Advances in stem cells treatment of diabetic wounds: A bibliometric analysis via CiteSpace.

Diabetes is a chronic medical condition that may induce complications such as poor wound healing. Stem cell therapies have shown promise in treating diabetic wounds with pre-clinical and clinical studies. However, little bibliometric analysis has been carried out on stem cells in the treatment of diabetic wounds. In this study, we retrieved relevant papers published from January 1, 2003, to December 31, 2023, from Chinese and English databases. CiteSpace software was used to analyze the authors, institutions, and keywords by standard bibliometric indicators. Our analysis findings indicated that publications on stem cells in the treatment of diabetic wounds kept increasing. The most prolific author was Qian Cai (n = 7) and Mohammad Bayat (n = 16) in Chinese and English databases, respectively. Institutions distribution analysis showed that Chinese institutions conducted most publications, and the most prolific institution was the Chinese People's Liberation Army General Hospital (n = 9) and Shahid Beheshti University of Medical Sciences (n = 17) in Chinese and English databases, respectively. The highest centrality keyword in Chinese and English databases was "wound healing" (0.54) and "in vitro" (0.13), respectively. There were 8 and 11 efficient and convincing keyword clusters produced by a log-likelihood ratio in the Chinese and English databases, respectively. The strongest burst keyword was "exosome" (strength 3.57) and "endothelial progenitor cells" (strength 7.87) in the Chinese and English databases, respectively. These findings indicated a direction for future therapies and research on stem cells in the treatment of diabetic wounds.

Electrospun PCL/gelatin/arbutin nanofiber membranes as potent reactive oxygen species scavengers to accelerate cutaneous wound healing.

The presence of excessive reactive oxygen species (ROS) at a skin wound site is an important factor affecting wound healing. ROS scavenging, which regulates the ROS microenvironment, is essential for wound healing. In this study, we used novel electrospun PCL/gelatin/arbutin (PCL/G/A) nanofibrous membranes as wound dressings, with PCL/gelatin (PCL/G) as the backbone, and plant-derived arbutin (hydroquinone-ß-d-glucopyranoside, ARB) as an effective antioxidant that scavenges ROS and inhibits bacterial infection in wounds. The loading of ARB increased the mechanical strength of the nanofibres, with a water vapour transmission rate of more than 2500 g/(m2 × 24 h), and the water contact angle decreased, indicating that hydrophilicity and air permeability were significantly improved. Drug release and degradation experiments showed that the nanofibre membrane controlled the drug release and exhibited favourable degradability. Haemolysis experiments showed that the PCL/G/A nanofibre membranes were biocompatible, and DPPH and ABTS+ radical scavenging experiments indicated that PCL/G/A could effectively scavenge ROS to reflect the antioxidant activity. In addition, haemostasis experiments showed that PCL/G/A had good haemostatic effects in vitro and in vivo. In vivo animal wound closure and histological staining experiments demonstrated that PCL/G/A increased collagen deposition and remodelled epithelial tissue regeneration while showing good in vivo biocompatibility and non-toxicity. In conclusion, we successfully prepared a multifunctional wound dressing, PCL/G/A, for skin wound healing and investigated its potential role in wound healing, which is beneficial for the clinical translational application of phytomedicines.

Adriamycin resistance-associated prohibitin gene inhibits proliferation of human osteosarcoma MG63 cells by interacting with oncogenes and tumor suppressor genes.

The resistance of cancer cells to chemotherapeutic agents is a major obstacle for successful chemotherapy, and the mechanism of chemoresistance remains unclear. The present study developed an adriamycin-resistant human osteosarcoma MG-63 sub-line (MG-63/ADR), and identified differentially expressed proteins that may be associated with adriamycin resistance. Two dimensional gel electrophoresis, matrix-assisted laser desorption ionization time-of-flight mass spectrometry analysis and a protein identification assay were performed. Western blot analysis was used to examine the prohibitin (PHB) levels in the MG-63/ADR cells. Quantitative polymerase chain reaction was utilized to detect adriamycin resistant-associated genes. Laser-scanning confocal microscope was employed to examine the colocalization of PHB with v-myc avian myelocytomatosis viral oncogene homolog (c-myc), FBJ murine osteosarcoma viral oncogene homolog (c-fos), tumor protein p53 and retinoblastoma 1 (Rb). In addition, the full length of the open reading frame of human PHB was subcloned into a lentiviral vector pLVX-puro. The proliferative rate of MG-63 cells was also investigated. The overall protein expression in MG-63/ADR cells was clearly suppressed. Three notable protein regions, representing high mobility group box 1, Ras homolog gene family, member A, and PHB, were identified to be significantly altered in MG-63/ADR cells when compared with its parental cells. Therefore, PHB modulated the chemoresistance of MG-63/ADR cells by interacting with multiple oncogenes or tumor suppressor genes (c-myc, c-fos, p53 and Rb). In addition, overexpression of PHB decreases the proliferative rate of MG-63 cells. In conclusion, PHB is an adriamycin resistance-associated gene, which may inhibit the proliferation of human osteosarcoma MG-63 cells by interacting with the oncogenes or tumor suppressor genes, c-myc, c-fos, p53 and Rb.

Melittin inhibits tumor angiogenesis modulated by endothelial progenitor cells associated with the SDF-1α/CXCR4 signaling pathway in a UMR-106 osteosarcoma xenograft mouse model.

Endothelial progenitor cells (EPCs) are important in tumor angiogenesis. Stromal cell-derived factor-1α (SDF-1α) and its receptor C-X-C chemokine receptor type 4 (CXCR4) are key in stem cell homing. Melittin, a component of bee venom, exerts antitumor activity, however, the underlying mechanisms remain to be elucidated. The present study aimed to assess the effects of melittin on EPCs and angiogenesis in a mouse model of osteosarcoma. UMR­106 cells and EPCs were treated with various concentrations of melittin and cell viability was determined using the MTT assay. EPC adherence, migration and tube forming ability were assessed. Furthermore, SDF­1α, AKT and extracellular signal­regulated kinase (ERK)1/2 expression levels were detected by western blotting. Nude mice were inoculated with UMR­106 cells to establish an osteosarcoma mouse model. The tumors were injected with melittin, and its effects were assessed by immunohistochemistry and immunofluorescence. Melittin decreased the viability of UMR­106 cells and EPCs. In addition, it decreased EPC adhesion, migration and tube formation when compared with control and SDF­1α­treated cells. Melittin decreased the expression of phosphorylated (p)­AKT, p­ERK1/2, SDF­1α and CXCR4 in UMR­106 cells and EPCs when compared with the control. The proportions of cluster of differentiation (CD)34/CD133 double­positive cells were 16.4±10.4% in the control, and 7.0±4.4, 2.9±1.2 and 1.3±0.3% in tumors treated with 160, 320 and 640 µg/kg melittin per day, respectively (P<0.05). At 11 days, melittin reduced the tumor size when compared with that of the control (control, 4.8±1.3 cm3; melittin, 3.2±0.6, 2.6±0.5, and 2.0±0.2 cm3 for 160, 320 and 640 µg/kg, respectively; all P<0.05). Melittin decreased the microvessel density, and SDF­1α and CXCR4 protein expression levels in the tumors. Melittin may decrease the effect of osteosarcoma on EPC­mediated angiogenesis, possibly via inhibition of the SDF-1α/CXCR4 signaling pathway.