Curcumin Attenuates Angiotensin II‐Induced Abdominal Aortic Aneurysm by Inhibition of Inflammatory Response and ERK Signaling Pathways

Hao, Qingqing; Xu, Chen; Wang, Xiaoyu; Dong, Bo; Yang, Chuanhua

doi:10.1155/2014/270930

Cited by 27 publications

(13 citation statements)

References 26 publications

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“…These results were confirmed in a recent study by Monfoulet et al, who demonstrated that curcumin pre-exposure reduces endothelial permeability and monocyte adhesion in both static and flow conditions [65]. In addition, most of the in vitro and in vivo studies confirm that curcumin administration determines the lowering of MCP-1 levels by downregulation of the MAPK and NF-κB signaling pathway [66][67][68]. The anti-inflammatory effects of curcumin on EC inflammatory markers were demonstrated also in vivo in various animal models.…”

Section: Introductionsupporting

confidence: 65%

Phenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular Diseases

et al. 2020

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Atherosclerosis is the main process behind cardiovascular diseases (CVD), maladies which continue to be responsible for up to 70% of death worldwide. Despite the ongoing development of new and potent drugs, their incomplete efficacy, partial intolerance and numerous side effects make the search for new alternatives worthwhile. The focus of the scientific world turned to the potential of natural active compounds to prevent and treat CVD. Essential for effective prevention or treatment based on phytochemicals is to know their mechanisms of action according to their bioavailability and dosage. The present review is focused on the latest data about phenolic compounds and aims to collect and correlate the reliable existing knowledge concerning their molecular mechanisms of action to counteract important risk factors that contribute to the initiation and development of atherosclerosis: dyslipidemia, and oxidative and inflammatory-stress. The selection of phenolic compounds was made to prove their multiple benefic effects and endorse them as CVD remedies, complementary to allopathic drugs. The review also highlights some aspects that still need clear scientific explanations and draws up some new molecular approaches to validate phenolic compounds for CVD complementary therapy in the near future.In the last decade the scientific researchers turned their attention to phytochemicals, as effective, safe and low-cost natural bioactive compounds for CVD treatment.Dyslipidemia consists of increased blood concentrations of total cholesterol (TC), low density lipoproteins-cholesterol (LDL-C) and/or triglycerides (TG), and decreased high density lipoproteins-cholesterol (HDL-C) [6]. The lipid metabolism is complex and the candidate mechanisms that could generate dyslipidemia include: (i) excessive dietary lipid absorption in the small intestine; (ii) packing of exogenous lipids with cholesterol and fatty acids produced de novo in the liver and their secretion as very low density lipoproteins (VLDL); (iii) hydrolysis of TG from VLDL by lipases and their conversion into LDL, which are taken up by the peripheral tissues through LDL receptor (LDL-R) and scavenger receptors; (iv) diminished production of HDL by the liver and small intestine, thereby decreasing reverse cholesterol transport (RCT) from the peripheral tissues to the liver; (v) lowered excess cholesterol excretion from the liver into gallbladder or to the intestinal lumen through the ATP-binding cassette G5 and G8 transporters (ABCG5/G8) that facilitate trans-intestinal cholesterol efflux (TICE). Dyslipidemia is associated with the accumulation of LDL in the sub-endothelium of the artery wall. At this site, LDL undergoes oxidative modifications (oxLDL) that trigger inflammatory responses, and is taken up by the monocyte-derived macrophages infiltrated in the sub-endothelium which thus become lipid-loaded foam cells, the hallmark of atheroma development [7]. Until now, the most effective lipid-lowering treatment for hyperlipidemic patients was the statin therapy. But recen...

