Celastrol attenuates angiotensin II mediated human umbilical vein endothelial cells damage through activation of Nrf2/ERK1/2/Nox2 signal pathway

Li, Miao; Liu, Xin; He, Yongpeng; Zheng, Qingyin; Wang, Min; Wu, Yu; Zhang, Yuanpeng; Wang, Chaoyun

doi:10.1016/j.ejphar.2017.01.027

Cited by 47 publications

(34 citation statements)

References 52 publications

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“…Celastrol is the main active ingredient of Tripterygium wilfordii Hook. f [82]. Liu et al [53] administered Celastrol (100 μ g/kg) intraperitoneally for three weeks to HFD-induced obese mice and found that Celastrol suppressed food intake, improved energy expenditure, and leads up to 45% weight loss in hyperleptinemic diet-induced obese mice by increasing leptin sensitivity.…”

Section: Resultsmentioning

confidence: 99%

Herbal Medicine for the Treatment of Obesity: An Overview of Scientific Evidence from 2007 to 2017

Liu

Sun

Yao

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Obesity is a very common global health problem, and it is known to be linked to cardiovascular and cerebrovascular diseases. Western medical treatments for obesity have many drawbacks, including effects on monoamine neurotransmitters and the potential for drug abuse and dependency. The safety of these medications requires improvement. Herbal medicine has been used for treatment of disease for more than 2000 years, and it has proven efficacy. Many studies have confirmed that herbal medicine is effective in the treatment of obesity, but the mechanisms are not clear. This article will discuss the possible effects and mechanisms of herbal medicine treatments for obesity that have been reported in the past decade.

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Section: Resultsmentioning

confidence: 99%

Herbal Medicine for the Treatment of Obesity: An Overview of Scientific Evidence from 2007 to 2017

Liu

Sun

Yao

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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“…Human studies indicated that mean plasma Ang II levels were 18.4 ± 3.3 p M in healthy humans by ESI-LC-MS/MS assay [35]. Li et al [36] demonstrated that 400 nmol/L of Ang II induced HUVEC apoptosis via the Nrf2/ERK1/2/Nox2 pathway. In our study, the data indicated that Ang II significantly decreased endogenous antioxidant enzyme activity, induced mitochondrial dysfunction, elevated NOX activity, and induced ROS generation, eventually enhancing the apoptosis of HUVECs.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

et al. 2017

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Introduction: This study aimed to investigate whether epigallocatechin-3-gallate (EGCG) shows antioxidant activity against angiotensin II (Ang II)-induced human umbilical vein endothelial cell (HUVEC) apoptosis. Materials and Methods: The viability of HUVECs was revealed by MTT and LDH assay. The cell apoptosis was detected by FITC-PI assay. A fluorescent probe assay was used to measure the reactive oxygen species (ROS) generation in HUVECs. Mitochondrial permeability transition pore (MPTP) opening, mitochondrial membrane potential, and caspase-3, -4, -8, -9 activities were also measured. Results: We found that Ang II treatment increased the generation of ROS, enhanced MPTP opening and cytochrome c release, activated caspase-3/9, and consequently induced HUVEC apoptosis. EGCG treatment-suppressed Ang II induces the oxidative stress of HUVECs and mitochondria-related cell apoptosis. We also showed that the antioxidant activity pathway, including cytochrome c release, MPTP opening, and caspase-3/9 activation, is a key endogenous defensive system in HUVECs, provoking Ang II exposure. Our study revealed that increased expression of Nrf2 by EGCG could partially repress Ang II-induced injury effects. Conclusions: All of our findings indicated that EGCG treatment provides a protective effect for Ang II-induced HUVEC apoptosis by decreasing oxidative stress and ameliorating mitochondrial injury.

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“…The concentration of protein carbonyl was calculated using a commercially available enzyme-linked immunosorbent assay (ELISA) kit (Cell Biolabs, San Diego, CA, USA) [26]. …”

Section: Methodsmentioning

confidence: 99%

“…The levels of TNF-α and IL-8 were analyzed using sandwich ELISA kits (Abcam) following the manufacturer’s protocols [26]. …”

Section: Methodsmentioning

confidence: 99%

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

et al. 2019

J Vasc Res

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Vitamin D has an important protective effect on chronic inflammatory disease. Angiotensin II (AngII) triggers vascular damage and plays a key role in vascular diseases via several mechanisms, including inflammation. Conversely, vitamin D has been shown to have an important protective effect on chronic inflammation. There is evidence showing that vitamin D can reverse the effects of AngII, but the molecular mechanisms by which this occurs are not known. Our results demonstrate that vitamin D improved the viability, migration ability, and tube formation of AngII-pretreated endothelial progenitor cells (EPCs) and inhibited the apoptosis of EPCs induced by AngII. Vitamin D also reversed reactive oxygen species production, vascular inflammatory cytokine generation, and nuclear factor kappa-B activation in EPCs induced by AngII. Furthermore, EPC pretreatment with GW9662 (the antagonist for PPAR-γ) or siHO-1 decreased the protective effect of vitamin D on AngII-induced EPC injury. Overall, our data indicate that vitamin D ameliorated AngII-induced abnormal EPC injury by decreasing oxidative stress and inflammatory cytokine levels. These findings also suggest that vitamin D protected EPCs from AngII-induced vascular injury via the activation of the PPAR-γ/HO-1 signaling pathway.

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Celastrol attenuates angiotensin II mediated human umbilical vein endothelial cells damage through activation of Nrf2/ERK1/2/Nox2 signal pathway

Cited by 47 publications

References 52 publications

Herbal Medicine for the Treatment of Obesity: An Overview of Scientific Evidence from 2007 to 2017

Herbal Medicine for the Treatment of Obesity: An Overview of Scientific Evidence from 2007 to 2017

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

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