Yi Tao1,
Bing Zhou2,
Jie Zou1,
Yixian Yu3,
Jing Zhao1,
Naijia Xu1,
Qiong Wang1 
1Department of Endocrinology, Wuhan Hospital of Traditional Chinese Medicinal, Wuhan, China;
2Department of Acupuncture, Wuhan Hospital of Traditional Chinese Medicinal, Wuhan, China;
3Department of Neurology, Wuhan Hospital of Traditional Chinese Medicinal, Wuhan, China.
For correspondence:- Qiong Wang
Email: heyk@crceg-na.com Tel:+8618672992705
Accepted: 18 January 2022
Published: 28 February 2021
Citation:
Tao Y, Zhou B, Zou J, Yu Y, Zhao J, Xu N, et al.
Nicorandil alleviates inflammation and oxidation in diabetic cardiomyopathy. Trop J Pharm Res 2022; 21(2):273-279
doi:
10.4314/tjpr.v21i2.9
© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Abstract
Purpose: To examine the effect of nicorandil on high glucose-induced cardiomyocyte inflammation and oxidative stress.
Methods: H9C2 cardiomyocytes were divided into control group, high glucose group and nicorandil group. The survival rate of cardiomyocytes was determined using the CCK-8 method. The contents of reactive oxygen species (ROS) of cardiomyocytes were determined by flow cytometry. The contents of MDA and LDH in cell supernatant were determined by kit. Western blot and real-time PCR were used to assess oxidative stress, inflammation and apoptosis related factors in each group of cardiomyocytes. The expression levels of IL-1β were determined by immunofluorescence. Tunnel staining was used to determine the apoptosis level of each group.
Results: The expressions of SOD1 and SOD2 in the high glucose group were significantly decreased (p < 0.05). Also, the contents of MDA and LDH were significantly increased (p < 0.05). Furthermore, IL-1β, TNF-α, caspase 3 and Bax expressions were increased, while Bcl-2 expression was inhibited. IL-1β and Tunnel fluorescence also increased significantly. NF-κB and Ikkα were significantly increased, while IκB-α was inhibited. Furthermore, nicorandil inhibited oxidative stress and apoptosis, as well as NF-κB pathway and downstream factor Ikkα.
Conclusion: Nicorandil ameliorates the inflammation and oxidative damage of cardiomyocytes induced by high glucose, by inhibiting NF-κB pathway, thereby lowering apoptosis. Thus, the findings provide new insight into the development of new agents for the treatment of diabetic cardiomyopathy.
Keywords: Diabetic cardiomyopathy, H9C2, Oxidative Stress, Inflammatory, Nuclear Factor-κB
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