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Chinese Journal of Anesthesiology ; (12): 105-108, 2019.
Article in Chinese | WPRIM | ID: wpr-745673

ABSTRACT

Objective To evaluate the effect of bone marrow-derived mesenchymal stem cells (BMSCs) on transforming growth factor-β1 (TGF-β1)/Smad signaling pathway during acute lung injury (ALI) in rats.Methods Healthy clean-grade adult male Sprague-Dawley rats,aged 4-5 weeks,weighing 100-120 g,were selected,and BMSCs were prepared and cultured in vitro.Eighty-four healthy clean-grade adult male Sprague-Dawley rats,aged 4 weeks,weighing 170-190 g,were selected and divided into 4 groups (n=21 each) using a random number table method:control group (group C),group ALI,ALI plus BMSCs group (group ALI + BMSCs),and ALI plus phosphate buffer solution (PBS)group (group ALI+PBS).ALI was induced by intraperitoneally injecting 5 mg/kg lipopolysaccharide 0.5 ml in anesthetized rats.In group ALI+BMSCs,1×104 cells/ml BMSCs 0.5 ml (in PBS) was injected via the tail vein after intraperitoneal injection of lipopolysaccharide.PBS 0.5 ml was injected via the tail vein after intraperitoneal injection of lipopolysaccharide in group ALI+PBS.Arterial blood samples were collected at 6,24 and 48 h after injecting BMSCs for blood gas analysis and for determination of wet to dry weight ratio (W/D ratio),pathological changes (using haematoxylin and eosin staining),and expression of TGF-β1,Smad2 and Smad3 in lung tissues (by Western blot).Results Compared with group C,PaO2 was significantly decreased,PaCO2 and W/D ratio were increased,the expression of TGF-β1,Smad2 and Smad3 in lung tissues was up-regulated (P<0.05),and the pathological changes of lung tissues were accentuated in ALI,ALI+BMSCs and ALI+PBS groups.Compared with group ALI,PaO2 was significantly increased,PaCO2and W/D ratio were decreased,the expression of TGF-β1,Smad2 and Smad3 in lung tissues was down-regulated (P<0.05),and the pathological changes of lung tissues were significantly reduced in group ALI+BMSCs.Conclusion The mechanism by which BMSCs mitigates ALI may be associated with inhibiting TGF-β1/Smad signaling pathway in rats.

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