Although IL-1beta monocyte release was markedly elevated in patients with atherogenic dyslipidemias, IL-1beta gene expression was only slightly and nonsignificantly higher in the studied groups versus control.
Meanwhile, DISO resulted in strong inhibition against the elevation of hepatic injury marker (AST, ALT, and ALP) activities and dyslipidemia (TC, TG, LDL-C, and HDL-C), as well as liver inflammatory cytokine (IL-1, IL-6, TNF-α, and TNF-β) release in l-carnitine-fed mice (<i>p</i> < 0.05).
Dyslipidemia caused significant (p < 0.05) increase in OS (lipid peroxidation, nitric oxide, and protein carbonyl), pro-inflammatory cytokine (CRP, IL-1β, MCP-1, and TNF-α), and eicosanoid (PGE<sub>2</sub>, LTB<sub>4</sub>, and LTC<sub>4</sub>) level in serum of both young and aged rats.