Objective To observe the effect of electroacupuncture(EA) at “Zusanli”(ST36) pretreatment on lung functions

inflammatory response

and levels of angiotensin-converting enzyme 2(ACE2) and angiotensin(1-7) [Ang(1-7)] in rats with sepsis-induced acute lung injury(ALI)

so as to explore its mechanisms underlying improvement of ALI. Methods Thirty male SD rats were randomly divided into normal

model and EA groups(n=10 in each group). The sepsis-related ALI model was established by intraperitoneal injection of lipopolysaccharide(LPS

5 mg/kg). Rats of the EA group received EA(4 Hz/20 Hz

1—3 mA) stimulation at bilateral ST36 for 30 min

once each day

for 7 days before modeling. The lung functions including forced vital capacity(FVC)

forced expiratory volume at 0.1 second(FEV0.1) and FEV0.3 were detected using a respiratory function detector for small animals at 3 h after modeling. The bronchoalveolar lavage fluid(BALF) was collected for assaying the contents of Ang(1-7)

tumor necrosis factor-α(TNF-α) and interleukin-1 β(IL-1β) using ELISA. The lung wet/dry weight(W/D) ratio

FEV0.1/FVC

and FEV0.3/FVC were calculated. The histopathological changes of lung tissues were displayed by hematoxylin-eosin(H.E.) staining. The expression of ACE2 and mitochondrial assembly receptor(MasR) mRNAs and proteins in the lung tissue was detected by fluorescence quantitative real-time PCR and Western blot

separately. Results Following modeling

the levels of FVC

FEV0.1

FEV0.3

ratio of FEV0.1/FVC and FEV0.3/FVC

content of Ang(1-7) in the BALF

and the expression levels of ACE2 and MasR mRNAs and proteins in the lung tissue were significantly decreased(P<0.01)

while the level of W/D ratio and TNF-α and IL-1β contents in the BALF significantly increased(P<0.01) in the model group relevant to the normal group. In comparison with the model group

the levels of FVC

FEV0.1

FEV0.3

ratio of FEV0.1/FVC and FEV0.3/FVC

content of Ang(1-7) in the BALF

and expression levels of ACE2 and MasR mRNAs and proteins in the lung tissue were significantly increased(P<0.05

P<0.01)

whereas the level of W/D ratio

and TNF-α and IL-1β contents in the BALF were significantly decreased(P<0.05

P<0.01) in the EA group. H.E. staining showed pulmonary interstitial edema and alveolar septum thickening with severe inflammatory cell infiltration in the model group

which was relatively milder in the EA group. Conclusion EA preconditioning at ST36 can improve pulmonary function in sepsis-related ALI rats

which may be related to its effects in inhibiting inflammatory response and up-regulating ACE2 and MasR expression and Ang(1-7) content in the lung tissue.