Resveratrol alleviate hypoxic pulmonary hypertension via anti-inflammation and anti-oxidant pathways in rats

Xu, Dan; Li, Yan; Zhang, Bo; Wang, Yanxia; Liu, Yi; Luo, Ying; Niu, Wen; Dong, Minyue; Liu, Manling; Dong, Huijuan; Zhao, Peng; Li, Zhichao

doi:10.7150/ijms.16810

Cited by 90 publications

(67 citation statements)

References 43 publications

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“…The inhibitory effect of resveratrol on arginase II was PI3K-Akt signaling pathway-dependent [99]. Similar results were found in rat PASMC [100], in hypoxic pulmonary hypertension rats [101], and in monocrotaline-induced PAH [102].…”

Section: Flavonoids and Other Polyphenolssupporting

confidence: 81%

Impact of Nutrition on Pulmonary Arterial Hypertension

et al. 2020

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Pulmonary arterial hypertension (PAH) is characterized by sustained vasoconstriction, vascular remodeling, inflammation, and in situ thrombosis. Although there have been important advances in the knowledge of the pathophysiology of PAH, it remains a debilitating, limiting, and rapidly progressive disease. Vitamin D and iron deficiency are worldwide health problems of pandemic proportions. Notably, these nutritional alterations are largely more prevalent in PAH patients than in the general population and there are several pieces of evidence suggesting that they may trigger or aggravate disease progression. There are also several case reports associating scurvy, due to severe vitamin C deficiency, with PAH. Flavonoids such as quercetin, isoflavonoids such as genistein, and other dietary polyphenols including resveratrol slow the progression of the disease in animal models of PAH. Finally, the role of the gut microbiota and its interplay with the diet, host immune system, and energy metabolism is emerging in multiple cardiovascular diseases. The alteration of the gut microbiota has also been reported in animal models of PAH. It is thus possible that in the near future interventions targeting the nutritional status and the gut dysbiosis will improve the outcome of these patients.

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Section: Flavonoids and Other Polyphenolssupporting

confidence: 81%

Impact of Nutrition on Pulmonary Arterial Hypertension

et al. 2020

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“…Decreased apoptosis and increased autophagy Rat H9c2 cardiomyoblasts [94] questionable. However, resveratrol has been implicated as a cardioprotective drug for many cardiovascular diseases both in preclinical studies [121] and in man [122], and this is thought to be largely due to its anti-inflammatory and anti-oxidant action [123]. Of specific interest for the topic of this review, resveratrol has been shown to lead to activation of AMPK and to reduce cardiac fibrosis and hypertrophy in a mouse model of pressure overload by transverse aortic constriction [124].…”

Section: Resveratrolmentioning

confidence: 99%

The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity

Timm

Tyler

2020

Cardiovasc Drugs Ther

129

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Doxorubicin is a commonly used chemotherapeutic agent for the treatment of a range of cancers, but despite its success in improving cancer survival rates, doxorubicin is cardiotoxic and can lead to congestive heart failure. Therapeutic options for this patient group are limited to standard heart failure medications with the only drug specific for doxorubicin cardiotoxicity to reach FDA approval being dexrazoxane, an iron-chelating agent targeting oxidative stress. However, dexrazoxane has failed to live up to its expectations from preclinical studies while also bringing up concerns about its safety. Despite decades of research, the molecular mechanisms of doxorubicin cardiotoxicity are still poorly understood and oxidative stress is no longer considered to be the sole evil. Mitochondrial impairment, increased apoptosis, dysregulated autophagy and increased fibrosis have also been shown to be crucial players in doxorubicin cardiotoxicity. These cellular processes are all linked by one highly conserved intracellular kinase: adenosine monophosphate-activated protein kinase (AMPK). AMPK regulates mitochondrial biogenesis via PGC1α signalling, increases oxidative mitochondrial metabolism, decreases apoptosis through inhibition of mTOR signalling, increases autophagy through ULK1 and decreases fibrosis through inhibition of TGFβ signalling. AMPK therefore sits at the control point of many mechanisms shown to be involved in doxorubicin cardiotoxicity and cardiac AMPK signalling itself has been shown to be impaired by doxorubicin. In this review, we introduce different agents known to activate AMPK (metformin, statins, resveratrol, thiazolidinediones, AICAR, specific AMPK activators) as well as exercise and dietary restriction, and we discuss the existing evidence for their potential role in cardioprotection from doxorubicin cardiotoxicity.

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“…The resultant product exhibited a distinct thin layer chromatographic signal from the reactants (data not shown). 1 HNMR was utilized to verify the chemical structure of the product. possesses a hydrophilic property, whereas the oleoyl moiety is hydrophobic.…”

Section: Synthesis and Identification Of N-oleoyld-galactosaminementioning

confidence: 99%

“…Resveratrol (RES) is a natural polyphenol which is rich in a variety of plants and fruits, such as grapes, peanut and mulberry. This compound has been shown of possessing multiple pharmacological and healthy benefits, including anti-inflammation/ oxidation, 1 antitumor, 2 and immunoregulation. 3 Currently, the French Paradox, a low incidence of cardiovascular diseases relative to a high saturated fats diet, makes this compound become popular.…”

Section: Introductionmentioning

confidence: 99%

Galactosylated PLGA nanoparticles for the oral delivery of resveratrol: enhanced bioavailability and in vitro anti-inflammatory activity

Siu

Lin

et al. 2018

IJN

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BackgroundResveratrol (RES) is a natural anti-inflammatory and antioxidant compound with poor water solubility and oral bioavailability. The present study takes the advantages of nanocarriers combined with a ligand (galactose) anchoring to orally deliver RES in an attempt to improve its bioavailability and pharmacological activity.MethodsRES-loaded galactosylated nanoparticles (RES-GNPs) were prepared by solvent diffusion technique using poly(lactic-co-glycolic acid), synthesized N-oleoyl-d-galactosamine and Tween 80. RES-GNPs were characterized by particle size, morphology, entrapment efficiency (EE) and in vitro release. Oral bioavailability and in vitro anti-inflammatory activity were investigated in rats and lipopolysaccharides-induced RAW 264.7 cells, respectively.ResultsThe resulting RES-GNPs were 108.4 nm around in particle size with a polydispersity index of 0.217. Furthermore, RES-GNPs possessed a high EE and a slow drug release in water. After oral administration, RES-GNPs significantly enhanced the oral bioavailability of RES, up to 335.7% relative to RES suspensions. In situ single-pass intestinal perfusion and cellular uptake experiments showed that GNPs could improve the intestinal permeability and transcellular transport of RES. Moreover, the anti-inflammatory efficacy of RES-GNPs in RAW 264.7 cells model was superior to free RES and RES-GNPs.ConclusionThe results indicate that RES-GNPs can effectively promote the intestinal absorption of RES and strengthen its bioactivity, which may be a promising system for the treatment of inflammatory diseases.

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Resveratrol alleviate hypoxic pulmonary hypertension via anti-inflammation and anti-oxidant pathways in rats

Cited by 90 publications

References 43 publications

Impact of Nutrition on Pulmonary Arterial Hypertension

Impact of Nutrition on Pulmonary Arterial Hypertension

The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity

Galactosylated PLGA nanoparticles for the oral delivery of resveratrol: enhanced bioavailability and in vitro anti-inflammatory activity

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