Curcumin attenuates migration of vascular smooth muscle cells via inhibiting NFκB-mediated NLRP3 expression in spontaneously hypertensive rats

Han, Ying; Sun, Hai-Jian; Tong, Ying; Chen, Yunzhi; Ye, Chao; Qiu, Yun; Zhang, Feng; Chen, Aidong; Qi, Xinming; Chen, Qi; Li, Yuehua; Kang, Yu-Ming; Zhu, Guo‐Qing

doi:10.1016/j.jnutbio.2019.07.003

Cited by 31 publications

(22 citation statements)

References 40 publications

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“…SMC, an important component of the vascular wall, participates in the characteristic inflammatory process of atherosclerosis. In an in vitro study, Han et al demonstrated that migration of human aortic SMC isolated from spontaneously hypertensive rats (SHR) or normal rats exposed to angiotensin II (AngII) was significantly inhibited by curcumin through the reduction of NLRP3/NF-κB signaling pathway [70]. The results were confirmed in vivo; it was demonstrated that administration of curcumin in SHR reduced intima-media thickness due to the inhibition of NF-κB and NLRP3 inflammasome and matrix metallopeptidase 9 (MMP-9) expression [70,71].…”

Section: Introductionmentioning

confidence: 99%

“…In an in vitro study, Han et al demonstrated that migration of human aortic SMC isolated from spontaneously hypertensive rats (SHR) or normal rats exposed to angiotensin II (AngII) was significantly inhibited by curcumin through the reduction of NLRP3/NF-κB signaling pathway [70]. The results were confirmed in vivo; it was demonstrated that administration of curcumin in SHR reduced intima-media thickness due to the inhibition of NF-κB and NLRP3 inflammasome and matrix metallopeptidase 9 (MMP-9) expression [70,71]. Yin et al showed that curcumin inhibited caspase-1 activation and IL-1β secretion through suppressing lipopolysaccharide (LPS) priming and NLRP3 inflammasome in mouse bone marrow-derived macrophages, and confirmed these results in vivo in a model of high-fat diet-induced insulin resistance in wild-type C57BL/6 mice [72].…”

Section: Introductionmentioning

confidence: 99%

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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: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2020

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“…LCN-2 can combine with matrix metalloprotein-9 (MMP-9) to form a heterodimer protein (15). The reduced decomposition or activation of MMP-9 during endothelial dysfunction promotes vascular smooth musclerelated vascular remodeling (16), which can aggravate endothelial dysfunction and promote PE. LCN-2 is also increased in insulin-resistant individuals (12), who are often more susceptible to PE (17).…”

Section: Discussionmentioning

confidence: 99%

Expression and significance of serum soluble fms-like tyrosine kinase 1 (sFlt-1), CXC chemokine ligand 16 (CXCL16), and lipocalin 2 (LCN-2) in pregnant women with preeclampsia

