Degraded the transplanted bone marrow cells blood collagen fibers and reduced liver fibrosis, the strong expression of matrix metalloproteinases , particularly MMP-9. The reason for the strong expression of MMP-9 still unknown, the authors report, but report that it is somehow related to the migration of bone marrow cells in inflammatory liver damage and in those cells ‘ degradation of the liver fibrosis. For the for the treatment of liver fibrosis, The present study clearly shows that this subpopulation of blood marrow cells is induced for the resolution of liver fibrosis by CCI4 treatment, the authors conclude, and..
The researchers first caused liver fibrosis in mice by injection of carbon tetrachloride twice a week for four weeks. Weeks. The mice the green fluorescent protein groups, and a bone marrow cells with the green fluorescent protein-positive blood. They treated the control group with saline. All mice continued to be treated with carbon tetrachloride. 3 or 4 weeks, the researchers assessed the extent of liver fibrosis in mice. To measure survival rates were 15 mice in the experimental group and 15 from the control group treated with carbon tetrachloride, then for a further 25 weeks.Iron mirror in animal models of excess iron problems of or instead, to lymphocyte deficiencies have been again excess iron in the excess iron in the the body and is incomplete additional assistance de Sousa ‘immuno iron ideas ‘.. From this work, we know now that hemochromatosis patients do and defective, and more, that your excess iron levels of correlate with their lymphocytes deficiency lymphocyte to lower they have heavier the disease.
Even in a position to place the protein is the possibility that hepdicin may fact ‘this missing link’theory to the de Sousa.. Nevertheless remained to the exact mechanism of how this happened seriouslyBut hepdicin, the central piece of iron regulating is known to also a major player in the immune response, to increases possible did that it in the her its to note for this problem. In fact, amounts of iron, hepcidin shut the ‘door’by which ferrous leaving the cell reducing iron availability plasma and therefore to monitor to infection such as bacterial must divide iron.