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2018 ; 42
(2
): 926-934
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Knockdown of TNF?? alleviates acute lung injury in rats with intestinal ischemia
and reperfusion injury by upregulating IL?10 expression
#MMPMID29767265
Yang Z
; Zhang XR
; Zhao Q
; Wang SL
; Xiong LL
; Zhang P
; Yuan B
; Zhang ZB
; Fan SY
; Wang TH
; Zhang YH
Int J Mol Med
2018[Aug]; 42
(2
): 926-934
PMID29767265
show ga
Intestinal ischemia and reperfusion (II/R) injury often triggers severe injury in
remote organs, with the lungs being considered the main target. Excessive
elevation of proinflammatory cytokines is a major contributor in the occurrence
and development of II/R?induced acute lung injury (ALI). Therefore, the present
study aimed to investigate whether blocking tumor necrosis factor?? (TNF??)
expression could protect the lungs from injury following II/R, and to explore the
possible underlying mechanism involving interleukin?10 (IL?10). Briefly, II/R was
induced in rats by 40 min occlusion of the superior mesenteric artery and celiac
artery, followed by 8, 16 or 24 h of reperfusion. Subsequently, lentiviral
vectors containing TNF?? short hairpin (sh)RNA were injected into the right lung
tissues, in order to induce TNF?? knockdown. The severity of ALI was determined
according to lung injury scores and lung edema (lung wet/dry weight ratio). The
expression levels of TNF?? were analyzed by quantitative polymerase chain
reaction (qPCR), western blotting and immunofluorescence (IF) staining. IL?10
expression, in response to TNF?? knockdown, was detected in lung tissues by qPCR
and IF. The results detected marked inflammatory responses, and increased levels
of lung wet/dry weight ratio and TNF?? expression, in the lungs of II/R rats.
Conversely, treatment with TNF?? shRNA significantly alleviated the severity of
ALI and upregulated the expression levels of IL?10 in lung tissues. These
findings suggested that TNF?? RNA interference may exert a protective effect on
II/R?induced ALI via the upregulation of IL?10. Therefore, TNF?? knockdown may be
considered a potential strategy for the prevention or treatment of ALI induced by
II/R in future clinical trials.
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