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首页> 外文期刊>American Journal of Physiology >Hyaluronic acid is radioprotective in the intestine through a TLR4 and COX-2-mediated mechanism
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Hyaluronic acid is radioprotective in the intestine through a TLR4 and COX-2-mediated mechanism

机译：透明质酸通过TLR4和COX-2介导的机制在肠道内具有辐射防护作用

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The intestinal epithelium is sensitive to radiation injury. Damage to the intestinal epithelium is dose limiting in radiation therapy of abdominal cancers. There is a need for agents that can be given before radiation therapy to protect the intestinal epithelium. C57BL6 mice were subjected to 12 Gy of total body radiation. Some mice received intraperitoneal hyaluronic acid (HA) before radiation. Mice were killed 6 h after radiation to assess radiation-induced apoptosis in the intestine; other mice were killed at 84 h to assess crypt survival. Total body radiation (12 Gy) resulted in increased expression of HA synthases and HA in the intestine and increased plasma HA (5-fold). Intraperitoneal injection of HA (30 mg/kg) before radiation resulted in a 1.8-fold increase in intestinal crypt survival and a decrease in radiation-induced apoptosis. The radioprotective effects of HA were not seen in Toll-like receptor 4 (TLR4)- or cyclooxygenase-2 (COX-2)-deficient mice. Intraperitoneal injection of HA induced a 1.5-fold increase in intestinal COX-2 expression, a 1.5-fold increase in intestinal PGE2, and the migration of COX-2-expressing mesenchymal stem cells from the lamina propria in the villi to the lamina propria near the crypt. We conclude that 1) radiation induces increased HA expression through inducing HA synthases, 2) intraperitoneal HA given before radiation reduces radiation-induced apoptosis and increases crypt survival, and 3) these radioprotective effects are mediated through TLR4, COX-2, and the migration of COX-2-expressing mesenchymal stem cells.
机译：肠上皮对辐射损伤敏感。在腹部癌症的放射治疗中，对肠上皮的损害是剂量限制。需要可以在放射治疗之前给予以保护肠上皮的药物。对C57BL6小鼠进行了12 Gy的全身辐射。一些小鼠在放射前接受腹膜内透明质酸（HA）。辐射后6小时杀死小鼠以评估辐射诱导的肠细胞凋亡。其他小鼠在84 h处死以评估隐窝存活率。全身辐射（12 Gy）导致肠道内HA合酶和HA的表达增加，血浆HA升高（5倍）。放射前腹腔注射HA（30 mg / kg）可使肠道隐窝存活增加1.8倍，并减少放射诱导的细胞凋亡。在Toll样受体4（TLR4）或环氧合酶2（COX-2）缺陷型小鼠中未观察到HA的放射防护作用。腹膜内注射HA诱导肠道COX-2表达增加1.5倍，使肠道PGE2增加1.5倍，表达COX-2的间充质干细胞从绒毛固有层迁移至附近的固有层地穴。我们得出的结论是：1）辐射通过诱导HA合酶来诱导HA表达增加; 2）辐射前给予腹膜内HA可减少辐射诱导的细胞凋亡并增加隐窝存活率; 3）这些放射防护作用是通过TLR4，COX-2和迁移介导的表达COX-2的间充质干细胞

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