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Objective. Methane saline (MS) can be used to treat many diseases via its anti-inflammatory, antiapoptotic, and antioxidative activities. However, to date, there is no published evidence as to whether MS has any effect on traumatic brain injury (TBI). The Wnt signalling pathway regulates cell proliferation, differentiation, migration, and apoptosis; however, whether the Wnt signalling pathway regulates any effect of MS on TBI is unknown. This study was designed to explore the role of MS in the treatment of TBI and whether the Wnt pathway is involved. Methods. Sprague-Dawley rats were randomly divided into five groups: sham, TBI, TBI+10 ml/kg MS, TBI+20 ml/kg MS, and TBI+30 ml/kg MS. After induction of TBI, MS was injected intraperitoneally once daily for seven consecutive days. Neurological function was evaluated by the Neurological Severity Score (NSS) at 1, 7, and 14 days after TBI. Haematoxylin-eosin (HE) staining, inflammatory factors, neuron-specific enolase (NSE) staining, oxidative stress, and cell apoptosis were measured and compared 14 d after TBI to identify the optimal dose of MS and to investigate the effect of MS on TBI. In the second experiment, Sprague-Dawley rats were randomly divided into four groups: sham, TBI, TBI+20 ml/kg MS, and TBI+20 ml/kg MS+Dickkopf-1 (DKK-1, a specific inhibitor of the Wnt pathway). NSE, caspase-3, superoxide dismutase (SOD), Wnt3a, and β-catenin were detected by real-time PCR and Western blotting. The results from each group were compared 14 d after TBI to determine the regulatory role of the Wnt pathway. Results. Methane saline significantly inhibited inflammation, oxidative stress, and cell apoptosis, thus protecting neurons within 14 days of TBI. The best treatment effect against TBI was obtained with 20 ml/kg MS. When the Wnt pathway was inhibited, the treatment effect of MS was impaired. Conclusion. Methane saline ameliorates TBI through its anti-inflammatory, antiapoptotic, and antioxidative effects via activation of the Wnt signalling pathway, which plays a part but is not the only mechanism underlying the effects of MS. Thus, MS may be a novel strategy for treating TBI.

The completed skeletal muscle regeneration resulted from severe injury and muscle-related disease is still a challenge. Here, we developed an injectable muscle-adhesive antioxidant conductive bioactive photothermo-responsive nanomatrix for regulating the myogenic differentiation and promoting the skeletal muscle regeneration in vivo. The multifunctional nanomatrix was composed of polypyrrole@polydopamine (PPy@PDA, 342 ± 5.6 nm) nanoparticles-crosslinked Pluronic F-127 (F127)-polycitrate matrix (FPCP). The FPCP nanomatrix demonstrated inherent multifunctional properties including excellent photothermo-responsive and shear-thinning behavior, muscle-adhesive feature, injectable ability, electronic conductivity (0.48 ± 0.03 S/m) and antioxidant activity and photothermal function. The FPCP nanomatrix displayed better photothermal performance with near-infrared irradiation, which could provide the photo-controlled release of protein (91% ± 2.6% of BSA was released after irradiated 3 times). Additionally, FPCP nanomatrix could significantly enhance the cell proliferation and myogenic differentiation of mouse myoblast cells (C2C12) by promoting the expressions of myogenic genes (MyoD and MyoG) and myosin heavy chain (MHC) protein with negligible cytotoxicity. Based on the multifunctional properties, FPCP nanomatrix efficiently promoted the full-thickness skeletal muscle repair and regeneration in vivo, through stimulating the angiogenesis and myotube formation. This study firstly indicated the vital role of multifunctional PPy@PDA nanoparticles in regulating myogenic differentiation and skeletal muscle regeneration. This work also suggests that rational design of bioactive matrix with multifunctional feature would greatly enhance the development of regenerative medicine., Graphical abstract Image 1, Highlights • Multifunctional muscle-adhesive nanomatrix was designed. • Nanomatrix showed good injectability, conductivity and antioxidant ability. • Nanomatrix displayed good photothermal function and biocompatibility. • Nanomatrix significantly enhanced cell proliferation and myogenic differentiation. • Nanomatrix efficiently promoted the full-thickness skeletal muscle regeneration.

