الفهرس 
Contents
InflammationOnly 14 pages are availabe for public view
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Abstract
CLP induced elevation in total and differential cell count in BALF and increase in serum levels of hepatic enzymes: ALT, AST, total bilirubin, γ-GT, in addition to, IL-6 and IL-10 serum levels. Moreover, CLP produced a notable inflammation in the liver tissue of rats with dense inflammatory cells infiltration. CLP increased nuclear translocation and expression of NF-κB/p65 and upregulated mRNA expression of IL-6, IL-10, NFκBia, TLR-4and 5-LOX in liver tissues. However, pretreatment with either BML-111 or celastrol decreased CLP-induced increase in serum hepatic enzymes and IL-6. Conversely, BML-111 further elevated serum IL-10 and celastrol didn’t produce a notable effect on CLP-induced increase in serum IL-10. Moreover, BML-111 and celastrol produced restoration in the liver histology of CLP rats. Either BML-111 or celastrol ceased nuclear expression of NF-κB/p65, which showed notable cytoplasmic expression and downregulated IL-6, NFκBia, TLR-4 and 5-LOX mRNA expression. Conversely, BML-111 further increased the CLP-induced elevation in IL-10 expression, while celastrol didn’t produce a notable effect on IL-10 elevation. Therefore, both BML-111 and celastrol protected against CLP-induced acute hepatic dysfunction in rats through their anti-inflammatory effect, which induced: (a) restoration of the normal hepatic function, (b) reduction in NFκBia, TLR-4, and 5-LOX hepatic mRNA expression, (c) suppression of NF-κB/p65 nuclear expression, (d) reduction in serum level and mRNA expression of IL-6 and (e) elevation in the serum level and hepatic mRNA expression of IL-10, which wasn’t affected with celastrol. In conclusion, BML-111 and celastrol produced prevention of acute hepatic dysfunction induced by CLP.