Parthenolide reduces cisplatin-induced renal damage

NF-κB in Renal Inflammation

“…The increasing awareness of NF-B diversity in terms of regulatory components and actions calls for more detailed preclinical studies to pinpoint the timeframe and optimal target for potential clinical therapy. 79 Decreased proteinuria Diabetic nephropathy 80 Decreased inflammation AKI, sepsis 39 Decreased inflammation AKI; zymosan 81 Decreased inflammation 5/6 renal ablation model 82 Decreased inflammation AngII-infused renal injury 54,83 Decreased inflammation Parthenolide Glomerulonephritis 56 Decreased inflammation, proteinuria AKI; cisplatin 87 Decreased inflammation, proteinuria AngII-induced kidney injury 67 Decreased inflammation gliotoxin Glomerulonephritis 56 Decreased inflammation, proteinuria DHMEQ Glomerulonephritis 88 Decreased inflammation, proteinuria Specific approaches decoy B ODN Glomerulonephritis, crescentic 90 Decreased inflammation Allogenic renal transplant 92 Decreased inflammation AKI, ischemia-reperfusion 89 Decreased inflammation UUO 91 Decreased inflammation p50 siRNA AKI, sepsis 39 Improved renal function, decreased inflammation p50 knockout AKI, endotoxemia 40 Prolonged inflammation, increased mortality IB␣ super-repressor Protein overload proteinuria 93 Decreased inflammation DHMEQ, dehydroxymethyl-epoxyquinomicin; ODN, oligodeoxynucleotides; PDTC, pyrrolidinedithiocarbamate; siRNA, small interfering RNA; UUO, unilateral ureteral obstruction.…”

“…57 Parthenolide also decreases interstitial monocyte accumulation in AngII-mediated and cisplatin-induced renal injury. 88 Dehydroxymethyl-epoxyquinomicin is an inhibitor of RelA nuclear translocation that does not modify IB. 89 There is more specific evidence linking NF-B with renal disease.…”

Attenuation of Cisplatin-Induced Renal Injury by Inhibition of Soluble Epoxide Hydrolase Involves Nuclear Factor κB Signaling

“…Both TNFR2 and TNF␣ have NF-B binding sites, which could account for their induction in response to cisplatin treatment (Santee and Owen-Schaub, 1996;Yao et al, 1997). Further downstream effects of NF-B activation include induction of ICAM-1 and subsequent neutrophil infiltration Reeves, 2002, 2003;Francescato et al, 2007). The ability of EETs to interfere with NF-B signaling is consistent with the findings that sEH inhibition attenuates the effect of cisplatin on TNF␣, TNFR, and ICAM-1 expression and provides a plausible mechanism for the observed renoprotection afforded by sEH inhibition.…”

Regulation and Pathological Role of p53 in Cisplatin Nephrotoxicity

“…NF-B is a family of transcription factors that regulate the expression of a number of genes involved in diverse cellular responses, such as immune reaction, inflammation, cell proliferation, and apoptosis (Pahl, 1999). The activation of NF-B and its role in cisplatin-induced renal injury have been suggested in a series of in vivo and in vitro studies (Ramesh and Reeves, 2004;Li et al, 2005;Lee et al, 2006a,b;Francescato et al, 2007b;Luo et al, 2008). Notably, cisplatin-induced oxidative stress appears to be a potent activator of NF-B because the antioxidants can attenuate ROS generation and NF-B activation and thus protect the renal cells against cisplatin injury (Lee et al, 2006b;Luo et al, 2008).…”