOD and NO, but notably raised inflammatory factors C-reactive protein (CRP) and matrix metalloproteinase-9 (MMP-9) and vascular endothelial function indices MDA and ET (p < 0.05). CONCLUSION: The occurrence of LA is implicated with the increasing levels of inflammatory factors in the patients, aggregation of cognitive dysfunction and impairment vascular endothelial functions.