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

In this study, we investigated the effect of celastrol on lipopolysaccharides (LPS)-induced inflammation and organ injuries in mice. Following celastrol pretreatment, mice showed increased mortality rate and aggravated inflammation evidenced by further enhanced inflammatory markers of IL-6, IL-1β, TNF-α, IL-18, MCP-1, and ICAM-1 in circulation, liver, and kidney after LPS treatment. The serum levels of ALT, AST, and LDH were further increased in parallel with the deteriorated liver morphological damage (H&E) and oxidative stress in celastrol-treated mice, indicating an aggravated liver injury. In kidney, the expressions of tubular injury markers of kidney injury molecule-1 (KIM-1) and gelatinase-associated lipocalin (NGAL) were further upregulated along with higher levels of blood urea nitrogen (BUN), creatinine (Cr), and MDA in celastrol-treated mice. These findings not only indicated a detrimental role of celastrol therapy in LPS-induced inflammation and organ injuries but also suggested the restriction of celastrol usage in sepsis patients. PMID: 30093945 [PubMed]
Source: American Journal of Translational Research - Category: Research Tags: Am J Transl Res Source Type: research