This study investigated the efficacy and feasibility of inducing the differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) into hepatocyte-like cells in vitro using Sprague Dawley rats, as a model of hepatocyte generation for cell transplantation. BMSCs were isolated and grown using the adherent method and exposed to 5 or 10% liver tissue homogenate, before being collected for analysis after 0, 7, 14, and 21 days. Immunofluorescence and western blotting were employed to detect the liver-specific markers a-fetoprotein (AFP) and albumin (ALB).
Bone marrow mesenchymal stem cells
In this study, we examined the treatment and mechanism of BMMSC on a deep II degree scald of the hamster skin. A deep II degree scald model on the skin of 40 hamsters was duplicated and divided randomly into a stem cell plantation group (group A) and model control group (group B). Skin cells were cultured in vitro until the allogeneic BMMSCs of the 5th generation formed with a cell count of 1 x 107/mL. Local injection plus liquid supernatant smearing was used to plant the cells into the position of the scald in the stem cell plantation group.
This study investigated the effect of bone marrow mesenchymal stem cells (BMCs) on the transforming growth factor-β1 (TGF-β1)-induced activation of the Smad signaling pathway in rat hepatic stellate cells (HSCs). There were four experimental groups: 1) a blank control group, 2) a TGF-β1 treatment group, 3) an MSC-combined group, and 4) an induced MSC-combined group. Isolation and culture of rat liver HSCs in vitro and the proliferation of HSCs in each group were detected by MTT method.
We studied the survival and gene expression of glial cell line-derived neurotrophic factor (GDNF) and GDNF receptor α-1 (GFRα-1) double-genetically modified rat bone marrow mesenchymal stem cells (BMSCs) transplanted into the intestinal walls of the rat models with congenital megacolon and determine the feasibility of treatment by transplantation of double-genetically modified rat BMSCs. The rat colorectal intestinal wall nerve plexus was treated with the cationic surface active agent benzalkonium chloride to establish an experimental megacolon model.