Background

Paraquat poisoning leads to lung injury and pulmonary fibrosis. The effect of paraquat encapsulation by previously described Pectin/Chitosan/Tripolyphosphate nanoparticles on its pulmonary toxicity was investigated in present study in a rat model of poison inhalation.

Material and method

The rats inhaled nebulized different formulation of paraquat (n = 5) for 30 min in various experimental groups. Lung injury and fibrosis scores, Lung tissue enzymatic activities, apoptosis markers were determined compared among groups.

Results

Encapsulation of paraquat significantly rescued both lung injury and fibrosis scores. Lung MDA level was reduced by encapsulation. Paraquat poisoning led to lung tissue apoptosis as was evidenced by higher Caspase-3 and Bax/Bcl2 expressions in rats subjected to paraquat inhalation instead of normal saline or free nanoparticles. Again, nanoencapsulation reduced these apoptosis markers significantly. Alpha-SMA expression was also reduced by encapsulation. Nanoparticles per se have no or little toxicity as was evidenced by inflammatory and apoptotic markers and histological scores.

Conclusion

In a rat model of inhalation toxicity of paraquat, loading of this herbicide on PEC/CS/TPP nanoparticles reduced acute lung injury and fibrosis. The encapsulation also led to lower apoptosis, oxidative stress and alpha-SMA expression in the lung tissue.

中文翻译：

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果胶/壳聚糖/三聚磷酸盐胶囊保护大鼠肺免受吸入百草枯诱导的纤维化和细胞凋亡

背景

百草枯中毒会导致肺损伤和肺纤维化。本研究在大鼠吸入毒物模型中研究了先前描述的果胶/壳聚糖/三聚磷酸盐纳米颗粒包裹百草枯对其肺毒性的影响。

材料和方法

 在不同的实验组中，大鼠吸入不同配方的百草枯 ( n = 5) 30 分钟。比较各组间肺损伤和纤维化评分、肺组织酶活性、细胞凋亡标志物。

结果

包封百草枯显着挽救了肺损伤和纤维化评分。通过封装降低了肺 MDA 水平。百草枯中毒导致肺组织凋亡，这一点可以通过吸入百草枯而不是生理盐水或游离纳米颗粒的大鼠中更高的 Caspase-3 和 Bax/Bcl2 表达来证明。同样，纳米封装显着减少了这些细胞凋亡标志物。Alpha-SMA 表达也通过封装减少。正如炎症和凋亡标志物以及组织学评分所证明的那样，纳米颗粒本身没有毒性或毒性很小。

结论

在百草枯吸入毒性大鼠模型中，在 PEC/CS/TPP 纳米颗粒上加入这种除草剂可减少急性肺损伤和纤维化。封装还导致肺组织中较低的细胞凋亡、氧化应激和 α-SMA 表达。