Ghrelin ameliorates impaired angiogenesis of ischemic myocardium through GHSR1a-mediated AMPK/eNOS signal pathway in diabetic rats

Wang, Li; Chen, Qingwei; Li, Guiqiong; Ke, Danxia

doi:10.1016/j.peptides.2015.09.004

Cited by 24 publications

(14 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ghrelin has been also found to stimulate angiogenesis in rat model of myocardial infarction [ 53 ], and this effect was associated with an anti-apoptotic effect and significant increase in vascular endothelial growth factor (VEGF) expression in the peri-infarct zone. In harmony with these findings is observation that administration of ghrelin ameliorates impaired angiogenesis in ischemic myocardium of diabetic rats with myocardial infarction [ 54 ]. This effect has been shown to involve AMPK/eNOS signal pathway by upregulated expression of hypoxia-inducible factor-1α (HIF-1α), VEGF, fetal liver kinase-1 (Flk-1), and fms-like tyrosine kinase-1 (Flt-1).…”

Section: Discussionmentioning

confidence: 68%

Exogenous Ghrelin Accelerates the Healing of Acetic Acid-Induced Colitis in Rats

Matuszyk

Ceranowicz

Warzecha

et al. 2016

IJMS

View full text Add to dashboard Cite

Previous studies have shown that ghrelin reduces colonic inflammation induced by trinitrobenzene sulfonic acid and dextran sodium sulfate. In the present study we determined the effect of treatment with ghrelin on the course of acetic acid-induced colitis in rats. Rectal administration of 3% acetic acid solution led to induction of colitis in all animals. Damage of the colonic wall was accompanied by an increase in mucosal concentration of pro-inflammatory interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), as well mucosal activity of myeloperoxidase. Moreover, induction of colitis led to a reduction in colonic blood flow and DNA synthesis. Administration of ghrelin after induction of colitis led to faster regeneration of the colonic wall and reduction in colonic levels of IL-1β, TNF-α, and myeloperoxidase. In addition, treatment with ghrelin improved mucosal DNA synthesis and blood flow. Our study disclosed that ghrelin exhibits a strong anti-inflammatory and healing effect in acetic acid-induced colitis. Our current observation in association with previous findings that ghrelin exhibits curative effect in trinitrobenzene sulfonic acid- and dextran sodium sulfate-induced colitis suggest that therapeutic effect of ghrelin in the colon is universal and independent of the primary cause of colitis.

show abstract

Section: Discussionmentioning

confidence: 68%

Exogenous Ghrelin Accelerates the Healing of Acetic Acid-Induced Colitis in Rats

Matuszyk

Ceranowicz

Warzecha

et al. 2016

IJMS

View full text Add to dashboard Cite

show abstract

“…In addition, VEGF is a VP enhancer whose potency is 5000 times stronger than histamine and plays an important role in the incidence of OHSS (Yan et al 1993, Neulen et al 1995, Wang et al 2002. Thus, VEGF promotes OHSS onset by regulating nitric oxide (NO) and junction proteins and thereby increasing VP (Farkkila et al 2011, Wang et al 2015. Apart from being a powerful mediator of VP, VEGF also participates in the formation of the corpus luteum by mediating vascularization (Aboulghar & Mansour 2003, Harada et al 2010.…”

Section: Introductionmentioning

confidence: 99%

Kisspeptin-10 inhibits OHSS by suppressing VEGF secretion

Zhai¹,

Liu²,

Zhao³

et al. 2017

Reproduction

View full text Add to dashboard Cite

The aim of the present study was to elucidate the effects of kisspeptin-10 (Kp-10) on ovarian hyperstimulation syndrome (OHSS) and its related mechanism in OHSS rat models, human umbilical vein endothelial cells (HUVECs) and human luteinized granulosa cells. OHSS is a systemic disorder with high vascular permeability (VP) and ovarian enlargement. KISS1R (KISS1 receptor) is the specific receptor of kisspeptin. The kisspeptin/KISS1R system inhibits the expression of vascular endothelial growth factor (VEGF), which is the main regulator of VP. In our study, decreased expression of Kiss1r was observed in both ovaries and lung tissue of OHSS rats. Injection of exogenous Kp-10 inhibited the increase of VP and VEGF while promoting the expression of Kiss1r in both the ovarian and lung tissue of OHSS rats. Using HUVECs, we revealed that a high level of 17-β estradiol (E), a feature of OHSS, suppressed the expression of KISS1R and increased VEGF and nitric oxide (NO) through estrogen receptors (ESR2). Furthermore, mRNA also decreased in the luteinized human granulosa cells of high-risk OHSS patients, and was consistent with the results in rat models and HUVECs. In conclusion, Kp-10 prevents the increased VP of OHSS by the activation of KISS1R and the inhibition of VEGF.

show abstract

“…It has been reported that AMPK reduces ROS generation and increases the anti‐oxidant MnSOD . AMPK also suppresses the resistin‐induced membrane assembly of NADPH oxidase and increases eNOS activity in endothelial cells . Hence, in the present study, we first observed the effects of Dex on heart function parameters, infarct size and proinflammatory cytokines following MIR surgery.…”

Section: Introductionmentioning

confidence: 73%

Dexmedetomidine protects mice against myocardium ischaemic/reperfusion injury by activating an AMPK/PI3K/Akt/eNOS pathway

Sun

Jiang

et al. 2017

Clin Exp Pharma Physio

View full text Add to dashboard Cite

Acute myocardial ischaemia/reperfusion (MIR) injury leads to severe arrhythmias and has a high rate of lethality. In the present study, we aim to determine the effect of dexmedetomidine (Dex) on heart injury parameters following MIR surgery. We examined the effects of Dex on heart function parameters and infarct size following MIR surgery. Proinflammatory cytokines, oxidative products and anti-oxidative enzymes in the myocardium were measured to evaluate the anti-inflammatory and anti-oxidative effects of Dex. The role of the adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/phosphatidylino-sitol 3-kinase (PI3k)/Akt/endothelial nitric oxide synthase (eNOS) pathway was investigated using their inhibitors. The alteration of haemodynamic parameters, histopathological results, and infarct size caused by MIR was attenuated by Dex. The interleukine-1 beta (IL-1β), IL-6, tumour necrosis factor-a (TNF-α) and myeloperoxidase (MPO) were all significantly decreased. Anti-oxidative enzymes superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) were restored by Dex. Oxidative products8-OHdG, MDA and protein carbonyl were all decreased by Dex (P<.05). Dex activated AMPK expression, eNOS and Akt phosphorylation. The influence of Dex on cardiac function was reversed by the inhibitors of the eNOS, AMPK and PI3K/Akt pathways. These results indicate that Dex protected the cardiac functional, histological changes, inflammation and oxidative stress induced by MIR. Our results present a novel signalling mechanism that Dex protects MIR injury by activating an AMPK/PI3K/Akt/eNOS pathway.

show abstract

Ghrelin ameliorates impaired angiogenesis of ischemic myocardium through GHSR1a-mediated AMPK/eNOS signal pathway in diabetic rats

Cited by 24 publications

References 51 publications

Exogenous Ghrelin Accelerates the Healing of Acetic Acid-Induced Colitis in Rats

Exogenous Ghrelin Accelerates the Healing of Acetic Acid-Induced Colitis in Rats

Kisspeptin-10 inhibits OHSS by suppressing VEGF secretion

Dexmedetomidine protects mice against myocardium ischaemic/reperfusion injury by activating an AMPK/PI3K/Akt/eNOS pathway

Contact Info

Product

Resources

About