α-Mangostin protects against high-glucose induced apoptosis of human umbilical vein endothelial cells

Luo, Yanli; Lei, Minxiang

doi:10.1042/bsr20170779

Cited by 18 publications

(24 citation statements)

References 44 publications

(45 reference statements)

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“…Importantly, supplementation of α-MG partially maintained the balance between Bax and Bcl-2, resulting in the prevention of mitochondrial dysfunction caused by APAP. In fact, our results were supported by a recent reports by Luo et al, who reported that α-MG exerted anti-apoptotic effects on high-glucose-induced vascular endothelial cell dysfunction via upregulation of Bcl-2 and downregulation of Bax protein expression [ 40 ].…”

Section: Discussionsupporting

confidence: 90%

Dietary α-Mangostin Provides Protective Effects against Acetaminophen-Induced Hepatotoxicity in Mice via Akt/mTOR-Mediated Inhibition of Autophagy and Apoptosis

Yan

Sun

Ren

et al. 2018

IJMS

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Acetaminophen overdose-induced hepatotoxicity is the most common cause of acute liver failure in many countries. Previously, alpha-mangostin (α-MG) has been confirmed to exert protective effects on a variety of liver injuries, but the protective effect on acetaminophen-induced acute liver injury (ALI) remains largely unknown. This work investigated the regulatory effect and underlying cellular mechanisms of α-MG action to attenuate acetaminophen-induced hepatotoxicity in mice. The increased serum aminotransferase levels and glutathione (GSH) content and reduced malondialdehyde (MDA) demonstrated the protective effect of α-MG against acetaminophen-induced hepatotoxicity. In addition, α-MG pretreatment inhibited increases in tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β) caused by exposure of mice to acetaminophen. In liver tissues, α-MG inhibited the protein expression of autophagy-related microtubule-associated protein light chain 3 (LC3) and BCL2/adenovirus E1B protein-interacting protein 3 (BNIP3). Western blotting analysis of liver tissues also proved evidence that α-MG partially inhibited the activation of apoptotic signaling pathways via increasing the expression of Bcl-2 and decreasing Bax and cleaved caspase 3 proteins. In addition, α-MG could in part downregulate the increase in p62 level and upregulate the decrease in p-mTOR, p-AKT and LC3 II /LC3 I ratio in autophagy signaling pathways in the mouse liver. Taken together, our findings proved novel perspectives that detoxification effect of α-MG on acetaminophen-induced ALI might be due to the alterations in Akt/mTOR pathway in the liver.

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Section: Discussionsupporting

confidence: 90%

Dietary α-Mangostin Provides Protective Effects against Acetaminophen-Induced Hepatotoxicity in Mice via Akt/mTOR-Mediated Inhibition of Autophagy and Apoptosis

Yan

Sun

Ren

et al. 2018

IJMS

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“…After that, we detected the aSMase activity, ceramide content, eNOS expression, NO production and vascular function. Desipramine is able to inhibit aSMase activity and ceramide accumulation 8,23‐25 . Here, we used desipramine as an aSMase inhibitor control in this study.…”

Section: Methodsmentioning

confidence: 99%

Alpha‐mangostin improves endothelial dysfunction in db/db mice through inhibition of aSMase/ceramide pathway

Jiang

Huang

Liu

et al. 2021

J Cellular Molecular Medi

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Diabetic vascular complications are the leading causes of death and disability in patients with diabetes. Alpha‐mangostin has been reported to have anti‐diabetic capacity in recent years. Here, we investigated the protective function of alpha‐mangostin on endothelium in vitro and in vivo experiments. We also observed that alpha‐mangostin improved impaired endothelium‐dependent vasodilation (EDV) of diabetic animals while it limited the aSMase/ceramide pathway and up‐regulated eNOS/NO pathway in aortas from diabetic mice. Meanwhile, alpha‐mangostin inhibited elevated aSMase/ceramide pathway and reversed impaired EDV induced by high glucose in isolated mouse aortas. In addition, alpha‐mangostin increased phosphorylation of eNOS and NO production in high glucose‐treated aortas. Alpha‐mangostin normalized high glucose‐induced activation of aSMase/ceramide pathway and improved eNOS/NO pathway in endothelial cells with high glucose. In conclusion, alpha‐mangostin regulates eNOS/NO pathway and improves EDV in aortas of diabetic mice through inhibiting aSMase activity and endogenous ceramide accumulation.

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“…The cells were seeded in a six-well plate and received different treatments, such as NC (normal control, 5 mM D-glucose), HG (high glucose, 25 mM D-glucose), LG (L-glucose, 25 mM L-glucose + 5 mM D-glucose), DES (desipramine, 10 μM). The desipramine concentrations used were based on our previous study [14].…”

Section: Methodsmentioning

confidence: 99%

Inhibition of acid sphingomyelinase activity ameliorates endothelial dysfunction in db/db mice

et al. 2019

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Acid sphingomyelinase (aSMase) plays an important role in endothelial dysfunction. Here, we show that elevated aSMase activity and ceramide content were reduced by desipramine treatment in diabetic animals. The inhibitor of aSMase, desipramine, improved vascular dysfunction in db/db mice. High glucose (HG)-induced up-regulation of aSMase activity and ceramide levels were restored by treatment with aSMase siRNA or desipramine in endothelial cells. In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG. These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.

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α-Mangostin protects against high-glucose induced apoptosis of human umbilical vein endothelial cells

Cited by 18 publications

References 44 publications

Dietary α-Mangostin Provides Protective Effects against Acetaminophen-Induced Hepatotoxicity in Mice via Akt/mTOR-Mediated Inhibition of Autophagy and Apoptosis

Dietary α-Mangostin Provides Protective Effects against Acetaminophen-Induced Hepatotoxicity in Mice via Akt/mTOR-Mediated Inhibition of Autophagy and Apoptosis

Alpha‐mangostin improves endothelial dysfunction in db/db mice through inhibition of aSMase/ceramide pathway

Inhibition of acid sphingomyelinase activity ameliorates endothelial dysfunction in db/db mice

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