Recent studies have suggested that exosomes exert similar therapeutic effects to those of mesenchymal stem cells (MSCs) in regenerative medicine and MSCs-derived exosomes exhibit therapeutic effects on steroid-induced osteonecrosis of the femoral head (ONFH). Furthermore, reparative functions of exosomes from MSCs are enhanced by hypoxia treatment of the cells. However, there are no related reports about whether exosomes derived from hypoxia-preconditioned MSCs could show better therapeutic effects on steroid-induced ONFH. In vitro, we investigated the effects of hypoxia precondition on exosomes derived from bone marrow mesenchymal stem cells (BMMSCs) from rats and the proangiogenic ability of exosomes derived from hypoxia-preconditioned BMMSCs. In vivo, we investigated the role of exosomes from hypoxia-preconditioned BMMSCs on angiogenesis and protecting osteonecrosis in a rat ONFH model. We found that the potential of the proangiogenic ability of exosomes derived from hypoxia-preconditioned BMMSCs was higher than exosomes derived from BMMSCs cultured under normoxia. Exosomes derived from hypoxia-preconditioned BMMSCs significantly promoted proliferation, migration, vascular endothelial growth factor (VEGF) expression, and tube formation of human umbilical vein endothelial cells (HUVECs) compared with exosomes derived from BMMSCs cultured under normoxia. Administration of exosomes derived from hypoxia-preconditioned BMMSCs significantly prevented bone loss and increased vessel volume in the femoral head compared with exosomes derived from BMMSCs cultured under normoxia. Taken together, our data suggest that exosomes derived from hypoxia-preconditioned BMMSCs exert better therapeutic effects on steroid-induced ONFH by promoting angiogenesis and preventing bone loss.

Purpose To discuss the reason and treatment method of helical blade over-unlocking. Methods The case reported in this paper is that the helical blade cannot be locked due to over-unlocking during the treatment of intertrochanteric fracture with PFNA, which is very rare. We expound why it happens and how to deal with it. Results When the helical blade is over-unlocking, if the aiming arm is not disassembled, you can try to take out the helical blade and fix it again. If the aiming arm has been removed, it is not recommended to remove the helical blade, we suggest that we should consider adding a screw from the lateral wall through the femoral neck for anti-rotation, or you can observe the tail of helical blade and find suitable screw driver to fix it if there is one. Conclusions In order to avoid over-unlocking of the helical blade, intraoperative fluoroscopy should not only pay attention to the position of the helical blade, but also pay more attention to the abnormal shape of the helical blade itself. Once the helical blade is over-unlocking, it needs to be handled in time.

Objectives: Spinal cord injury (SCI) is a most debilitating traumatic injury, and cytotherapy is a promising alternative treatment strategy. Here we investigated the effect and mechanism of adipose-derived stem/stromal cells (ASCs) with overexpressing brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) (BDNF-NT3) in combination with silk fibroin/chitosan scaffold (SFCS) in SCI.Methods: Female Sprague-Dawley rats were used as an SCI model. SFCS,SFCS and ASCs, or ASCs overexpressing NT3, BDNF, and BDNF-NT3 were implanted into SCI rats. Basso, Beattie, and Bresnahan score, pathological changes, and spinal cord tissue and nerve fiber morphology were observed and assayed. GAP-43, GFAP, and caspase-3 expression was determined using immunohistochemistry and western blotting.Results: Smoother spinal cords, less scar tissue, and lower inflammatory activity were found in the SFCS, SFCS and ASCs, ASCs with NT3, BDNF, and BDNF-NT3 overexpression treatment than in the untreated SCI rat groups. Increasing formation of nerve fibers was observed in the above groups in order. GAP-43 expression significantly increased, while GFAP and caspase-3 expression significantly decreased. These results indicated obvious alleviation in pathological changes and BDNF-NT3 overexpression in ASCs combined with SFCS treatment in SCI rats.Conclusion: Thus, BDNF-NT3 overexpression from ASCs with SFCS had synergistic neuroprotective effects on SCI and may be a treatment option for SCI.

