Sepsis-induced acute lung injury (ALI) remains one of the most common disorders in hospitals. The aim of this research was to explore the underlying characteristics and mechanisms of artesunate (AS) in protecting rat lungs from sepsis. The sepsis-induced ALI model was generated in SD rats by the intratracheal administration of lipopolysaccharide (LPS, 5 mg/kg) for 24 h. The rats were randomly assigned into 4 groups: Sham, LPS, LPS + AS, and LPS + AS + LY294002. Pathological evaluation of the lungs was conducted by HE staining, immunofluorescence, and TUNEL assay, and the MPO activity and the W/D ratio of each group were evaluated. The levels of inflammatory mediators (TNF-α and IL-6) were measured by immunoblotting, immunofluorescence and real-time PCR. Western blotting was used to determine the protein levels of PI3K, cleaved Caspase-3, p-mTOR, mTOR, p-Akt, and Akt in the lungs. The MPO activity, W/D ratio and lung injury score were obviously elevated after induction of ALI by LPS. Nevertheless, these alterations could be inhibited by AS. In addition, sepsis decreased the levels of p-mTOR, p-Akt, and PI3K and elevated the expression of cl-caspase-3, TNF-α, and IL-6 in the lungs. After AS administration, these alterations were obviously decreased, but treatment with the PI3K antagonist LY294002 inhibited the function of AS. AS could partially protect against LPS-induced ALI by inhibiting apoptosis and inflammatory mediator production, and this function is perhaps associated with the regulation of the mTOR/AKT/PI3K axis. These findings suggest that AS may possess certain beneficial characteristics in protecting the lungs from sepsis.

脓毒症引起的急性肺损伤（ALI）仍然是医院中最常见的疾病之一。这项研究的目的是探讨青蒿琥酯（AS）在保护大鼠肺部脓毒症中的潜在特征和机制。气管内注射脂多糖（LPS，5 mg / kg）持续24 h，在SD大鼠中产生败血症诱导的ALI模型。将大鼠随机分为4组：假手术，LPS，LPS + AS和LPS + AS + LY294002。通过HE染色，免疫荧光和TUNEL法进行肺的病理学评估，并评估每组的MPO活性和W / D比。通过免疫印迹，免疫荧光和实时PCR测量炎性介质（TNF-α和IL-6）的水平。Western印迹法用于测定PI3K，裂解的Caspase-3，p-mTOR，肺中的mTOR，p-Akt和Akt。LPS诱导ALI后，MPO活性，W / D比和肺损伤评分明显升高。但是，这些改变可能会被AS抑制。此外，脓毒症降低了肺中p-mTOR，p-Akt和PI3K的水平，并提高了cl-caspase-3，TNF-α和IL-6的表达。服用AS后，这些改变明显减少，但是用PI3K拮抗剂LY294002治疗抑制了AS的功能。AS可以通过抑制细胞凋亡和炎症介质的产生来部分防御LPS诱导的ALI，并且该功能可能与mTOR / AKT / PI3K轴的调控有关。这些发现表明，AS在保护肺部免受脓毒症的侵袭中可能具有某些有益的特征。LPS诱导ALI后，W / D比和肺损伤评分明显升高。但是，这些改变可能会被AS抑制。此外，脓毒症降低了肺中p-mTOR，p-Akt和PI3K的水平，并提高了cl-caspase-3，TNF-α和IL-6的表达。服用AS后，这些改变明显减少，但是用PI3K拮抗剂LY294002治疗抑制了AS的功能。AS可以通过抑制细胞凋亡和炎症介质的产生来部分防御LPS诱导的ALI，并且该功能可能与mTOR / AKT / PI3K轴的调控有关。这些发现表明，AS在保护肺部免受脓毒症的侵袭中可能具有某些有益的特征。LPS诱导ALI后，W / D比和肺损伤评分明显升高。但是，这些改变可能会被AS抑制。此外，脓毒症降低了肺中p-mTOR，p-Akt和PI3K的水平，并提高了cl-caspase-3，TNF-α和IL-6的表达。服用AS后，这些改变明显减少，但是用PI3K拮抗剂LY294002治疗抑制了AS的功能。AS可以通过抑制细胞凋亡和炎症介质的产生来部分防御LPS诱导的ALI，并且该功能可能与mTOR / AKT / PI3K轴的调控有关。这些发现表明，AS在保护肺部免受脓毒症的侵袭中可能具有某些有益的特征。这些改变可以被AS抑制。此外，脓毒症降低了肺中p-mTOR，p-Akt和PI3K的水平，并提高了cl-caspase-3，TNF-α和IL-6的表达。服用AS后，这些改变明显减少，但是用PI3K拮抗剂LY294002治疗抑制了AS的功能。AS可以通过抑制细胞凋亡和炎症介质的产生来部分防御LPS诱导的ALI，并且该功能可能与mTOR / AKT / PI3K轴的调控有关。这些发现表明，AS在保护肺部免受脓毒症的侵袭中可能具有某些有益的特征。这些改变可以被AS抑制。此外，脓毒症降低了肺中p-mTOR，p-Akt和PI3K的水平，并提高了cl-caspase-3，TNF-α和IL-6的表达。服用AS后，这些改变明显减少，但是用PI3K拮抗剂LY294002治疗抑制了AS的功能。AS可以通过抑制细胞凋亡和炎症介质的产生来部分防御LPS诱导的ALI，并且该功能可能与mTOR / AKT / PI3K轴的调控有关。这些发现表明，AS在保护肺部免受脓毒症的侵袭中可能具有某些有益的特征。这些改变明显减少，但是用PI3K拮抗剂LY294002治疗抑制了AS的功能。AS可以通过抑制细胞凋亡和炎症介质的产生来部分防御LPS诱导的ALI，并且该功能可能与mTOR / AKT / PI3K轴的调控有关。这些发现表明，AS在保护肺部免受脓毒症的侵袭中可能具有某些有益的特征。这些改变明显减少，但是用PI3K拮抗剂LY294002治疗抑制了AS的功能。AS可以通过抑制细胞凋亡和炎症介质的产生来部分防御LPS诱导的ALI，并且该功能可能与mTOR / AKT / PI3K轴的调控有关。这些发现表明，AS在保护肺部免受脓毒症的侵袭中可能具有某些有益的特征。