Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress

Coptisine is the major bioactive protoberberine alkaloid found in <i>Rhizoma Coptidis.</i> Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including...

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Main Authors: Yan Zhou, Chunxiu Zhou, Xutao Zhang, Chi Teng Vong, Yitao Wang, Wai San Cheang
Format: Article
Language:English
Published: MDPI AG 2021-07-01
Series:Molecules
Subjects:
Online Access:https://www.mdpi.com/1420-3049/26/14/4210
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author Yan Zhou
Chunxiu Zhou
Xutao Zhang
Chi Teng Vong
Yitao Wang
Wai San Cheang
author_facet Yan Zhou
Chunxiu Zhou
Xutao Zhang
Chi Teng Vong
Yitao Wang
Wai San Cheang
author_sort Yan Zhou
collection DOAJ
description Coptisine is the major bioactive protoberberine alkaloid found in <i>Rhizoma Coptidis.</i> Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for <i>ex vivo</i> treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.
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spelling doaj.art-77f37b1a70be47658576a234f5e3b6252023-11-22T04:30:16ZengMDPI AGMolecules1420-30492021-07-012614421010.3390/molecules26144210Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative StressYan Zhou0Chunxiu Zhou1Xutao Zhang2Chi Teng Vong3Yitao Wang4Wai San Cheang5State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR 999078, ChinaState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR 999078, ChinaState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR 999078, ChinaState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR 999078, ChinaState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR 999078, ChinaState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR 999078, ChinaCoptisine is the major bioactive protoberberine alkaloid found in <i>Rhizoma Coptidis.</i> Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for <i>ex vivo</i> treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.https://www.mdpi.com/1420-3049/26/14/4210coptisinediabetesendoplasmic reticulum stressendothelial dysfunctionoxidative stress
spellingShingle Yan Zhou
Chunxiu Zhou
Xutao Zhang
Chi Teng Vong
Yitao Wang
Wai San Cheang
Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress
Molecules
coptisine
diabetes
endoplasmic reticulum stress
endothelial dysfunction
oxidative stress
title Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress
title_full Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress
title_fullStr Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress
title_full_unstemmed Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress
title_short Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress
title_sort coptisine attenuates diabetes associated endothelial dysfunction through inhibition of endoplasmic reticulum stress and oxidative stress
topic coptisine
diabetes
endoplasmic reticulum stress
endothelial dysfunction
oxidative stress
url https://www.mdpi.com/1420-3049/26/14/4210
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AT yitaowang coptisineattenuatesdiabetesassociatedendothelialdysfunctionthroughinhibitionofendoplasmicreticulumstressandoxidativestress
AT waisancheang coptisineattenuatesdiabetesassociatedendothelialdysfunctionthroughinhibitionofendoplasmicreticulumstressandoxidativestress