Li¹,

Ling²,

Mei³

et al. 2021

Ann Palliat Med

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Background: To explore the value of serum soluble fms-like tyrosine kinase 1 (sFlt-1), CXC chemokine ligand 16 (CXCL16), and lipocalin 2 (LCN-2) in the diagnosis and grading of preeclampsia (PE).Methods: A total of 186 patients with PE diagnosed and treated in our hospital were included. According to the disease severity, the patients were divided into the mild PE group (99 cases) and the severe PE group (87 cases). A total of 72 healthy pregnant women who underwent antenatal care were selected as the healthy control group. The levels of serum sFlt-1, CXCL16, and LCN-2 before medication were compared among the patients, and the diagnosis and grading value of the above 3 indicators were analyzed. Results: For PE patients vs. healthy controls, the levels of sFlt-1 (132.71±14.49 vs. 68.43±9.28 μg/L), CXCL16 (2.15±0.35 vs. 0.61±0.12 μg/L), and LCN-2 (70.81±8.25 vs. 19.22±3.14 μg/L) were all significantly higher in PE patients than in the healthy controls (P<0.05). For severe PE vs. mild PE, the levels of sFlt-1 (142.16±20.23 vs. 124.41±10.36 μg/L), CXCL16 (2.87±0.59 vs. 1.51±0.28 μg/L), and LCN-2 (90.76±10.16vs. 53.27±6.19 μg/L) in the severe PE group were higher than those in the mild PE group (P<0.05). Receiver operating characteristic curve (ROC) analysis showed that when the cut-off values of sFlt-1, CXCL16, and LCN-2 were 99.65, 1.36, and 0.84 μg/L, respectively, the diagnostic efficacy of PE was the highest. With these cut-off values, the diagnostic sensitivities of sFlt-1, CXCL16, and LCN-2 were 86.67%, 73.33%, and 93.33%, respectively. The specificities of sFlt-1, CXCL16, and LCN-2 were 80.00%, 86.67%, and 60.00%, respectively. The areas under the curves (AUC) of sFlt-1, CXCL16, and LCN-2 were 0.764, 0.769, and 0.831, respectively. When the cut-off values for sFlt-1, CXCL16, and LCN-2 were 135.16, 2.24, and 70.38 μg/L, respectively, the efficacy was the highest in distinguishing mild and severe PE. With these cut-off values, the AUC values of sFlt-1, CXCL16, and LCN-2 were 0.837, 0.808, and 0.869, respectively.Conclusions: sFlt-1, CXCL16, and LCN-2 have certain significance in the diagnosis and grading of PE.Among them, LCN-2 has the highest correlation with the diagnosis and grading of PE.

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“…Of note, a recent paper showed that curcumin (1,7‐bis(4‐hydroxy‐3‐methoxyphenyl)‐1,6‐heptadiene‐3,5‐dione), a bioactive component of Curcuma longa L., endowed with anti‐inflammatory, antioxidant, and anticancer properties, attenuated hypertension, vascular inflammation, and remodeling in SHR, via the suppression of NFκB‐mediated NLRP3 expression 170 …”

Section: Effects Of the Pharmacological Modulation Of Nlrp3 Inflammasome In Cardiovascular Diseasesmentioning

confidence: 99%

NLRP3 inflammasome in cardiovascular diseases: Pathophysiological and pharmacological implications

Pellegrini

Martelli

Antonioli

et al. 2021

Medicinal Research Reviews

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Growing evidence points out the importance of nucleotide‐binding oligomerization domain leucine‐rich repeat and pyrin domain‐containing protein 3 (NLRP3) inflammasome in the pathogenesis of cardiovascular diseases (CVDs), including hypertension, myocardial infarct (MI), ischemia, cardiomyopathies (CMs), heart failure (HF), and atherosclerosis. In this regard, intensive research efforts both in humans and in animal models of CVDs are being focused on the characterization of the pathophysiological role of NLRP3 inflammasome signaling in CVDs. In addition, clinical and preclinical evidence is coming to light that the pharmacological blockade of NLRP3 pathways with drugs, including novel chemical entities as well as drugs currently employed in the clinical practice, biologics and phytochemicals, could represent a suitable therapeutic approach for prevention and management of CVDs. On these bases, the present review article provides a comprehensive overview of clinical and preclinical studies about the role of NLRP3 inflammasome in the pathophysiology of CVDs, including hypertension, MI, ischemic injury, CMs, HF and atherosclerosis. In addition, particular attention has been focused on current evidence on the effects of drugs, biologics, and phytochemicals, targeting different steps of inflammasome signaling, in CVDs.

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Curcumin attenuates migration of vascular smooth muscle cells via inhibiting NFκB-mediated NLRP3 expression in spontaneously hypertensive rats

Cited by 31 publications

References 40 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

Expression and significance of serum soluble fms-like tyrosine kinase 1 (sFlt-1), CXC chemokine ligand 16 (CXCL16), and lipocalin 2 (LCN-2) in pregnant women with preeclampsia

NLRP3 inflammasome in cardiovascular diseases: Pathophysiological and pharmacological implications

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