J Toxicol Sci. 2011 Aug;36(4):493-8. doi: 10.2131/jts.36.493.
Previous studies have shown that prenatal and postnatal exposure to diesel exhaust (DE), which is known to be one of the main constituents of air pollution, enhances the persistence of endometriosis in a rat model. The aim of this study is to investigate the pathological changes induced by DE exposure in a rat model of endometriosis. Pregnant Sprague-Dawley rats were exposed to DE or clean air beginning on gestational day 2 and neonatal rats were persistently exposed to DE or clean air. Endometriosis was induced by autotransplantation of endometrium onto the peritoneum of eight-week-old female offspring. Endometriotic lesions were examined at 7 and 14 days post-transplantation. As a result, infiltration of activated mast cells remained in deeper area of peritoneal tissue around the endometriosis model compared to the control group at 14 days post-autotransplantation. In the DE exposure group, 14 days post-transplant, the remaining lesions contained fibroblasts and activated mast cells, which were surrounded by collagen fibers. The data showed that prenatal and postnatal DE exposure enhances the activation of mast cells and prolongs the persistence of collagen fibers in the induced rat model of endometriosis.
先前的研究表明，产前和产后暴露于柴油废气（DE）会增强子宫内膜异位症在大鼠模型中的持续性，DE 已知是空气污染的主要成分之一。本研究旨在探讨 DE 暴露在子宫内膜异位症大鼠模型中引起的病理变化。从妊娠第 2 天开始，将怀孕的 Sprague-Dawley 大鼠暴露于 DE 或清洁空气中，并且新生大鼠持续暴露于 DE 或清洁空气中。通过将子宫内膜自体移植到 8 周龄雌性后代的腹膜上来诱导子宫内膜异位症。在移植后 7 和 14 天检查子宫内膜异位症病变。结果显示，与对照组相比，在自体移植后 14 天，子宫内膜异位症模型周围腹膜组织的深部区域仍有活化的肥大细胞浸润。在 DE 暴露组中，移植后 14 天，残留的病变包含成纤维细胞和活化的肥大细胞，这些细胞被胶原纤维包围。数据表明，产前和产后 DE 暴露可增强肥大细胞的活化，并延长诱导的子宫内膜异位症大鼠模型中胶原纤维的持续性。
