Using a rat model of lipopolysaccharide (LPS)-induced ALI, we aimed investigate whether efferocytosis is involved in the underlying mechanism of EA therapy for ALI.
Three-month-old rats were randomly divided into the control, LPS, and LPS + EA groups (n = 3). Daily EA was applied at the bilateral ST36 (Zusanli) and LU5 (Chize) sites in the LPS + EA group. After intervention, lung tissue was collected to assess lung tissue damage and cell apoptosis via histological analysis. The serum levels of TNFα, IL-1β, IL-6, and IL-10 were measured by ELISA. Factors associated with apoptosis and efferocytosis were evaluated by qPCR and Western blotting.
Histopathological examination demonstrated that EA alleviated LPS-induced lung tissue damage and inflammatory cells infiltration. The serum levels of TNFα, IL-1β, and IL-6 notably decreased after EA treatment, while the IL-10 levels increased. We further confirmed that EA treatment inhibited cells apoptosis in ALI rats by downregulating the overexpression of caspase-3 and caspase-8 and reducing the abundance of TUNEL-positive cells. In addition, the LPS-induced downregulation of Axl, Mertk and Rac1 expressions along with the upregulation of Gas6 expression were reversed by EA intervention.
EA alleviated lung tissue damage and suppressed inflammatory response and apoptosis in LPS-induced ALI rats. This protective effect might be related to the enhancement of efferocytosis by EA.
These results provided convincing evidence for the use of EA to treat LPS-induced ALI.
Electroacupuncture
Efferocytosis
