ABSTRACT. This study aimed to isolate mesenchymal stem cells from bone mesenchymal stem cells (BMSCs), determine their therapeutic potential for treating rats with acute liver failure (ALF), further explore the factors that induce liver failure mechanisms, and elucidate the role of bone marrow stem cell therapy and BMSCs on liver homing. We found that differentiation potential was present in BMSCs expressing high levels of CD29 and CD90. These cells improved liver functioning in vivo after transplantation into rat livers with D-galactosamine damage, as evidenced by the levels of alanine aminotransferase and aspartate aminotransferase returning to normal (low levels) in recipient ALF rats. A significant improvement in the liver functional test and histological findings was observed in the Stem cells and acute liver failure transplantation group after 120 and 168 h of transplantation (P < 0.05). Histological data revealed that hepatocyte cell apoptosis was lower in the transplantation group compared to the control groups (P < 0.05), and that the transplantation of BMSCs reduced liver inflammation, decreased hepatic denaturation and necrosis, and promoted liver regeneration. These ameliorations were not recorded in the control groups. The results of in situ hybridization, immunofluorescence staining, and Western blot confirmed the presence of transplanted BMSCs in recipient rat livers. Stromal cell derived factor-1 alpha and vascular endothelial growth factor were significantly upregulated after the intraportal transplantation of BMSCs, with significantly higher levels being found in the portal vein and the tail vein groups (P < 0.05). In conclusion, BMSCs have a therapeutic effect against ALF rats, evoke endogenous repair mechanisms in the liver, and may represent a novel form of therapeutic intervention for the disease. Furthermore, intraportal transplantation serves as a more effective pathway compared to tail vein transplantation.
ABSTRACT. This study investigated the effects induced by co-culturing human primary basic fibroblasts (HPBFs) with 16-human bronchial epithelial cells (16-HBE) infected with respiratory syncytial virus (RSV), in particular the transformation of HPBFs into myofibroblasts and secretion of extracellular matrix proteins. HPBFs were co-cultured with 16-HBE cells infected with RSV and quantitatively analyzed. We constructed models of HPBFs co-cultured with 16-HBE cells that were either uninfected (control group) or infected with RSV (experimental group). Following initiation of cocultures, HPBFs and supernatants were collected at 24-h intervals up to 120 h. Expression of α-smooth muscle actin (α-SMA) was detected by indirect immunofluorescence and western blotting, while type I collagen (Col I) and fibronectin were analyzed by competitive enzyme-linked immunosorbent assays. After 72 h, α-SMA expression increased in HPBFs cultured with RSV-infected 16-HBE relative to uninfected controls, reaching its highest level at 96 h. Similarly, Col I secretion was also higher in HPBFs co-cultured with RSV-infected 16-HBE relative to uninfected controls; Col I secretion increased with time and reached its highest level at 120 h. HPBFs were transformed into myofibroblasts following co-culture with RSV-infected 16- HBE, which when combined with the observed increase in Col I secretion suggests that airway remodeling would then be promoted.
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