Open Access

Anthocyanins inhibit high glucose-induced renal tubular cell apoptosis caused by oxidative stress in db/db mice

  • Authors:
    • Jinying Wei
    • Haijiang Wu
    • Haiqiang Zhang
    • Fang Li
    • Shurui Chen
    • Baohua Hou
    • Yonghong Shi
    • Lijuan Zhao
    • Huijun Duan
  • View Affiliations

  • Published online on: January 10, 2018     https://doi.org/10.3892/ijmm.2018.3378
  • Pages: 1608-1618
  • Copyright: © Wei et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Oxidative stress is an important contributory factor resulting the development of kidney injury in patients with diabetes. Numerous in vitro and in vivo studies have suggested that anthocyanins, natural phenols commonly existing in numerous fruits and vegetables, exhibit important antioxidative, anti‑inflammatory and antihyperlipidemic effects; however, their effects and underlying mechanisms on diabetic nephropathy (DN) have not yet been fully determined. In the present study, the regulation of apoptosis metabolism and antioxidative effects exhibited by anthocyanins [grape seed procyanidin (GSPE) and cyanidin‑3‑O‑β‑glucoside chloride (C3G)] were investigated, and the molecular mechanism underlying this process was investigated in vivo and in vitro. GSPE administration was revealed to suppress renal cell apoptosis, as well as suppress the expression of Bcl‑2 in diabetic mouse kidneys. Furthermore, GSPE administration was demonstrated to suppress the expression of thioredoxin interacting protein (TXNIP), in addition to enhancing p38 mitogen‑activation protein kinase (MAPK) and extracellular signal‑regulated kinase 1/2 (ERK1/2) oxidase activity in diabetic mouse kidneys. In vitro experiments using HK‑2 cells revealed that C3G suppressed the generation of HG‑mediated reactive oxygen species, cellular apoptosis, the expression of cleaved caspase‑3 and the Bax/Bcl‑2 ratio; and enhanced the expression of cytochrome c released from mitochondria. Furthermore, treatment with C3G was revealed to suppress the expression of TXNIP, in addition to the phosphorylation of p38 MAPK and ERK1/2 oxidase activity in HK‑2 cells under HG conditions. In addition, treatment with C3G was revealed to attenuate the HG‑induced suppression of the biological activity of thioredoxin, and to enhance the expression of thioredoxin 2 in HK‑2 cells under HG conditions. In conclusion, the present study demonstrated that anthocyanins may exhibit protective effects against HG‑induced renal injury in DN via antioxidant activity.
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March 2018
Volume 41 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

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APA
Wei, J., Wu, H., Zhang, H., Li, F., Chen, S., Hou, B. ... Duan, H. (2018). Anthocyanins inhibit high glucose-induced renal tubular cell apoptosis caused by oxidative stress in db/db mice. International Journal of Molecular Medicine, 41, 1608-1618. https://doi.org/10.3892/ijmm.2018.3378
MLA
Wei, J., Wu, H., Zhang, H., Li, F., Chen, S., Hou, B., Shi, Y., Zhao, L., Duan, H."Anthocyanins inhibit high glucose-induced renal tubular cell apoptosis caused by oxidative stress in db/db mice". International Journal of Molecular Medicine 41.3 (2018): 1608-1618.
Chicago
Wei, J., Wu, H., Zhang, H., Li, F., Chen, S., Hou, B., Shi, Y., Zhao, L., Duan, H."Anthocyanins inhibit high glucose-induced renal tubular cell apoptosis caused by oxidative stress in db/db mice". International Journal of Molecular Medicine 41, no. 3 (2018): 1608-1618. https://doi.org/10.3892/ijmm.2018.3378