Background

Exposure to airborne fine particulate matter (PM_2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM_2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM_2.5 exposure in vivo and in vitro.

Results

In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM_2.5 (PM_2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM_2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM_2.5 exposure.

Conclusions

Taken together, our findings indicated that PM_2.5 induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.

中文翻译：

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PM 2.5暴露通过激活大鼠和HK-2细胞的自噬途径而引起肾损伤

背景

已宣布暴露于空气传播的细颗粒物质（PM _2.5）对人体肾脏有害。然而，自噬途径的激活在由PM _2.5暴露引起的肾毒性中是否起关键作用仍知之甚少。这项研究的目的是探讨体内和体外暴露于PM _2.5后肾脏损害的机制。

结果

在本研究中，在浓缩的PM _2.5（PM _2.5）组和过滤的空气（FA）组之间观察到饮水量，尿流率和平均血压的统计学显着变化。暴露的动物表现出严重的肾小管上皮细胞水肿，毛细血管充血，肾小球泌尿空间减少和早期促纤维化状态。此外，在暴露的大鼠中观察到早期肾脏损伤标志物水平的显着增加，并且这些动物在肾细胞中表现出更高的凋亡率。此外，PM _2.5暴露激活了自噬途径，如LC3-I向LC3-II的转化，P62和beclin-1的活化所证明。在暴露于PM _2.5后，体内和体外均存在更多的自噬体，所有这些影响是同时存在的。

结论

两者合计，我们的发现表明PM _2.5通过激活肾小管上皮细胞中的自噬途径诱导肾功能损害。