Introduction Spinal cord impact is a mature method for building models of spinal cord injury (SCI). However, a common problem is that the degree of elicited paralysis may not be identical even though animals receive the same impact. We hypothesize that this difference may be caused by the difference in the secondary injury mechanism of SCI and there might be an impact dosage named “median paralyzing dose (PD50)”, similar as the “median lethal dose (LD50)” in pharmacology. In addition, since SCI is a result of multiple mechanisms, we hypothesize that it is more suitable to employ multiple regression analysis to analyze the related factors for complete paraplegia. So the present study aimed to calculate the existence of PD50 and analyze the related factors of SCI-induced complete paralysis using logistic regression under the PD50 which represents identical primary injury. Material and methods Rat models of SCI were built using the weight-drop method under PD50. PD50 was calculated by Karber’s method. Rats were allocated into two groups according to whether they developed complete or incomplete paralysis 2 weeks after injury. Cavity and spared tissues in the two groups were compared. Neuronal preservation, microglia/macrophage reaction, T-lymphocyte infiltration, astrocyte activation and neuronal apoptotic were compared by immunohistochemistry. The logistic regression model was constructed and significant related factors of complete paralysis were selected. Results Of the two groups, the cavity in the injured spinal cord of the complete-paralysis rats was significantly larger and the spared white matter volume (SWMV%) was obviously smaller. Whereas, the spared grey matter volume was not different between groups. Macrophage reaction, T-lymphocyte infiltration and neuronal apoptosis were significantly more severe in the complete-paralysis rats. Astrocyte activation and neuronal preservation showed no difference between groups. Logistic regression analysis showed that cavity volume, SWMV%, microglia/macrophage reaction and neuronal apoptosis were significantly correlated with SCI-induced complete paralysis. Conclusion As a non-mainstream method, it is feasible to analyze the secondary factors of SCI-induced complete paralysis using multiple regression analysis in the condition of identical primary injury (PD50). SWMV% and microglia/macrophage reaction are important factors that contribute to complete paralysis at the early phase of severe SCI.

Small extracellular vesicles (sEVs) derived from bone marrow mesenchymal stem cells (BMMSCs) from individuals with steroid-induced osteonecrosis of the femoral head (ONFH) have not been studied. The objective of the present study was to compare the proosteogenic and proangiogenic effects of sEVs derived from BMMSCs from rats with steroid-induced ONFH (oBMMSCs-sEVs) and sEVs derived from BMMSCs from normal rats (nBMMSCs-sEVs). BMMSCs were isolated from steroid-induced ONFH rats and healthy rats. sEVs were isolated and characterized by Western blotting analysis of exosomal surface biomarkers and by transmission electron microscopy. The impacts of nBMMSCs-sEVs and oBMMSCs-sEVs on the proliferation and osteogenic differentiation of BMMSCs were determined via cell proliferation assay, alizarin red staining, and alkaline phosphatase activity assay. Enzyme-linked immunosorbent assay and tube formation assay were conducted to investigate the effect of nBMMSCs-sEVs and oBMMSCs-sEVs on the angiogenic potential of human umbilical vein endothelial cells (HUVECs). The expression of relevant genes was detected by quantitative real-time polymerase chain reaction analysis, and the expression of β-catenin was detected by immunofluorescence. Both nBMMSCs-sEVs and oBMMSCs-sEVs promoted proliferation, osteogenic differentiation, and β-catenin expression of BMMSCs and enhanced angiogenesis of HUVECs. However, compared with nBMMSCs-sEVs, oBMMSCs-sEVs exhibited attenuated effects. Our findings indicated that the proosteogenic and proangiogenic effects of sEVs were partially attenuated in steroid-induced ONFH. Therefore, this study might offer guidance for the selection of source cells for sEV therapy in the future.

The therapeutic effect of stem cell transplantation in traumatic spinal cord injury (SCI) has been extensively studied these days, and evidence has shown that stem cell-derived exosomes and exosome-shuttled miRNA (e.g. miR-21) contribute to the protective effects of stem cell transplantation against SCI. It has been reported that obesity, a prevalent metabolic disorder, reshapes stem cells and their extracellular vesicles. However, the effects of exosomes derived from obese rat stem cells on SCI and its underlying mechanism remain unknown. Here, we examined the effects of exosomes derived from obese rat mesenchymal stem cells (MSCs) on SCI, and tested the role of miR-21 in their effects. We found that exosomes derived from obese rat MSCs showed decreased miR-21 levels and did not exert protective effects against SCI. Overexpression of miR-21 in obese rat MSCs restored the protective effects of exosomes purified from obese rat MSCs against SCI. In addition, obese rat MSCs showed insulin resistance, and MSC insulin resistance decreased miR-21 levels in its secreted exosomes. These results suggested that miR-21 deficiency in obese rat MSCs contributes to the impaired protective effects of obese rat MSCs-derived exosomes against SCI, and further reinforced the notion that miR-21 is a potential molecule for treatment of SCI.

