Niclosamide ethanolamine inhibits artery constriction

Li, Shanliang; Yan, Jie; Zhang, Yanqiu; Zhen, Chang-Lin; Li, Mingyu; Jin, Jing; Gao, Jin-Lai; Xiao, Xiaolin; Shen, Xin; Tai, Yu Tzu; Hu, Nan; Zhang, Xinzi; Sun, Zeyu; Dong, De-Li

doi:10.1016/j.phrs.2016.11.008

Cited by 34 publications

(41 citation statements)

References 26 publications

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“…AMPK is involved in pathogenesis of neointimal hyperplasia and restenosis (Igata et al, ; Nagata et al, ; Song et al, ). Niclosamide (2 μM) induced AMPK activation (Figure A), in line with our previous finding that niclosamide ethanolamine (a salt of niclosamide) induced AMPK activation in A10 cells (Li et al, ). We further checked the effects of niclosamide on the expression of β‐catenin and the activities of ERK1/2 and Akt, signalling pathways known to be involved in smooth muscle cell proliferation and migration.…”

Section: Resultssupporting

confidence: 92%

“…Mitochondrial uncouplers have been reported to reverse hypertriglyceridemia, fatty liver disease, insulin resistance and diabetes (Fu et al, ; Perry et al, ; Perry et al, ; Tao et al, ) and protect against heart and renal ischaemic injury (Brennan et al, ; Kenwood et al, ). We previously found that mitochondrial uncouplers relaxed the constricted arteries through a mechanism involving AMPK activation (Li et al, ; Zhang et al, ; Zhang et al, ). However, the effects of chemical mitochondrial uncouplers on VSMC proliferation and migration have never been identified.…”

Section: Introductionmentioning

confidence: 97%

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Niclosamide inhibits vascular smooth muscle cell proliferation and migration and attenuates neointimal hyperplasia in injured rat carotid arteries

Xiao

Zhang

et al. 2018

British J Pharmacology

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Section: Resultssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 97%

Niclosamide inhibits vascular smooth muscle cell proliferation and migration and attenuates neointimal hyperplasia in injured rat carotid arteries

Xiao

Zhang

et al. 2018

British J Pharmacology

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“…Due to its mitochondrial uncoupling activity, niclosamide ethanolamine reduced the cellular ATP/ADP ratio in vascular smooth muscle cells and activated AMP-activated protein kinase (AMPK) activity in smooth muscle cells and rat thoracic aorta. Niclosamide ethanolamine treatment increased cytosolic [Ca 2 + ] i and depolarized mitochondrial membranes in vascular smooth muscle cells [82] . These results suggest that niclosamide has potential as an anti-hypertensive drug.…”

Section: Niclosamide and Artery Constrictionmentioning

confidence: 93%

Niclosamide: Beyond an antihelminthic drug

Chen

Mook

Premont

et al. 2018

Cellular Signalling

362

258

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Niclosamide is an oral antihelminthic drug used to treat parasitic infections in millions of people worldwide. However recent studies have indicated that niclosamide may have broad clinical applications for the treatment of diseases other than those caused by parasites. These diseases and symptoms may include cancer, bacterial and viral infection, metabolic diseases such as Type II diabetes, NASH and NAFLD, artery constriction, endometriosis, neuropathic pain, rheumatoid arthritis, sclerodermatous graft-versus-host disease, and systemic sclerosis. Among the underlying mechanisms associated with the drug actions of niclosamide are uncoupling of oxidative phosphorylation, and modulation of Wnt/β-catenin, mTORC1, STAT3, NF-κB and Notch signaling pathways. Here we provide a brief overview of the biological activities of niclosamide, its potential clinical applications, and its challenges for use as a new therapy for systemic diseases.

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“…The experiments were carried out according to our previous works [10, 16, 17]. The rats were sacrificed after anesthetized with sodium pentobarbitone.…”

Section: Methodsmentioning

confidence: 99%

Mitochondrial Fission Inhibitors Suppress Endothelin-1-Induced Artery Constriction

Chen¹,

Gao²,

Li³

et al. 2017

Cell Physiol Biochem

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558

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Background/Aims: Endothelin-1 is implicated in the pathogenesis of hypertension, but the underlying mechanisms remained elusive. Our previous study found that inhibition of mitochondrial fission of smooth muscle cells suppressed phenylephrine- and high K⁺-induced artery constriction. Here, we studied the effects of mitochondrial fission inhibitors on endothelin-1-induced vasoconstriction. Methods: The tension of rat mesenteric arteries and thoracic aorta was measured by using a multi-wire myograph system. Mitochondrial morphology of aortic smooth muscle cells was observed by using transmission electron microscopy. Results: Dynamin-related protein-1 selective inhibitor mdivi-1 relaxed endothelin-1-induced constriction, and mdivi-1 pre-treatment prevented endothelin-1-induced constriction of rat mesenteric arteries with intact and denuded endothelium. Mdivi-1 had a similar inhibitory effect on rat thoracic aorta. Another mitochondrial fission inhibitor dynasore showed similar effects as mdivi-1 in rat mesenteric arteries. Mdivi-1 inhibited endothelin-1-induced increase of mitochondrial fission in smooth muscle cells of rat aorta. Rho-associated protein kinase inhibitor Y-27632 which relaxed endothelin-1-induced vasoconstriction inhibited endothelin-1-induced mitochondrial fission in smooth muscle cells of rat aorta. Conclusion: Endothelin-1 increases mitochondrial fission in vascular smooth muscle cells, and mitochondrial fission inhibitors suppress endothelin-1-induced vasoconstriction.

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Niclosamide ethanolamine inhibits artery constriction

Cited by 34 publications

References 26 publications

Niclosamide inhibits vascular smooth muscle cell proliferation and migration and attenuates neointimal hyperplasia in injured rat carotid arteries

Niclosamide inhibits vascular smooth muscle cell proliferation and migration and attenuates neointimal hyperplasia in injured rat carotid arteries

Niclosamide: Beyond an antihelminthic drug

Mitochondrial Fission Inhibitors Suppress Endothelin-1-Induced Artery Constriction

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