Protective effect of HSF1 on mice with LPS-induced acute lung injury and screening of relevant differentially-expressed genes / 中国病理生理杂志
Chinese Journal of Pathophysiology
; (12): 2073-2077,2083, 2017.
Article
en Zh
| WPRIM
| ID: wpr-667319
Biblioteca responsable:
WPRO
ABSTRACT
AIM:To study the protective effect of heat shock factor1(HSF1) on the mice with lipopolysaccha-ride (LPS)-induced acute lung injury(ALI),and to screen the relevant differentially-expressed genes. METHODS:ALI mouse model was established by LPS intracheal instillation. The macroscopic and pathological changes of the lung tissue were observed,and the concentrations of total protein,TNF-α, IL-β, IL-6 and VEGF in the bronchoalveolar lavage fluid (BALF) were analyzed. Differentially-expressed genes in the lung tissues of HSF1 +/ +mice and HSF1 -/- mice with ALI induced by LPS were screened by gene chips. The key gene was verified by real-time qPCR. RESULTS:The macroscopic and pathological changes of the lung injury in HSF1 -/- +LPS mice were more serious than those in HSF1 +/ ++LPS mice.The concentrations of total protein,VEGF,TNF-α,IL-1β and IL-6 in the BALF of HSF1 -/- +LPS mice were significantly higher than those of HSF1 +/ ++LPS mice(P<0.05). Compared with the HSF1 +/ +mice,a total of 918 differentially-ex-pressed genes were indentified in the HSF1 -/- mice, among which the expression levels of 65 genes had obvious diffe-rence,with 28 genes up-regulated,including Atg7,ccr1,cxcr2,Tbl1xr1,Mmp9,Pparg,Plcb2,Arrb2,Cntn1,Col4a6, etc, and 37 genes down-regulated,including Fgfr1,Fgfr2,Map4k4,Ddx58,Tfg,Stat3,Smad4,Lamc1,Sdc3,etc. The results of real-time qPCR showed that the mRNA level of CXCR2 in HSF1 -/- + LPS mice was significantly higher than that in HSF1 +/ ++ LPS mice,which was consistent with the results of gene chips. CONCLUSION:HSF1 has protective effect on the mice with LPS-induced ALI. CXCR2 may be involved in the protective effect of HSF1 on this process.
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Índice:
WPRIM
Tipo de estudio:
Diagnostic_studies
/
Prognostic_studies
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Screening_studies
Idioma:
Zh
Revista:
Chinese Journal of Pathophysiology
Año:
2017
Tipo del documento:
Article