Background It was indicated that inhibition of PPARγ probably represents a novel therapy for steroid-related osteonecrosis. In this study, we investigated the preventive effects of PPARγ inhibition on steroid-related osteonecrosis in a rabbit model. Methods Rabbits were randomly divided into three groups (normal group, model group and BADGE group). Osteonecrosis was induced in rabbits in the model group and the BADGE group. The BADGE group also received bisphenol a diglycidyl ether(BADGE), a PPARγ antagonist, for 6 weeks. Results Histopathological results indicated that rabbits treated with BADGE exhibited significantly reduced osteonecrotic changes, incidence of osteonecrosis and bone marrow adiposity. Furthermore, BADGE-treated rabbits exhibited reduced intraosseous pressure and increased femoral blood perfusion. Micro-computed tomography and bone histomorphometry indicated that the BADGE group exhibited significantly improved bone quality and mineral appositional rate compared with the model group. Furthermore, the BADGE group showed a significant increase in circulating levels of the bone formation marker osteocalcin and reduced levels of the bone resorption marker TRACP. Overall, BADGE-treated rabbits exhibited reduced marrow adiposity concomitant with improved bone formation. Conclusions In conclusion, these observations demonstrated that pharmacological inhibition of PPARγ might represent an effective therapy for steroid-related osteonecrosis in the near future.

The increased prevalence of obesity is recognized as a serious public health problem affecting millions of people. Although some anti-obesity drugs are currently licensed for use, these drugs involve diverse side effects such as diarrhea, vomiting, and low efficiency. Here we developed a safe and efficient biomaterials-based anti-obesity nanosystem (PCG-EPL/miR33agonist), which was formed with poly (citric acid)-glycerol-polylysine (PCG-EPL) and miR33 agonist by self-assembly. The PCG-EPL could efficiently load, protect and deliver the miR33 agonist into the adipocytes and decreased the obesity-related IL-1β expression in adipocytes in vitro. The high-fat diet induced obese rat model experiment showed that the PCG-EPL/miR33agonist via caudal vein injection effectively reduced the body weight by enhancing lipid metabolism and decreasing the inflammatory factors expressions (IL-1β, TNF-α and IL-6) in vivo, without suppressing the appetite of rat. Compared with the obese mice, mice in PCG-EPL/miR33 had higher average food intake but lower energy conversion rate. PCG-EPL/miR33agonist significantly inhibited the growth of adipocytes. Noteworthy, this weight loss strategy is not only safe and efficient, but also does not need diet control. Thus, PCG-EPL may serve as an ideal platform for RNA drug delivery in anti-obesity therapy, especially for those who need to lose weight but unable to autonomously control their diet.

Rolipram, a phosphodiesterase-4 inhibitor, can activate the cyclic adenosine monophosphate (cAMP)/cAMP-responsive element binding protein (CREB) pathway to facilitate functional recovery following ischemic stroke. However, to date, the effects of rolipram on angiogenesis and cerebral ischemia-induced neuronal apoptosis are yet to be fully elucidated. In this study, the aim was to reveal the effect of rolipram on the angiogenesis and neuronal apoptosis following brain cerebral ischemia. Rat models of ischemic stroke were established following transient middle cerebral artery occlusion and rolipram was administered for three, seven and 14 days. The results were examined using behavioral tests, triphenyl tetrazolium chloride staining, immunostaining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) to evaluate the effects of rolipram therapy on functional outcome, angiogenesis and apoptosis. Western blot analysis was used to show the phosphorylated- (p-)CREB protein level in the ischemic hemisphere. The rolipram treatment group exhibited a marked reduction in infarct size and modified neurological severity score compared with the vehicle group, and rolipram treatment significantly promoted the microvessel density in the ischemic boundary region and increased p-CREB protein levels in the ischemic hemisphere. Furthermore, a significant reduction in the number of TUNEL-positive cells was observed in the rolipram group compared with the vehicle group. These findings suggest that rolipram has the ability to attenuate cerebral ischemic injury, stimulate angiogenesis and reduce neuronal apoptosis though the cAMP/CREB pathway.

