Aim: The study was to explore the effects of the fibroblast transdifferentiation for myofibroblast (MFB) in the pathogenesis of systemic sclerosis (SSc) and to research the effect mechanism of H2 Relaxin (H2-RLX) against fibrosis in SSc.
Methods: The fibroblasts derived from the skin lesion of the SSc patients and normal skin tissue were respectively cultured in vitro and demonstrated. The MFB proportion in fibroblast was known by α-smooth muscle actin (α-SMA) in fibroblast culture detected with immunohistochemistry for qualitative study and ELISA for quantitative analysis. The influence on fibroblast proliferation and transdifferentiation for MFB was observed by adding H2-RLX.
Results: There were no apparent differences for cell morphology between the fibroblasts from SSc patients and controls. The means of positive α-SMA in SSc group were higher than those in controls (P<0.01). With culture time extended, α-SMA levels of the two groups all increased gradually (P<0.01 all), but there were higher α-SMA levels in SSc group than those in controls separately at H24, H48, H72 in culture (P<0.05 all). Fibroblast proliferation and α-SMA levels were not influenced after adding 1 μg/L of H2-RLX, but 10 μg/L and 100 μg/L of it could completely inhibit the fibroblast proliferation and α-SMA levels (P<0.05 all), with the strongest repressing effect after adding 100 μg/L of it.
Conclusion: There is a specific property of fibroblasts transdifferentiation for MFB strongly from the skin lesion of the SSc patients. H2-RLX could give play to the antifibrotic effects by repressing the fibroblast proliferation and transdifferentiation for MFB in SSc.