Pro-inflammatory cytokines correlate with classical risk factors for atherosclerosis in the admixed Brazilian older women

Pires, Alause S.; Souza, Vinícius Carolino; Paula, Roberta; Toledo, Juliana Oliveira; Lins, Tulio Cesar de Lima; Moraes, Clayton Franco; Córdova, Cláudio; Pereira, Rinaldo Wellerson; Nóbrega, Otávio Tolêdo

doi:10.1016/j.archger.2014.10.004

Cited by 8 publications

(7 citation statements)

References 43 publications

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“…Many studies have shown that pro-inflammatory factors including IL-6 and TNF-α are of significance in the formation of atherosclerosis [7]. This study showed that simvastatin decreased the contents of TNF-α and IL-6 in serum of ApoE KO mice and downregulated the mRNA expression of TNF-α and IL-6 in atherosclerotic tissue.…”

Section: Discussionmentioning

confidence: 55%

“…Studies have demonstrated that pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) get involved in the formation of atherosclerosis [7]. TNF-α was reported to induce the early inflammatory reactions in atherosclerotic lesion of ApoE KO mice [8] and the inhibition of TNF-α resulted in diminished atherosclerosis [9].…”

Section: Introductionmentioning

confidence: 99%

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Downregulations of CD36 and Calpain-1, Inflammation, and Atherosclerosis by Simvastatin in Apolipoprotein E Knockout Mice

Yin¹,

Liu²,

Yu³

et al. 2017

J Vasc Res

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Background: In the previous in vitro study, we found that simvastatin decreased the protein expression of CD36, the scavenger receptor, and calpain-1, the Ca²⁺-sensitive cysteine protease, in oxidized low-density lipoprotein (oxLDL)-treated macrophages. In this in vivo study, we investigated whether simvastatin downregulates the expression of CD36 and calpain-1 and inhibits the inflammation and atherosclerosis in apolipoprotein E knockout (ApoE KO) mice. Methods: Twenty male 6-week-old ApoE KO mice were divided into 2 groups: the ApoE KO group and the ApoE KO + simvastatin (ApoE KO + Sim) group. Atherosclerotic lesions were evaluated and the expressions of CD68, CD36, and calpain-1 in aorta were examined. Results: Simvastatin inhibited the atherosclerotic lesion in ApoE KO mice. In addition, simvastatin reduced the contents of oxLDL, thiobarbituric acid reactive substances, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in serum, decreased the mRNA and protein expressions of CD36 and reduced the mRNA expression of TNF-α and IL-6 in the aortas. Furthermore, simvastatin reduced the calpain activity and the protein expression of calpain-1 in the aorta. Conclusion: The results suggested that the attenuation of atherosclerotic lesions in ApoE KO mice by simvastatin might be associated with the downregulations of CD36 and calpain-1 and with inflammation.

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Section: Discussionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Downregulations of CD36 and Calpain-1, Inflammation, and Atherosclerosis by Simvastatin in Apolipoprotein E Knockout Mice

Yin¹,

Liu²,

Yu³

et al. 2017

J Vasc Res

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“…This phenomena were observed, for instance, in the evaluation of the inflammatory response after ingestion of highly caloric meal (high fat content) in European young men, which showed an increase in plasma IL-8 concentrations [25]. Titers of IL-8 as well as of other immune mediators related to the inflammaging process have proven to differ between individuals according to health status, tending to be increased among carriers of chronic conditions [26]. In regard to this, we understand that our report poses a contribution by duly controlling our analyses for the presence of the most frequent, inflammation-boosted aging disorders (type 2 diabetes, systemic arterial hypertension and hyperlipidemia).…”

Section: Discussionmentioning

confidence: 93%

Habitual dietary intake and mediators of the inflammaging process in Brazilian older women

et al. 2015

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“…The investigation of inflammatory markers in vascular disorders reveals augmented levels of circulating cytokines and chemokines among carriers of classic risk factors for atherosclerosis. Dysregulation of the PPAR signaling pathway may explain the association of IL-8/12 and very low density lipoprotein (VLDL)-c in the promotion of dysglycemia ( 118 ). The PPAR signaling pathway was shown to be important in the modulation of inflammatory factors, including MCP-1, TNF-α, IL-1 and IL-6, COX-2, nicotinamide adenine dinucleotide phosphate, protein kinase C, vascular cell adhesion molecule-1, NF-κB and monocyte expressions in HUVECs.…”

Section: Potential Role Of Ppar Agonists In the Treatment Of Cabmentioning

confidence: 99%

The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns?(Review)

Zhou

Zhang

et al. 2016

Int J Mol Med

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Corneal alkali burns (CAB) are characterized by injury-induced inflammation, fibrosis and neovascularization (NV), and may lead to blindness. This review evaluates the current knowledge of the molecular mechanisms responsible for CAB. The processes of cytokine production, chemotaxis, inflammatory responses, immune response, cell signal transduction, matrix metalloproteinase production and vascular factors in CAB are discussed. Previous evidence indicates that peroxisome proliferator-activated receptor γ (PPAR-γ) agonists suppress immune responses, inflammation, corneal fibrosis and NV. This review also discusses the role of PPAR-γ as an anti-inflammatory, anti-fibrotic and anti-angiogenic agent in the treatment of CAB, as well as the potential role of PPAR-γ in the pathological process of CAB. There have been numerous studies evaluating the clinical profiles of CAB, and the aim of this systematic review was to summarize the evidence regarding the treatment of CAB with PPAR-γ agonists.

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Pro-inflammatory cytokines correlate with classical risk factors for atherosclerosis in the admixed Brazilian older women

Cited by 8 publications

References 43 publications

Downregulations of CD36 and Calpain-1, Inflammation, and Atherosclerosis by Simvastatin in Apolipoprotein E Knockout Mice

Downregulations of CD36 and Calpain-1, Inflammation, and Atherosclerosis by Simvastatin in Apolipoprotein E Knockout Mice

Habitual dietary intake and mediators of the inflammaging process in Brazilian older women

The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns?(Review)

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