Open Access

Kuwanon G protects HT22 cells from advanced glycation end product-induced damage

  • Authors:
    • Wen-Jun Gan
    • Chen-Lin Gao
    • Wen-Qian Zhang
    • Jun-Ling Gu
    • Ting-Ting Zhao
    • Heng-Li Guo
    • Hua Zhou
    • Yong Xu
    • Li-Li Yu
    • Li-Fang Li
    • Ding-Kun Gui
    • You-Hua Xu
  • View Affiliations

  • Published online on: February 25, 2021     https://doi.org/10.3892/etm.2021.9869
  • Article Number: 425
  • Copyright: © Gan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The incidence of diabetic encephalopathy is increasing as the population ages. Evidence suggests that formation and accumulation of advanced glycation end products (AGEs) plays a pivotal role in disease progression, but limited research has been carried out in this area. A previous study demonstrated that Kuwanon G (KWG) had significant anti-oxidative stress and anti-inflammatory properties. As AGEs are oxidative products and inflammation is involved in their generation it is hypothesized that KWG may have effects against AGE-induced neuronal damage. In the present study, mouse hippocampal neuronal cell line HT22 was used. KWG was shown to significantly inhibit AGE-induced cell apoptosis in comparison with a control treatment, as determined by both MTT and flow cytometry. Compared with the AGEs group, expression of pro-apoptotic protein Bax was reduced and expression of anti-apoptotic protein Bcl-2 was increased in the AGEs + KWG group. Both intracellular and extracellular levels of acetylcholine and choline acetyltransferase were significantly elevated after KWG administration in comparison with controls whilethe level of acetylcholinesterase decreased. These changes in protein expression were accompanied by increased levels of superoxide dismutase and glutathione peroxidase synthesis and reduced production of malondialdehyde and reactive oxygen species. Intracellular signaling pathway protein levels were determined by western blot and immunocytochemistry. KWG administration was found to prevent AGE-induced changes to the phosphorylation levels of Akt, IκB-α, glycogen synthase kinase 3 (GSK3)-α and β, p38 MAPK and NF-κB p65 suggesting a potential neuroprotective effect of KWG against AGE-induced damage was via the PI3K/Akt/GSK3αβ signaling pathway. The findings of the present study suggest that KWG may be a potential treatment for diabetic encephalopathy.
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May-2021
Volume 21 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Gan W, Gao C, Zhang W, Gu J, Zhao T, Guo H, Zhou H, Xu Y, Yu L, Li L, Li L, et al: Kuwanon G protects HT22 cells from advanced glycation end product-induced damage. Exp Ther Med 21: 425, 2021
APA
Gan, W., Gao, C., Zhang, W., Gu, J., Zhao, T., Guo, H. ... Xu, Y. (2021). Kuwanon G protects HT22 cells from advanced glycation end product-induced damage. Experimental and Therapeutic Medicine, 21, 425. https://doi.org/10.3892/etm.2021.9869
MLA
Gan, W., Gao, C., Zhang, W., Gu, J., Zhao, T., Guo, H., Zhou, H., Xu, Y., Yu, L., Li, L., Gui, D., Xu, Y."Kuwanon G protects HT22 cells from advanced glycation end product-induced damage". Experimental and Therapeutic Medicine 21.5 (2021): 425.
Chicago
Gan, W., Gao, C., Zhang, W., Gu, J., Zhao, T., Guo, H., Zhou, H., Xu, Y., Yu, L., Li, L., Gui, D., Xu, Y."Kuwanon G protects HT22 cells from advanced glycation end product-induced damage". Experimental and Therapeutic Medicine 21, no. 5 (2021): 425. https://doi.org/10.3892/etm.2021.9869