恶性胸水与水通道蛋白AQP1之间相关性探讨

Correlation between AQP1 and Malignant Pleural Effusion

目的:拟阐明水通道蛋白AQP1与恶性胸水产生机制的相关性,给予临床治疗提供科学依据。方法:利用免疫组织化学法和荧光定量PCR方法检测AQP1、CD34和TNF-αmRNA表达水平,并探讨其与胸水之间的相关性。结果:免疫组织化学方法检测结果提示AQP1在正常肺近胸膜下的毛细血管内皮细胞中强阳性表达,间皮细胞中弱表达。荧光定量PCR结果有胸水的肺癌组织中CD34和TNF-αmRNA的表达量比对照组、无胸水肺癌组织和炎性胸水相比增多,差异有统计学意义(P<0.05)。CD34的表达与VEGF有着密切的正相关,但AQP1的表达与CD34不相关,伴有胸水的肺癌组织中AQP1表达相对减少。结论:NSCLC伴有胸水时其癌组织中TNF-α和VEGF高表达导致新生毛细血管增多,即CD34表达增多;肿瘤来源TNF-α导致血管通透性增高,导致胸腔内渗出液不断增多;新生血管大量出现但相应的AQP1并未同步增多,导致机体水的严重失衡最后形成恶性胸水,推测癌性胸水与AOP1具有潜在联系。

Objective： To explore the correlation between aquaporin protein （ AQP1 ） and malignant pleural effusion as well as to provide scientific basis for related clinical treatment. Methods： The mechanisms of malignant pleural effusion were discussed, and the expression levels of AQP1, CD34, and TNF-α were determined using immunohistochemistry and fluorescent quantitation real-time polymerase chain reaction （ PCR ）. Results： Immunostaining results revealed the high expression of AQP 1 in the microvascular endothelia near the visceral pleura and a weak expression in the mesothelial cells in the visceral pleura. Quantitative PCR results showed that CD34 and TNF-α expression in the pleural effusion of cancer tissue significantly increased compared with the control group, and there were no spilled cancer tissue and inflammatory effusion （ P 〈 0.05 ）. CD34 expression is closely associated with VEGF, but not correlated with AQP 1 expression. This condition implies that the reduced expression of AQP1 under a cancer pathophysiological condition is associated with pleural effusion. Conclusion： High CD34 expression in the cancer tissue of non-small cell lung cancer with pleural effusion results in increased angiogenesis. High TNF-α expression can increase vascular permeability. These two mechanisms cause an increment in the pleural effusion, resulting in an increase of new blood vessels without a synchronous increase in AQP1. The latter finally disrupts the balance of water in the thorax and develops malignant pleural effusion. Further studies are needed to elucidate the potential pathophysiological role ofAQP 1 in malignant pleural effusion.