Wang Xin, Lv Lina, Chen Ying, Chen Jie
Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, PR China.
Toxicol Ind Health. 2010 Feb;26(1):47-53. doi: 10.1177/0748233709359274. Epub 2010 Jan 7.
Silicosis is a kind of pneumoconiosis caused by inhalation of silica dust, which is characterized by lung fibrosis. The biologically active form of transforming growth factor-beta1 (TGF-beta1) plays a key role in the development of lung fibrosis. CD36 is involved in the transformation of latent TGF-beta1 (L-TGF-beta1) to active TGF-beta1. The antagonistic effect of the synthetic peptide was analyzed by the administration of CD36 (93-110) synthetic peptide to the silicosis model of mice. The hydroxyproline content of the silica + CD36 (93-110) synthetic peptide group was significantly lower than that of the other experimental groups [silica and silica + CD36 (208-225) synthetic peptide groups] (p < .05). Inflammation, fibrotic degree and distribution of collagen fibers in silicotic nodules of the silica + CD36 (93-110) synthetic peptide group were less than those of the other experimental groups. The expressions of collagen I and III of the silica + CD36 (93-110) synthetic peptide group were significantly lower than those of the other experimental groups (p < .05). CD36 (93-110) synthetic peptide reduced the tissue fibrotic pathologies and collagen accumulation in the silicosis model of mice, resulting in the decreased severity of silica-induced lung fibrosis.
矽肺是一种因吸入二氧化硅粉尘引起的尘肺病，其特征为肺纤维化。转化生长因子-β1（TGF-β1）的生物活性形式在肺纤维化的发展过程中起关键作用。CD36参与潜伏性TGF-β1（L-TGF-β1）向活性TGF-β1的转化。通过给小鼠矽肺模型施用CD36（93-110）合成肽来分析该合成肽的拮抗作用。二氧化硅+CD36（93-110）合成肽组的羟脯氨酸含量显著低于其他实验组[二氧化硅组和二氧化硅+CD36（208-225）合成肽组]（p<0.05）。二氧化硅+CD36（93-110）合成肽组矽结节中的炎症、纤维化程度及胶原纤维分布均少于其他实验组。二氧化硅+CD36（93-110）合成肽组I型和III型胶原的表达显著低于其他实验组（p<0.05）。CD36（93-110）合成肽减轻了小鼠矽肺模型中的组织纤维化病变和胶原积累，导致二氧化硅诱导的肺纤维化严重程度降低。
