论文部分内容阅读
目的:探讨成纤维细胞(FB)向肌成纤维细胞(MFB)转分化在系统性硬化症(SSc)发病机制中的作用和H2松弛素(H2-RLX)在SSc中的抗纤维化作用机制。方法:体外培养SSc患者皮损和正常皮肤FB及鉴定;免疫细胞化学法定性、ELISA法定量检测FB中α-平滑肌肌动蛋白(α-SMA)而了解MFB比重;施加并观察H2-RLX对SSc FB增殖和转分化为MFB的影响。结果:两组FB的细胞形态无明显不同;SSc组α-SMA阳性率均值高于对照组(P<0.01);随培养时间的延长,两组α-SMA量均渐增多(P均<0.01),但在培养的24、48、72 h,SSc组α-SMA量分别高于对照组(P均<0.05);H2-RLX 1μg/L对FB增殖和α-SMA量无明显影响,而10μg/L和100μg/L则完全地抑制FB增殖和α-SMA量(P均<0.05),以100μg/L时抑制作用最强。结论:SSc患者皮损来源的FB存在强烈地向MFB转分化的特性,H2-RLX则可通过抑制FB增殖及转分化为MFB而在SSc中发挥抗纤维化作用。
OBJECTIVE: To investigate the role of fibroblasts (FB) transdifferentiation in myofibroblasts (MFB) in the pathogenesis of systemic sclerosis (SSc) and the anti-fibrosis mechanism of H2 relaxin (H2-RLX) in SSc . Methods: Skin lesions and normal skin FB were identified in SSc patients. Immunocytochemistry was used to detect the α-smooth muscle actin (α-SMA) in FB and the specific gravity of MFB was detected by ELISA. H2-RLX Effect of SSc FB proliferation and transdifferentiation on MFB. Results: The morphological changes of α-SMA in SSc group were higher than those in control group (P <0.01). The α-SMA levels in both groups increased gradually with the prolongation of culture time (P <0.01) ), But α-SMA levels in SSc group were higher than those in control group (P <0.05) at 24h, 48h and 72h respectively. H2-RLX 1μg / L had no significant effect on FB proliferation and α-SMA level, The inhibition of FB proliferation and the amount of α-SMA were all inhibited by 10μg / L and 100μg / L (P <0.05). CONCLUSIONS: FBs derived from skin lesions in SSc patients strongly transdifferentiate to MFBs. H2-RLX exerts anti-fibrotic effects in SSc by inhibiting FB proliferation and transdifferentiation into MFBs.