Decursin derivative-004 protect renal cell damage via p38 MAPK inhibition

  • Shin, Seon-Mi (Laboratory ot cell culture engineering, Graduate School of Boptechnollogy. Korea University) ;
  • Kim, Hyeon-Ho (Laboratory ot cell culture engineering, Graduate School of Boptechnollogy. Korea University) ;
  • Kim, Ik-Hwan (Laboratory ot cell culture engineering, Graduate School of Boptechnollogy. Korea University)
  • Published : 2002.10.01

Abstract

Hypertrophy and the alteration of renal cell growth have been reported as early abnormality in diabetic nephropathy. However, the effects ot high PKCglucose and its action mechanism in renal proximal tubular cell (PTC) have not been elucidated. High glucose condition increases diacyl glycerol (DAG) and activates protein kinase C (PKC) in renal tubular cells. The PKC activates mitogen-activated protein kinases (MAPK), such as extracellular regulated kinase (ERK) and p38 MAPK. (omitted)

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