Abstract:
:Angiotensin II (Ang II) plays an important role in inflammatory process. Acute lung injury (ALI), an inflammatory disorder of the lung, is commonly associated with endotoxemia; however, the mechanism that endotoxin (lipopolysaccharide, LPS) induces the inflammatory response in ALI is not well defined. Here, we showed, in LPS-induced ALI rat model, that Ang II and Ang II type 1 (AT(1)) receptor were significantly increased in lung tissues, compared with those in controls. Meanwhile, nuclear factor (NF)-kappaB-DNA-binding activity, tumor necrosis factor (TNF)-alpha mRNA, and pneumocytic apoptosis were significantly increased. Moreover, pretreatment of rats with losartan, an antagonist of AT(1) receptor for Ang II, improved the inflammation, reduced the elevation of Ang II and AT(1) receptor, and inhibited NF-kappaB-DNA-binding activity, expression of TNF-alpha mRNA, and pneumocytic apoptosis. The data indicate that Ang II may mediate the inflammatory process in LPS-induced ALI through AT(1) receptor, which can be blocked by losartan.
journal_name
Arch Biochem Biophysjournal_title
Archives of biochemistry and biophysicsauthors
Liu L,Qiu HB,Yang Y,Wang L,Ding HM,Li HPdoi
10.1016/j.abb.2008.09.019subject
Has Abstractpub_date
2009-01-01 00:00:00pages
131-6issue
1eissn
0003-9861issn
1096-0384pii
S0003-9861(08)00455-4journal_volume
481pub_type
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