摘要
We examined the role of a down stream of intracellular signaling pathway,extracellular signal-regulated kinase(ERK),in cephaloridine (CER)-induced nephrotoxicity in rats.The increase in phosphorylated ERK(pERK,activated ERK) was detected in nucleus fraction prepared from rat kidney cortex 24h after injections of antibiotic CER with the increase in BUN level.The slices prepared from rat kidney cortex were incubated in the medium containing PD980-59,a MEK1/2 inhibitor,for the measurement of free radical production and cell injure(LDH leakage).CER caused not only the increases in lipid peroxidation as an index of free radical production and LDH leakage,but also ERK activation in nucleus fraction.MEK1/2 inhibitor ameliorated CER-induced injury and suppressed ERK activation in the slices.These results suggest a possible role of MEK/ERK signaling pathway in free radical-induced CER nephrotoxicity.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
2002年第6期426-426,共1页
Chinese Journal of Pharmacology and Toxicology
