[Relationship between nuclear factor-kappaB activity and kidney injury in rats with postburn sepsis].
OBJECTIVE
To investigate the relationship between nuclear factor-KappaB (NF-KappaB) activity and kidney injury in rats with postburn sepsis.


METHODS
Rats subjected to 30% full-thickness scald injury, followed by intraperitoneal injection of lipopolysaccharide (LPS), were used in the present study. Fifty-four Wistar rats were randomly divided into normal control group, postburn sepsis 1, 2, 6, 12, 24 hours groups, and sepsis with NF-KappaB inhibitor pyrrolidine dithiocarbamate (PDTC) treatment 1, 2, and 6 hour groups. NF-KappaB activity, tumor necrosis factor-alpha (TNF-alpha) protein expression, and renal function were determined with electrophoretic mobility shift assay (EMSA), enzyme linked immunoadsorbent assay (ELISA), and automatic biochemistry analyzer, respectively.


RESULTS
NF-KappaB activity in kidney was markedly enhanced and reached its peak 1 hour after scalding and injection of LPS (all P<0.01), and was decreased remarkably after the administration of PDTC. PDTC could suppress the elevated plasma TNF-alpha protein expression (both P<0.01), but not renal TNF-alpha levels. PDTC could not reduce blood urea nitrogen and blood creatinine contents, which were increased after scalding followed by LPS challenge.


CONCLUSIONS
The results suggest that the treatment with NF-KappaB inhibitor PDTC could down-regulate the NF-KappaB activity in kidney, but it could not protect the renal function in rats with postburn sepsis.
Yao
Feng-hua
FH
Department of Nephrology, 304 th Hospital Affiliated to General Hospital of PLA, Beijing 100037, China.
Yao
Xiao-di
XD
Li
Ji-jun
JJ
Chai
Jia-ke
JK
D000818:Animals; D002056:Burns / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D007668:Kidney / Q000378:metabolism / Q000473:pathology*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha