Resistance to Tumor Necrosis Factor-α (TNF-α)-induced Apoptosis in Rat Hepatoma Cells Expressing TNF-α Is Linked to Low Antioxidant Enzyme Expression

Overexpression of Ref-1 Inhibits Lead-induced Endothelial Cell Death via the Upregulation of Catalase

“…This finding is consistent with a previous report, in which it was demonstrated that catalase levels declined significantly in vascular smooth muscle cells chronically exposed to lead (Ni et al, 2004). Catalase expression can be downregulated by lipopolysaccharide (Clerch et al, 1996), ionizing radiation (Ushakova et al, 1999;Nenoi et al, 2001), and tumor necrosis factor-alpha (Clerch and Massaro, 1992;Chovolou et al, 2003;Lupertz et al, 2008), which stimulated cell death or oxidative stress in the cells. Therefore, in this study, the downregulation of catalase was related to Pb-induced cell death in endothelial cells.…”

Madecassoside suppresses LPS-induced TNF-α production in cardiomyocytes through inhibition of ERK, p38, and NF-κB activity

“…One microgram of total RNA was reverse-transcribed into cDNA with 0.2 U/ml Superscript III reverse transcriptase according to the manufacturer's protocol. The following oligonucleotide primers were used: TNF-α, sense 5′-TACTGAACTTCGGGGTGATTGGTCC-3′, antisense 5′-CAGCCTTGT-CCCTTGAAGAGAACC-3′ [13], producing a 295 bp fragment; β-actin, sense 5′-GCTCGTCGTCGACAACGGCTC-3′, antisense 5′-CAAACAT-GATCTGGGTCATCTTCTC-3′, producing a 353 bp fragment. PCR products were separated by 2% agarose gel electrophoresis, stained with ethidium bromide, and visualized by UV transillumination.…”

An Updated Systematic Review of the Pharmacology of Silymarin

“…A widely expressed 60 kDa protein, named SODD (silencer of death domains), associated with the DD of TNF RI and suppresses TNF-induced cell death and NF-kB activation demonstrating its role as a negative regulatory protein for these signalling pathways. Silibinin prevents 'in vitro' the effect of TNF-α induced with α-amanitin in hepatocytes [20], possibly by ROS(reactive ocygen species)-dependent mechanisms [21]. In mice treated with 750 mg/kg/day silymarin by gavage and 2.25 mg/kg Fumonisin B1 (inhibitor of ceramide synthase), silymarin prevented the Fumonisin B1-induced increases in TNF receptor 1 (TNFR1) expression, TNFR1-associated apoptosis (induction of caspases) and induction of lymphotoxin ß and interferon(IFN)-γ, although silymarin itself slightly increased expression of hepatic TNF-α.…”