The specific pathogenesis of steroid‑induced osteonecrosis (ON) is yet to be elucidated and until recently effective prophylactic therapies have not been available. The local renin‑angiotensin system (RAS) exists in the bone and has an important role in local bone regulation. However, to the best of our knowledge, the interrelation between local bone RAS and steroid‑induced ON is yet to be investigated. In the present study, 45 rabbits were injected with a single intramuscular dose of 20 mg/kg methylprednisolone acetate (MPA) and were sacrificed 1 (group A), 2 (group B) and 3 (group C) weeks subsequent to MPA administration (n=15 per group). Ten rabbits were used as a control group (group N). The presence or absence of ON in the bilateral femoral heads was examined histopathologically. The mRNA and protein expression of components of the RAS, including angiotensin II (Ang II), angiotensin converting enzyme (ACE) and Ang II type 1 (AT1) and Ang II type 2 (AT2) receptors, were detected in the bone. Significant changes in Ang II, ACE, and AT1 and AT2 receptor expression were observed in the bone of the rabbits in the different groups. Moreover, the expression of Ang II and ACE was highest one week subsequent to administration of the glucocorticoid methylprednisolone and the expression of the AT1 and AT2 receptors was highest two weeks following methylprednisolone administration. ON occurs most significantly at three weeks following the administration of MPA in this animal model, thus the changes in Ang II, ACE and AT1 and AT2 receptor expression preceded this. The present study found that ON was strongly associated with the activation of the local bone RAS in rabbits.

Spinal cord injury (SCI) may lead to a devastating and permanent loss of neurological function, which may place a great economic burden on the family of the patient and society. Methods for reducing the death of neuronal cells, inhibiting immune and inflammatory reactions, and promoting the growth of axons in order to build up synapses with the target cells are the focus of current research. Target cells are located in the damaged spinal cord which create a connect with the scaffold. As tissue engineering technology is developed for use in a variety of different areas, particularly the biomedical field, a clear understanding of the mechanisms of tissue engineering is important. This review establishes how this technology may be used in basic experiments with regard to SCI and considers its potential future clinical use.

The use of tissue engineering technology in the repair of spinal cord injury (SCI) is a topic of current interest. The success of the repair of the SCI is directly affected by the selection of suitable seed cells and scaffold materials with an acceptable biocompatibility. In this study, adipose tissue-derived stem cells (ADSCs) were incorporated into a silk fibroin-chitosan scaffold (SFCS), which was constructed using a freeze-drying method, in order to assess the biocompatibility of the ADSCs and the SFCS and to provide a foundation for the use of tissue engineering technology in the repair of SCI. Following the seeding of the cells onto the scaffold, the adhesion characteristics of the ADSCs and the SFCS were assessed. A significant difference was observed between the experimental group (a composite of the ADSCs with the SFCS) and the control group (ADSCs without the scaffold) following a culture period of 6 h (P0.05). The use of an MTT assay to assess the proliferation of the cells on the scaffold revealed that there were significant differences between the experimental and control groups following culture periods of 2 and 4 days (P0.05). Scanning electron microscopy (SEM), using hematoxylin and eosin (H&E) staining, was used to observe the cellular morphology following seeding, and this revealed that the cells displayed the desired morphology. The results indicate that ADSCs have a good biocompatibility with a SFCS and thus provide a foundation for further studies using tissue engineering methods for the repair of SCI.

