Planta Med 2012; 78(16): 1757-1760
DOI: 10.1055/s-0032-1315257
Letters
Georg Thieme Verlag KG Stuttgart · New York

The In Vitro Protective Effects of Curcumin and Demethoxycurcumin in Curcuma longa Extract on Advanced Glycation End Products-Induced Mesangial Cell Apoptosis and Oxidative Stress

Authors

  • Ji-ping Liu

    1   Department of Pharmacology, Shaanxi University of Chinese Medicine, Xianyang, P. R. China
  • Liang Feng

    2   Key Laboratory of New Drug Delivery System of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Nanjing, P. R. China
  • Mao-mao Zhu

    2   Key Laboratory of New Drug Delivery System of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Nanjing, P. R. China
  • Ru-Shang Wang

    2   Key Laboratory of New Drug Delivery System of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Nanjing, P. R. China
  • Ming-hua Zhang

    2   Key Laboratory of New Drug Delivery System of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Nanjing, P. R. China
  • Shao-ying Hu

    2   Key Laboratory of New Drug Delivery System of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Nanjing, P. R. China
  • Xiao-bin Jia

    2   Key Laboratory of New Drug Delivery System of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Nanjing, P. R. China
  • Jin-Jie Wu

    3   Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Jiangsu Nanjing, P. R. China
Further Information

Publication History

received 26 February 2012
revised 24 July 2012

accepted 26 July 2012

Publication Date:
24 August 2012 (online)

Preview

Abstract

Curcuma longa L. (CLL), a traditional herbal medicine, has been widely used for the prevention of diabetic vascular complications in recent years. However, the protective effects of curcuminoids in CLL on the AGEs-induced damage to mesangial cell are not fully understood. In this present study, dihydroethidium, superoxide dismutase kit, malondialdehyde kit, and acridine orange/ethidium bromide staining methods were used to evaluate the activities of curcumin and demethoxycurcumin (10−11 − 10−9 M) on AGEs-induced oxidative stress and apoptosis, which were associated with the damage to mesangial cell. The results showed that these two compounds could significantly restore advanced glycation end products (AGEs)-induced apoptosis to normal levels (IC50 = 3.874 × 10−11 M for curcumin and IC50 = 6.085 × 10−11 M for demethoxycurcumin) and reduce remarkably reactive oxygen species generation in mesangial cell. Furthermore, curcumin and demethoxycurcumin dramatically elevated AGEs-decreased superoxide dismutase activity while significantly reducing AGEs-increased malondialdehyde content in cell culture supernatant. Our results suggest that both curcumin and demethoxycurcumin have a significant protective potential to the prevention of diabetic nephropathy.

