Objective

Evidence has shown that sevoflurane plays a protective role in acute lung injury (ALI) due to its anti-inflammatory and apoptotic-regulating activity. Nevertheless, the mechanism of sevoflurane is still not completely understood. This study intends to discuss the mechanism of sevoflurane on ALI and the possible mechanisms involved.

Methods

ALI model of rats was established through intravenous injection of endotoxin lipopolysaccharide. microRNA-34a-3p (miR-34a-3p) and signal transducers and activators of transcription 1 (STAT1) expression in lung tissues of ALI rats were detected. The optimal inhaled concentration of sevoflurane was screened, and then the modeled rats were injected with miR-34a-3p inhibitors, overexpressed STAT1 and inhaled 1.0 Minimum Alveolar Concentration (MAC) sevoflurane to determine mean arterial pressure (MAP) of rats, wet weight/dry weight ratio and myeloperoxidase (MPO) activity, oxidative stress- and inflammation-related factors in lung tissues of rats, along with lung cell viability and apoptosis.

Results

iR-34a-3p was downregulated while STAT1 was upregulated in ALI rats. Sevoflurane of 1.0 MAC was selected as the optimal inhalation concentration. Sevoflurane (1.0 MAC) increased MAP at T3 and reduced MPO activity, alleviated pathological damage, suppressed apoptosis, oxidative stress and inflammation, and induced cell viability in lung tissues of ALI rats. Down-regulated miR-34a-3p or up-regulated STAT reversed the functions of sevoflurane (1.0 MAC) on ALI rats.

Conclusion

Collectively, we demonstrate that sevoflurane reduces inflammatory factor expression, increases lung cell viability and inhibits lung cell apoptosis in ALI through upregulation of miR-34a-3p and downregulation of STAT1, which provides new clues for ALI treatment.

中文翻译：

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七氟醚通过microRNA-34a-3p上调和STAT1下调来降低炎性因子的表达，增加活力并抑制急性肺损伤中肺细胞的凋亡

目的

有证据表明，七氟醚具有抗炎和凋亡调节作用，在急性肺损伤（ALI）中起保护作用。然而，七氟醚的机理仍不完全清楚。这项研究旨在讨论七氟醚对ALI的作用机制及其可能的机制。

方法

通过静脉注射内毒素脂多糖建立大鼠ALI模型。检测了ALI大鼠肺组织中的microRNA-34a-3p（miR-34a-3p）以及信号转导子和转录激活因子1（STAT1）的表达。筛选最佳的七氟醚吸入浓度，然后向模型大鼠注射miR-34a-3p抑制剂，过表达的STAT1并吸入1.0的最低肺泡浓度（MAC）七氟醚以确定大鼠的平均动脉压（MAP），湿重/干重比和髓过氧化物酶（MPO）活性，大鼠肺组织中的氧化应激和炎症相关因子，以及肺细胞活力和凋亡。

结果

ALI大鼠中iR-34a-3p被下调，而STAT1被上调。选择1.0 MAC的七氟醚作为最佳吸入浓度。七氟醚（1.0 MAC）在T3时可增加MAP，降低MPO活性，减轻病理损伤，抑制凋亡，氧化应激和炎症，并诱导ALI大鼠肺组织细胞活力。下调的miR-34a-3p或上调的STAT可以逆转ALI大鼠的七氟醚（1.0 MAC）功能。

结论

集体地，我们证明七氟醚通过上调miR-34a-3p和下调STAT1来降低ALI中炎性因子的表达，增加肺细胞的活力并抑制肺细胞的凋亡，这为ALI治疗提供了新的线索。