Effects of Puerariae Radix extract on Cisplatin-Induced Apoptosis of Rat Mesangial Cells

갈근(葛根) 추출물이 cisplatin에 의해 유도된 rat mesangial cell의 apoptosis에 미치는 영향

  • Hong, Jae-Eui (Department of Internal Medicine, Wonkwang University) ;
  • Shin, Jo-Young (Department of Internal Medicine, Wonkwang University) ;
  • Ju, Sung-Min (Department of Pathology, College of Oriental Medicine, Wonkwang University) ;
  • Jeon, Byung-Hun (Department of Pathology, College of Oriental Medicine, Wonkwang University) ;
  • Lee, Si-Hyeong (Department of Internal Medicine, Wonkwang University)
  • 홍재의 (원광대학교 한의과대학 폐계내과학교실) ;
  • 신조영 (원광대학교 한의과대학 폐계내과학교실) ;
  • 주성민 (원광대학교 한의과대학 병리학교실) ;
  • 전병훈 (원광대학교 한의과대학 병리학교실) ;
  • 이시형 (원광대학교 한의과대학 폐계내과학교실)
  • Received : 2010.03.16
  • Accepted : 2010.04.13
  • Published : 2010.04.25

Abstract

Puerariae radix (PR) is a popular natural herb and a traditional food in Asia, which has antithrombotic and anti-allergic properties and stimulates estrogenic activity. One of the major side effects of cisplatin is nephrotoxicity, leading to acute renal failure. Recent study has suggested a role of ROS and p53 in renal cell injury by cisplatin. We studied that protective effects of PR on cisplatin-induced apoptosis in rat mesangial cell. Rat mesangial cell was preincubated with PR (50, 100, 150 and 200 ${\mu}g/m{\ell}$) for 12 hr and then treated with 30 ${\mu}M$ cisplatin for 24 hr. Protective effect of PR on cisplatin-induced apoptosis in ECV304 cells was determined using MTT assay, FDA-PI staining, flow cytometric analysis, caspase-3 activity assay, ROS assay and western blot. Our results showed that PR inhibited in cisplatin-induced apoptosis and ROS production in ECV304 cells. Moreover, PR reduced ERK, p38 and JNK activation that increased in cisplatin-treated rat mesangial cell. Furthermore, activation of p53 by cisplatin in rat mesangial cell was inhibited by PR treatment. These results suggest that protective effect of PR on cisplatin-induced apoptosis in rat mesangial cell may be associated with reduction of ERK, p38, JNK, p53 activation.

Keywords

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