Supporting Information

 
  • References

  • 1 Menini S, Iacobini C, Ricci C, Oddi G, Pesce C, Pugliese F, Block K, Abboud HE, Giorgio M, Migliaccio E, Pelicci PG, Pugliese G. Ablation of the gene encoding p 66Shc protects mice against AGE-induced glomerulopathy by preventing oxidant-dependent tissue injury and further AGE accumulation. Diabetologia 2007; 50: 1997-2007
  • 2 Yamagishi S, Matsui T. Advanced glycation end products, oxidative stress and diabetic nephropathy. Oxid Med Cell Longev 2010; 3: 101-108
  • 3 Kim KM, Kim YS, Jung DH, Lee J, Kim JS. Increased glyoxalase I levels inhibit accumulation of oxidative stress and an advanced glycation end product in mouse mesangial cells cultured in high glucose. Exp Cell Res 2012; 318: 152-159
  • 4 Liang YJ, Jian JH, Liu YC, Juang SJ, Shyu KG, Lai LP, Wang BW, Leu JG. Advanced glycation end products-induced apoptosis attenuated by PPARdelta activation and epigallocatechin gallate through NF-kappaB pathway in human embryonic kidney cells and human mesangial cells. Diabetes Metab Res Rev 2010; 26: 406-416
  • 5 Pharmacopoeia Commission of PRC. Pharmacopoeia of the Peopleʼs Republic of China, Volume 1. Beijing: China Medical Science Press; 2010. 247.
  • 6 Takahashi M, Inafuku K, Miyagi T, Oku H, Wada K, Imura T, Kitamoto D. Efficient preparation of liposomes encapsulating food materials using lecithins by a mechanochemical method. J Oleo Sci 2006; 56: 35-42
  • 7 Cheng J, Weijun K, Yun L, Jiabo W, Haitao W, Qingmiao L, Xiaohe X. Development and validation of UPLC method for quality control of Curcuma longa L.: Fast simultaneous quantitation of three curcuminoids. J Pharm Biomed Anal 2010; 53: 43-49
  • 8 Yang FQ, Wang YT, Li SP. Simultaneous determination of 11 characteristic components in three species of Curcuma rhizomes using pressurized liquid extraction and high-performance liquid chromatography. J Chromatogr A 2006; 1134: 226-231
  • 9 Qin NY, Yang FQ, Wang YT, Li SP. Quantitative determination of eight components in rhizome (Jianghuang) and tuberous root (Yujin) of Curcuma longa using pressurized liquid extraction and gas chromatography-mass spectrometry. J Pharm Biomed Anal 2007; 43: 486-492
  • 10 Mukherjee S, Roy M, Dey S, Bhattacharya RK. A mechanistic approach for modulation of arsenic toxicity in human lymphocytes by curcumin, an active constituent of medicinal herb Curcuma longa L. J Clin Biochem Nutr 2007; 41: 32-42
  • 11 Haddad M, Sauvain M, Deharo E. Curcuma as a parasiticidal agent: a review. Planta Med 2011; 77: 672-678
  • 12 Adaramoye OA, Anjos RM, Almeida MM, Veras RC, Silvia DF, Oliveira FA, Cavalcante KV, Araújo IG, Oliveira AP, Medeiros IA. Hypotensive and endothelium-independent vasorelaxant effects of methanolic extract from Curcuma longa L. in rats. J Ethnopharmacol 2009; 124: 457-462
  • 13 Sharma S, Kulkarni SK, Chopra K. Curcumin, the active principle of turmeric (Curcuma longa), ameliorates diabetic nephropathy in rats. Clin Exp Pharmacol Physiol 2006; 33: 940-945
  • 14 Arun N, Nalini N. Efficacy of turmeric on blood sugar and polyol pathway in diabetic albino rats. Plant Foods Hum Nutr 2002; 57: 41-52
  • 15 Madkor HR, Mansour SW, Ramadan G. Modulatory effects of garlic, ginger turmeric and their mixture on hyperglycaemia, dyslipidaemia and oxidative stress in streptozotocin-nicotinamide diabetic rats. Br J Nutr 2011; 105: 1210-1217
  • 16 Xiang M, Qian ZY, Zhou CH, Liu J, Li WN. Crocetin inhibits leukocyte adherence to vascular endothelial cells induced by AGEs. J Ethnopharmacol 2006; 107: 25-31
  • 17 Soetikno V, Sari FR, Veeraveedu PT, Thandavarayan RA, Harima M, Sukumaran V, Lakshmanan AP, Suzuki K, Kawachi H, Watanabe K. Curcumin ameliorates macrophage infiltration by inhibiting NF-κB activation and proinflammatory cytokines in streptozotocin induced-diabetic nephropathy. Nutr Metab (Lond) 2011; 8: 35
  • 18 Chiu J, Khan ZA, Farhangkhoee H, Chakrabarti S. Curcumin prevents diabetes-associated abnormalities in the kidneys by inhibiting p 300 and nuclear factor-kappaB. Nutrition 2009; 25: 964-972
  • 19 Soetikno V, Watanabe K, Sari FR, Harima M, Thandavarayan RA, Veeraveedu PT, Arozal W, Sukumaran V, Lakshmanan AP, Arumugam S, Suzuki K. Curcumin attenuates diabetic nephropathy by inhibiting PKC-α and PKC-β1 activity in streptozotocin-induced type I diabetic rats. Mol Nutr Food Res 2011; 55: 1655-1665
  • 20 Lin J, Tang Y, Kang Q, Feng Y, Chen A. Curcumin inhibits advanced glycation end-products (AGEs)-induced gene expression of receptor for AGEs (RAGE) in hepatic stellate cells in vitro by elevating PPARγ activity and attenuating oxidative stress. Br J Pharmacol 2012;
  • 21 Bamba Y, Yun YS, Kunugi A, Inoue H. Compounds isolated from Curcuma aromatica Salisb. inhibit human P450 enzymes. J Nat Med 2011; 65: 583-587
  • 22 Feng L, Xu YH, Wang SS, Au-Yeung W, Zheng ZG, Wang RS, Zhu Q, Xiang P. Preventative effects of 4,4′-diphenylmethane-bis(methyl) carbamate isolated from Cortex Mori on human umbilical vein endothelial cell dysfunction induced by advanced glycation end products. Phytother Res 2012; 26: 412-419
  • 23 Maeda S, Matsui T, Takeuchi M, Yoshida Y, Yamakawa R, Fukami K, Yamagishi S. Pigment epithelium-derived factor (PEDF) inhibits proximal tubular cell injury in early diabetic nephropathy by suppressing advanced glycation end products (AGEs)-receptor (RAGE) axis. Pharmacol Res 2011; 63: 241-248