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The Journal of Internal Korean Medicine > Volume 30(1); 2009 > Article
The Journal of Internal Korean Medicine 2009;30(1): 36-50.
地骨皮가 H2O2에 의한 LLC-PK1 세포의 Redox Status 및 NF-κB Signaling에 미치는 영향
최규호, 신현철
대구한의대학교 한의과대학 내과학교실
The Effects of Lycium Chinense Milie on the H2O2-treated LLC-PK1 Cell's Redox Status and NF-κB Signaling
Gyu-ho Choi, Hyeon-cheol Shin
Dept. of Internal Medicine, College of Oriental Medicine, Daegu Haany University
Correspondence  Hyeon-cheol Shin ,Tel: 054-281-0055, Fax: 054-281-7464, Email: ungaeshin@naver.com
  Published online: March 30, 2009.
ABSTRACT
Objectives:
This study was aimed to verify the cytoprotective function, antioxidative effect and inflammation genes inhibitory effects of Lycium chinense Milie. Therefore the generation of superoxide anion radical (O2-), peroxynitrite (ONOO-), nitric oxide (NO) and prostaglandin E2 (PGE2) was investigated in the renal epithelial cells of mouse. Effects of Lycium chinense Milie on the expression of inflammation-related proteins, IKK-α, p-IKK-αβ, p-IκB-α, NF-κB (p50, p65), COX-2 and iNOS, were examined by western blotting.

Methods :
For this study, the fluorescent probes were used, namely dihydrorhodamine 123 (DHR 123), 4,5-diaminofluorescein (DAF-2) and 2',7'-dichlorodihydrofluorescein diacetate (DCFDA). Western blotting was performed using anti-IKK-α, anti-phospho IKK-αβ, anti-phospho IκB-α, anti-NF-κB (p50, p65), anti-COX-2 and anti-iNOS, respectively.

Results:
Lycium chinense Milie reduced H2O2-induced cell death dose-dependently. It inhibited the generation of O2-, ONOO-, NO and PGE2 in the H2O2-treated renal epithelial cells of mouse in vitro. Lycium chinense Milie inhibited the expression of IKK-α, p-IKK-αβ, p-IκB-α, COX-2 and iNOS genes by means of decreasing activation of NF-κB.

Conclusions:
According to above results, Lycium chinense Milie recommended to be applied in treatment for the inflammatory process and inflammation-related diseases.
Key words: Lycium chinense Milie, LLC-PK1 cell, H2O2, ․O2-, ONOO-, NO, PGE2, NF-κB, COX-2, iNOS
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