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目的：探讨活血化淤药物７６４３对细胞外间质合成的影响。方法：羟脯氨酸法、间接酶联免疫吸附法（ＥＬＩＳＡ）测定博莱霉素Ａ６（ＢＬＭＡ６）诱发的小鼠、大鼠肺纤维化模型肺组织胶原含量及合成，阿利新蓝法测定其糖胺多糖（ＧＡＧ）含量；３ＨＰｒｏ掺入法测定体外培养兔角膜瘢痕成纤维细胞中胶原合成，ＥＬＩＳＡ测定其纤维粘连蛋白（Ｆｎ）含量。结果：７６４３对模型肺组织胶原合成有明显的抑制作用，抑制率５０．５％，尤其能使肺组织中Ⅰ型胶原及ＧＡＧ明显减少；体外实验证实，７６４３可抑制３ＨＰｒｏ及３ＨＴｄＲ掺入成纤维细胞，且使其表面Ｆｎ明显减少。结论：７６４３抗纤维化作用机制的研究，应以细胞外间质组分———胶原合成为基点深入进行。
OBJECTIVE: To investigate the effect of activating blood detoxification drug 764 3 on extracellular matrix synthesis. METHODS: Hydroxyproline method and indirect enzyme-linked immunosorbent assay (ELISA) were used to determine collagen content and synthesis in lung tissue of mice and rats induced by bleomycin A6 (BLMA6). Aliski blue method The content of glycosaminoglycans (GAG) was determined. Collagen synthesis in fibroblasts of rabbits corneal scars was measured by 3HPro incorporation method. The fibronectin (Fn) content was measured by ELISA. RESULTS: 764 3 significantly inhibited the synthesis of collagen in lung tissue, and the inhibition rate was 50.5%. In particular, type I collagen and GAG in lung tissue were significantly reduced. In vitro experiments confirmed that 764 3 can inhibit 3H-Pro. And 3H-TdR incorporation into fibroblasts, and its surface significantly reduced Fn. Conclusion: The study of the mechanism of 764 3 anti-fibrosis should be based on the synthesis of extracellular matrix components—collagen synthesis.