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在放射性肺损伤的发展过程中,内皮细胞损伤会导致血-肺泡屏障破坏。

Endothelial cell damage induces a blood-alveolus barrier breakdown in the development of radiation-induced lung injury.

作者信息

Qiu Jun, Li Jian, He Tian-Chu

机构信息

Radiotherapy Department of The First Affiliated Hospital of Guangxi Medical University, Nanning, China.

出版信息

Asia Pac J Clin Oncol. 2011 Dec;7(4):392-8. doi: 10.1111/j.1743-7563.2011.01461.x.

Abstract

AIM

To investigate the role of endothelial cell damage in radiation-induced lung injury.

METHODS

A total of 60 male Sprague-Dawley rats were irradiated to the right hemithorax with a single dose of 0, 7.0 or 14.4 Gy. Serial studies were performed before and at 1, 7, 30 and 90 days after radiation, respectively. Pathological studies were carried out to detect changes in the lung after irradiation. Western blot studies were conducted to detect the expression of CD34 and of CD105 and vascular endothelial growth factor (VEGF).

RESULTS

Compared to controls, the irradiated rat lung showed a dose-dependent and time-dependent decrease in the expression of CD34. The level of CD105 was significantly reduced by irradiation except at 90 days after radiation. The expression of VEGF increased 1 day after radiation, and then decreased from day 30 onwards, to be lower than the control group at 90 days. Pulmonary fibrosis was observed at 90 days after 14.4 Gy exposure; however, most of these phenomena were not observed in the 7.0 Gy group.

CONCLUSION

These results support the notion that endothelial cells play an important role in radiation-induced lung injury, and may be critical to breakdown of the blood-alveolus barrier and microcirculation dysfunction related to radiation-induced inflammation and fibrosis.

摘要

目的

探讨内皮细胞损伤在放射性肺损伤中的作用。

方法

将60只雄性Sprague-Dawley大鼠的右半胸分别接受0、7.0或14.4 Gy的单次照射。分别在放疗前及放疗后1、7、30和90天进行系列研究。进行病理研究以检测照射后肺的变化。进行蛋白质印迹研究以检测CD34、CD105和血管内皮生长因子(VEGF)的表达。

结果

与对照组相比,照射后的大鼠肺组织中CD34的表达呈剂量和时间依赖性降低。除放疗后90天外,照射使CD105水平显著降低。放疗后1天VEGF表达增加,然后从第30天起下降,至90天时低于对照组。14.4 Gy照射后90天观察到肺纤维化;然而,在7.0 Gy组中未观察到这些现象中的大多数。

结论

这些结果支持内皮细胞在放射性肺损伤中起重要作用的观点,并且可能对与放射性炎症和纤维化相关的血-气屏障破坏和微循环功能障碍至关重要。

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