Effect of bioflavonoids quercetin and curcumin on ischemic renal injury - A new class of renoprotective agents

被引:180
作者
Shoskes, DA [1 ]
机构
[1] Univ Calif Los Angeles, Sch Med, Harbor UCLA Med Ctr, Dept Surg,Div Urol, Torrance, CA 90509 USA
关键词
D O I
10.1097/00007890-199807270-00001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background. Nonimmune renal injury plays an important role in acute and chronic rejection by triggering an injury response through cytokine and chemokine release. Bioflavonoids are agents with potential immunosuppressive and renoprotective properties. We studied the effects of quercetin and curcumin, two bioflavonoids, on ischemia-reperfusion in the rat. Methods. Rats underwent 30 min of left renal pedicle occlusion with simultaneous right nephrectomy and were pretreated with quercetin or curcumin, Serial serum creatinine was measured, and renal expression of the chemokines regulated upon activation, normal T-cell expressed and secreted (RANTES), monocyte chemoattractant protein-1 (MCP-1), and allograft inflammatory factor (AIF) was quantified by polymerase chain reaction. Results. Pretreatment with quercetin or curcumin resulted in preservation of histological integrity, with a decrease in tubular damage and interstitial inflammation. On day 2 after ischemia-reperfusion, quercetin pretreatment decreased the mean serum creatinine level from 6.5 +/- 1.4 to 3.3 +/- 0.5 mg/dl (P = 0.06). On day 7, the creatinine level for control animals was 7.5 +/- 1.5 mg/dl, which was significantly decreased by pretreatment with quercetin, curcumin, or both together (creatinine levels: 1.6 +/- 1.3, 1.8 +/- 0.2, and 2.0 +/- 0.4 mg/dl, respectively; all P < 0.05 vs. untreated). By semiquantitative polymerase chain reaction, RANTES, MCP-1, and AIF were detected at high levels in kidneys on day 2 but not in normal kidneys. Pretreatment with quercetin or curcumin strongly attenuated this expression. Conclusion. Quercetin and curcumin reduce ischemia-reperfusion injury and its inflammatory sequelae, The bioflavonoids hold promise as agents that can reduce immune and nonimmune renal injury, the key risk factors in chronic graft loss.
引用
收藏
页码:147 / 152
页数:6
相关论文
共 44 条
[31]   A molecular injury-response model for the understanding of chronic disease [J].
Satyanarayana, K ;
Shoskes, DA .
MOLECULAR MEDICINE TODAY, 1997, 3 (08) :331-334
[32]   Intragraft TGF-beta(1) mRNA: A correlate of interstitial fibrosis and chronic allograft nephropathy [J].
Sharma, VK ;
Bologa, RM ;
Xu, GP ;
Li, BG ;
Mouradian, J ;
Wang, J ;
Serur, D ;
Rao, V ;
Suthanthiran, M .
KIDNEY INTERNATIONAL, 1996, 49 (05) :1297-1303
[33]  
SHOSKES DA, 1990, TRANSPLANTATION, V50, P877
[34]   Delayed graft function in renal transplantation: Etiology, management and long-term significance [J].
Shoskes, DA ;
Halloran, PF .
JOURNAL OF UROLOGY, 1996, 155 (06) :1831-1840
[35]   INCREASED MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGEN EXPRESSION IN UNILATERAL ISCHEMIC ACUTE TUBULAR-NECROSIS IN THE MOUSE [J].
SHOSKES, DA ;
PARFREY, NA ;
HALLORAN, PF .
TRANSPLANTATION, 1990, 49 (01) :201-207
[36]   Nitric oxide synthase activity in renal ischemia-reperfusion injury in the rat - Implications for renal transplantation [J].
Shoskes, DA ;
Xi, YN ;
GonzalezCadavid, NF .
TRANSPLANTATION, 1997, 63 (04) :495-500
[37]   ACTIVATION OF TRANSCRIPTION FACTOR NF-KAPPA-B IS SUPPRESSED BY CURCUMIN (DIFERULOLYLMETHANE) [J].
SINGH, S ;
AGGARWAL, BB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (42) :24995-25000
[38]   QUERCETIN DOWN-REGULATES SIGNAL BREAST-CARCINOMA TRANSDUCTION IN HUMAN-CELLS [J].
SINGHAL, RL ;
YEH, YA ;
PRAJDA, N ;
OLAH, E ;
SLEDGE, GW ;
WEBER, G .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 208 (01) :425-431
[39]  
Soudamini K. K., 1992, Indian Journal of Physiology and Pharmacology, V36, P239
[40]  
SREEJAYAN N, 1994, J PHARM PHARMACOL, V46, P1013