Celastrol aggravates LPS-induced inflammation and injuries of liver and kidney in mice.

摘要: Sepsis, a life-threatening syndrome with uncontrolled inflammatory response, causes high morbidity and mortality worldwide. Currently, satisfactory treatments on sepsis are still lacking in clinic. Thus, new therapeutic strategies urgently required. Recently, celastrol, pentacyclic triterpene extracted from the traditional Chinese medicine Tripterygium Wilfordi plant, attracted great interest for its properties of anti-inflammation, anti-oxidative stress, metabolism remodeling. However, effect celastrol is unclear. In this study, we investigated lipopolysaccharides (LPS)-induced inflammation organ injuries mice. Following pretreatment, mice showed increased rate aggravated evidenced by further enhanced markers IL-6, IL-1β, TNF-α, IL-18, MCP-1, ICAM-1 circulation, liver, kidney after LPS treatment. The serum levels ALT, AST, LDH were parallel deteriorated liver morphological damage (H&E) oxidative stress celastrol-treated mice, indicating an injury. kidney, expressions tubular injury molecule-1 (KIM-1) gelatinase-associated lipocalin (NGAL) upregulated along higher blood urea nitrogen (BUN), creatinine (Cr), MDA These findings not only indicated detrimental role therapy LPS-induced but also suggested restriction usage patients.