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Section: Introductionsupporting

confidence: 65%

Phenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular Diseases

et al. 2020

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“…Increasing evidence suggests that ERK levels are dramatically increased during cardiac damage, as shown in an ischemic pig model and in the human heart [ 32 ]. In addition, activation of ERK seems to be a causal factor for cardiac inflammation by HMGB1, and phosphorylated ERK has been associated with the macrophage polarization and inflammatory process [ 33 ]. Here we observed that gallein treatment effectively attenuated the phosphorylation of ERK1/2 in the hearts of EAM rats.…”

Section: Discussionmentioning

confidence: 99%

Small molecule disruption of G protein βγ subunit signaling reprograms human macrophage phenotype and prevents autoimmune myocarditis in rats

Karuppagounder¹,

Bajpai²,

Meng³

et al. 2018

PLoS ONE

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The purpose of this study was to determine whether blocking of G protein βγ (Gβγ) signaling halts heart failure (HF) progression by macrophage phenotype manipulation. Cardiac Gβγ signaling plays a crucial role in HF pathogenesis. Previous data suggested that inhibiting Gβγ signaling reprograms T helper cell 1 (Th1) and Th2 cytokines, suggesting that Gβγ might be a useful drug target for treating HF. We investigated the efficacy of a small molecule Gβγ inhibitor, gallein, in a clinically relevant, experimental autoimmune myocarditis (EAM) model of HF as well as in human macrophage phenotypes in vitro. In the myocardium of HF patients, we observed that G protein coupled receptor kinase (GRK)2 levels were down-regulated compared with healthy controls. In rat EAM, treatment with gallein effectively improved survival and cardiac function, suppressed cardiac remodeling, and further attenuated myocardial protein expression of GRK2 as well as high mobility group box (HMGB)1 and its cascade signaling proteins. Furthermore, gallein effectively inhibited M1 polarization and promoted M2 polarization in vivo in the EAM heart and in vitro in human monocyte-derived macrophages. Taken together, these data suggest that the small molecule Gβγ inhibitor, gallein, could be an important pharmacologic therapy for HF as it can switch the phenotypic reprogramming from M1 to M2 phenotype in a rat model of EAM heart and in human macrophages.

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“…ERK1/2 enters the cell nucleus and acts as a transcription factor, accelerating the transcription and expression of certain genes and is closely associated with cell proliferation and differentiation (35). Studies have indicated that ERK1/2 mediates the stress and inflammatory response (36,37). ERK1/2 is an essential signal transduction pathway in the MAPK family and it has been demonstrated that ERK1/2 is closely associated with atherosclerosis (38).…”

Section: Discussionmentioning

confidence: 99%

Rutin inhibits coronary heart disease through ERK1/2 and Akt signaling in a porcine model

Yao

Zhao

et al. 2017

Exp Ther Med

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Abstract.Rutin has a variety of pharmacological actions, including radical reactivity, and protective activity against lipid peroxidation, viruses and acute pancreatitis; thus, it may be used as a treatment for many diseases. The present study aimed to investigate whether rutin inhibits coronary heart disease through extracellular signal-regulated kinase (ERK) 1/2 and Akt signaling in a porcine model. Male Chinese miniature pigs were randomly divided into four groups: A sham group, a coronary heart disease (CHD) model group, a group receiving 15 mg/kg rutin for 8 weeks following CHD modeling and a group receiving 45 mg/kg rutin for 8 weeks following CHD modeling. The results suggested that treatment with rutin suppressed the reduction in left ventricular ejection fraction and increase in systolic internal diameter that occurred in CHD model pigs. Rutin administration reduced the infarct size of the myocardium, attenuated LVEF, increased LVID and inhibited urine protein concentration, BUN and Scr expression levels in CHD model pigs. Results from western blot analysis demonstrated that in CHD pigs treated with 45 mg/kg rutin, the CHD-associated increases in transforming growth factor β1 and SMAD2 expression and reductions in phosphorylated (p)-ERK1/2 and p-Akt expression were attenuated. The present study suggests that rutin inhibits coronary heart disease through ERK1/2 and Akt signaling pathways in a porcine model.

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Curcumin Attenuates Angiotensin II‐Induced Abdominal Aortic Aneurysm by Inhibition of Inflammatory Response and ERK Signaling Pathways

Cited by 27 publications

References 26 publications

Phenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular Diseases

Phenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular Diseases

Small molecule disruption of G protein βγ subunit signaling reprograms human macrophage phenotype and prevents autoimmune myocarditis in rats

Rutin inhibits coronary heart disease through ERK1/2 and Akt signaling in a porcine model

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