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Updated: Oct 2, 2026
Non-Invasive Endotracheal Administration of Lipopolysaccharide to Induce Acute Lung Injury in Rodents
Published on: December 5, 2025
Electroacupuncture Attenuates Lipopolysaccharide-Induced Acute Lung Injury via Enhanced Efferocytosis
Jing Liu1,2,3, Fang Liu1,2,3, Guihua Lai1,2,3
1The First Affiliated Hospital, Rehabilitation Medicine Center, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Introduction:
This study aimed to investigate whether efferocytosis, the phagocytic clearance of apoptotic cells, contributes to the therapeutic mechanism of EA in a lipopolysaccharide (LPS)-induced rat model of Acute Lung Injury (ALI).
Methods:
Three-month-old rats were randomly assigned to control, LPS, and LPS + EA groups (n = 8/group). Daily EA was administered at the bilateral ST36 (Zusanli) and LU5 (Chize) acupoints in the LPS + EA group. Lung tissue damage and cellular death were assessed using histological analysis and TUNEL staining. Serum concentrations of TNF-α, IL-1β, IL-6, and IL-10 were quantified by ELISA. Key markers associated with apoptosis and efferocytosis were assessed by qRT-PCR and Western blotting.
Results:
Histopathological examination showed that EA alleviated LPS-induced lung tissue damage and attenuated inflammatory cell infiltration. Following EA intervention, serum levels of TNF-α, IL-1βand IL-6 were decreased, while the level of IL-10 was increased. Massive accumulation of dead cells was observed in the lung tissue of ALI rats; LPS exposure significantly downregulated the mRNA and protein expression levels of Axl, Mertk and Rac1, while upregulating the expression level of Gas6 in lung tissue. After EA intervention, the number of dead cells was markedly reduced, and the transcriptional levels of caspase-3/8 were decreased. Meanwhile, EA significantly upregulated the expressions of Axl, Mertk and Rac1, while downregulating that of Gas6.
Discussion:
These results indicate that EA exerts a lung-protective effect by inhibiting the inflammatory response and repairing damaged lung tissue of LPS-induced ALI rats. Efferocytosis function was suppressed in the LPS-induced ALI model. Whereas EA may enhance the efferocytotic function of lung tissue.
Conclusion:
EA intervention exerts significant protective effects against LPS-induced ALI in rats. This therapeutic benefit may be partially mediated by the activation of efferocytosis, thereby suggesting a novel mechanism for EA in ALI.
