Kawai Y, Gemba M
Division of Pharmacology, Osaka University of Pharmaceutical Sciences, Japan.
Jpn J Pharmacol. 1996 Sep;72(1):67-70. doi: 10.1254/jjp.72.67.
We investigated the effects of a phosphodiesterase inhibitor and dibutyryl cAMP (dBcAMP) on the cell injury induced by cephaloridine (CER) in an established renal epithelial cell LLC-PK1. CER increased the leakage of lactate dehydrogenase (LDH) from LLC-PK1 cells to the medium and the level of lipid peroxidation in the cells. 3-Isobutyl-1-methylxanthine, a phosphodiesterase inhibitor, increased cAMP content in LLC-PK1 cells and ameliorated the increase in LDH leakage induced by CER, dBcAMP reduced the cell injury induced by CER. Our results suggest that a signalling pathway of cAMP protects against CER-induced renal cell injury, which is probably due to generation of oxygen radicals.
我们研究了磷酸二酯酶抑制剂和二丁酰环磷腺苷(dBcAMP)对已建立的肾上皮细胞LLC-PK1中头孢菌素(CER)诱导的细胞损伤的影响。CER增加了乳酸脱氢酶(LDH)从LLC-PK1细胞向培养基中的泄漏以及细胞中脂质过氧化的水平。磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤增加了LLC-PK1细胞中的环磷腺苷含量,并改善了CER诱导的LDH泄漏增加,dBcAMP减轻了CER诱导的细胞损伤。我们的结果表明,环磷腺苷的信号通路可预防CER诱导的肾细胞损伤,这可能是由于氧自由基的产生。