Materials and Methods: Ten swab samples from equine infected wounds were collected and bacteria isolation and identification were performed. The antibacterial effect of the ionized water of pH 2.5, 4.5, 7.0, and 11.5 was tested on Staphylococcus aureus, Staphylococcus pseudintermedius, Staphylococcus intermedius, Escherichia coli, Pantoea agglomerans, and Klebsiella pneumoniae. The time-kill profiles of the ionized waters were determined at time 0, 2, 4, 6, and 8 h.
Results: Ionized water of pH 2.5 and 4.5 showed antibacterial activity against S. aureus, S. pseudintermedius, and S. intermedius with significant (p>0.05) reduction in colony-forming unit/mL within 2-8 h. The degree of bactericidal effect of the acidic ionized water differs between the species with S. intermedius more susceptible. However, there was no antibacterial effect at pH 2.5, 4.5, 7.0, and 11.5 on the Gram-negative bacteria tested.
Conclusion: Ionized water of pH 2.5 and 4.5 is effective in minimizing the growth of Gram-positive bacteria; thus it could be of clinical importance as an antiseptic for surface wound lavage in horses.
METHODS: Sprague-Dawley rats were injected with CCl4 for 8 weeks to induce irreversible liver fibrosis. Ex-vivo expanded, pooled human MSCs obtained from BM and WJ were intravenously administered into rats with liver fibrosis at a dose of 10 × 106 cells/animal. Sham control and vehicle-treated animals served as negative and disease controls, respectively. The animals were sacrificed at 30 and 70 days after cell transplantation and hepatic-hydroxyproline content, histopathological, and immunohistochemical analyses were performed.
RESULTS: BM-MSCs treatment showed a marked reduction in liver fibrosis as determined by Masson's trichrome and Sirius red staining as compared to those treated with the vehicle. Furthermore, hepatic-hydroxyproline content and percentage collagen proportionate area were found to be significantly lower in the BM-MSCs-treated group. In contrast, WJ-MSCs treatment showed less reduction of fibrosis at both time points. Immunohistochemical analysis of BM-MSCs-treated liver samples showed a reduction in α-SMA+ myofibroblasts and increased number of EpCAM+ hepatic progenitor cells, along with Ki-67+ and human matrix metalloprotease-1+ (MMP-1+) cells as compared to WJ-MSCs-treated rat livers.
CONCLUSIONS: Our findings suggest that BM-MSCs are more effective than WJ-MSCs in treating liver fibrosis in a CCl4-induced model in rats. The superior therapeutic activity of BM-MSCs may be attributed to their expression of certain MMPs and angiogenic factors.