Introduction Adipose-derived stem cells (ADSCs) possess the potential of multi-differentiation which could differentiate into neuronal cells and Schwann cells under certain conditions. If we inoculate the ADSCs modified by Brain derived neurophic factor(BDNF) and Neurotrophin-3(NT-3)double genes on the silk fibroin/chitosan (SFCS), and transplant it into 2 mm pre-made spinal cord transection animal model, we can take advantage of the characteristic of ADSCs which could express BDNF and NT-3 stably after being double gene modified and the advantage of tissue engineering, we look forward to providing a new treatment method for spinal cord injury (SCI), which thereby could reduce SCI morbidity and mortality rate, so as to build up a solid theoretical foundation for the clinical treatment of SCI. Material and Methods According to the preliminary design, animal experiment is divided into seven groups: Group A: SFCS/ADSCs/Lenti-BDNF-GFP-NT-3-RFP, namely, BDNF and NT-3 double genes co-transfect ADSCs combining SFCS group; Group B: SFCS/ADSCs/Lenti-BDNF-GFP, namely, BDNF single gene transfect ADSCs combining SFCS group; Group C: SFCS/ADSCs/ Lenti-NT-3-RFP, namely, NT-3 single gene transfect ADSCs combining SFCS group; Group D: SFCS/ADSCs/Lenti-eGFP, namely, empty vector transfect ADSCs combining SFCS group; Group E:SFCS, namely, single SFCS group; Group F:only cut off spinal cord and without treatment; Group G: normal control group, just open the vertebral plate without any treatment. Group A, B, C, D and E transplant the scaffold into 2 mm spinal cord transection defect rat model. Group F cuts off spinal cord and makes 2 mm defect, Group G is normal group. Do a BBB scoring at 1 w, 4 w, 8 w and 12 w after surgery to analyze functional recovery, execute the rats 12 w later, take out the scaffolds, test them by HE staining, immunehistochemical staining (NSE, GAP-43, Caspase-3, GFAP), LFB staining, RT-PCR and Western blot, the purpose of which is to observe the effect of tissue engineering on the recovery of SCI. Results Group A (BDNF and NT-3 double genes modified ADSCs combining the use of SFCS group) has a better repair effect on rats spinal cord transection injury treatment, which reveals higher BBB scores, increased GAP-43 expression, more positive NSE cells, decreased expression of GFAP and Caspase-3. At the same time denser regenerating nerve fiber could move through the scaffold, and the most important thing is the repair effect of Group A is better than single gene modified Group B and Group C, which is better than Group D (empty vector transfect ADSCs combining SFCS group), which is better than Group E (single use SFCS), which is better than Group F (just cut off spinal cord and without treatment). Conclusion Under the guidance of tissue engineering method, ADSCs modified by BDNF and NT-3 double genes combining the use of SFCS can significantly reduce the inflammatory response after injury, inhibit scar hyperplasia and cell apoptosis and promote nerve fibers regeneration and the differentiation of ADSCs into neurons in vivo, so as to improve the repair effect of rat spinal cord transection injuries, which provides a new method for the treatment of SCI.

Spinal cord injury usually leads to permanent disability, which could cause a huge financial problem to the patient. Up to now there is no effective method to treat this disease. The key of the treatment is to enable the damage zone axonal regeneration and luckily it could go through the damage zone; last a connection can be established with the target neurons. This study attempts to combine stem cell, material science and genetic modification technology together, by preparing two genes modified adipose-derived stem cells and inducing them into neuron direction; then by compositing them on the silk fibroin/chitosan scaffold and implanting them into the spinal cord injury model, seed cells can have features of neuron cells. At the same time, it could stably express the brain-derived neurotrophic factor and neurotrophin-3, both of which could produce synergistic effects, which have a positive effect on the recovery of spinal cord. The spinal cord scaffold bridges the broken end of the spinal cord and isolates with the surrounding environment, which could avoid a scar effect on the nerve regeneration and provide three-dimensional space for the seed cell growth, and at last we hope to provide a new treatment for spinal cord injury with the tissue engineering technique.

To discuss the impact of adipose-derived stem cells (ADSCs) combined with vascular bundle implantation on vascularized tissue engineering scaffolds in vivo so as to provide a theoretical basis for the repair of avascular necrosis of the femoral head.ADSCs were isolated from 4-month-old Sprague Dawley (SD) rats and cultured, then were induced to osteogenesis and identified. ADSCs at the 3rd passage were seeded on the nano-hydroxyapatite/polyamide-66 (nHA/PA66) to prepare the composite scaffolds. The compound condition of cells and scaffold materials were observed under scanning electronic microscope (SEM). Twenty-four 4-month-old SD rats (weighing 350-400 g) were randomly divided into 3 groups (n=8). In group A and group B, the inferior epigastric artery and vein of rats were implanted into composite scaffold cultured for 10 days or simple nHA/PA66 scaffold, respectively. In group C, two composite scaffolds cultured for 10 days were embedded into quadriceps femoris muscle of both thighs, respectively. After 2 and 4 weeks of operation, angiogenesis was observed by HE staining and CD34 immunohistochemical staining.Cells isolated from adipose were identified as ADSCs. SEM showed that the number of cells increased after being cultured for 10 days, cell morphology stretched fully with a shape of long spindle. HE staining and immunohistochemical staining showed that a large number of angiogenesis was observed around the implanted artery and vein in group A, which was superior to groups B and C in the number of blood vessels and the maturity of blood vessel wall. After 2 and 4 weeks of operation, the blood vessel density and blood vessel diameter were significantly higher in group A than in group B and group C, and in group B than in group C (P0.05).Combined application of ADSCs and vascular bundle implantation can promote the degree of vascularization, which could make the scaffold vascularization reliable.