2008Di-san junyi daxue xuebaoRequires access

PPARγ expressions in rat lung tissues after acute lung injury

Qian Gui-sheng

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Abstract

Objective To observe the changes of PPARγ expressions in acute lung injury (ALI) rats and explore the role of PPARγ in the pathogenesis of ALI. Methods ALI model was induced by lipopolysaccharide (LPS) in 32 male Wistar rats. Another 8 matched normal rats were used as control. At 1, 2, 4, 8 h after ALI, arterial blood gas analysis, lung tissue wet/dry weight ratio, lung histopathological changes were observed; The expressions of PPARγ and TNF-α mRNA were detected by RT-PCR; TNF-αcontent was examined with ELISA; PPARγ protein in lung tissues was detected by immunohistochemistry. Results Compared with control rats, PaO2 of ALI rats decreased significantly (P0.05); Lung wet/dry weight ratio rose (P0.05); Lung tissues were damaged histopathologically; The expressions of TNF-α mRNA in lung tissues and blood plasma increased markedly (P0.05). PPARγ expressed in lung tissues of control rats. PPARγ mRNA expressions in lung tissues decreased in 1 h after ALI, declined to the lowest level 2 h after ALI and kept at a low level to the end of observation peroid. Immunohistochemical staining of PPASγ showed that there was no difference between ALI rats and control rats at 1 h and 2 h after ALI, and significant decrease occurred 4 h after ALI and lasted to 8 h after ALI (P0.05). Conclusion Lung tissues of normal rats express PPARγ. The decreased PPARγ mRNA and protein expressions in the rats of ALI caused by LPS may be associated with inflammation and damage of lung tissues.

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Objective To observe the changes of PPARγ expressions in acute lung injury (ALI) rats and explore the role of PPARγ in the pathogenesis of ALI. Methods ALI model was induced by lipopolysaccharide (LPS) in 32 male Wistar rats. Another 8 matched normal rats were used as control. At 1, 2, 4, 8 h after ALI, arterial blood gas analysis, lung tissue wet/dry weight ratio, lung histopathological changes were observed; The expressions of PPARγ and TNF-α mRNA were detected by RT-PCR; TNF-αcontent was examined with ELISA; PPARγ protein in lung tissues was detected by immunohistochemistry. Results Compared with control rats, PaO2 of ALI rats decreased significantly (P0.05); Lung wet/dry weight ratio rose (P0.05); Lung tissues were damaged histopathologically; The expressions of TNF-α mRNA in lung tissues and blood plasma increased markedly (P0.05). PPARγ expressed in lung tissues of control rats. PPARγ mRNA expressions in lung tissues decreased in 1 h after ALI, declined to the lowest level 2 h after ALI and kept at a low level to the end of observation peroid. Immunohistochemical staining of PPASγ showed that there was no difference between ALI rats and control rats at 1 h and 2 h after ALI, and significant decrease occurred 4 h after ALI and lasted to 8 h after ALI (P0.05). Conclusion Lung tissues of normal rats express PPARγ. The decreased PPARγ mRNA and protein expressions in the rats of ALI caused by LPS may be associated with inflammation and damage of lung tissues.

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Available abstract

Objective To observe the changes of PPARγ expressions in acute lung injury (ALI) rats and explore the role of PPARγ in the pathogenesis of ALI. Methods ALI model was induced by lipopolysaccharide (LPS) in 32 male Wistar rats. Another 8 matched normal rats were used as control. At 1, 2, 4, 8 h after ALI, arterial blood gas analysis, lung tissue wet/dry weight ratio, lung histopathological changes were observed; The expressions of PPARγ and TNF-α mRNA were detected by RT-PCR; TNF-αcontent was examined with ELISA; PPARγ protein in lung tissues was detected by immunohistochemistry. Results Compared with control rats, PaO2 of ALI rats decreased significantly (P0.05); Lung wet/dry weight ratio rose (P0.05); Lung tissues were damaged histopathologically; The expressions of TNF-α mRNA in lung tissues and blood plasma increased markedly (P0.05). PPARγ expressed in lung tissues of control rats. PPARγ mRNA expressions in lung tissues decreased in 1 h after ALI, declined to the lowest level 2 h after ALI and kept at a low level to the end of observation peroid. Immunohistochemical staining of PPASγ showed that there was no difference between ALI rats and control rats at 1 h and 2 h after ALI, and significant decrease occurred 4 h after ALI and lasted to 8 h after ALI (P0.05). Conclusion Lung tissues of normal rats express PPARγ. The decreased PPARγ mRNA and protein expressions in the rats of ALI caused by LPS may be associated with inflammation and damage of lung tissues.

Key concepts: Lung, Lipopolysaccharide, Immunohistochemistry, Medicine, Endocrinology, Inflammation, H&E stain, Pathology

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