Malondialdehyde, lipoprotein-a, lipoprotein ratios, comprehensive lipid tetrad index and atherogenic index as surrogate markers for cardiovascular disease in patients with psoriasis: a case–control study

Wadhwa, Dhaarna; Mahajan, Vikram K.; Mehta, Karaninder S; Chauhan, Pushpinder S; Yadav, Rajinder S; Bhushan, Satya; Sharma, Vikas; Sharma, Abha; Sharma, Aditi; Chauhan, Shailja

doi:10.1007/s00403-019-01896-y

Cited by 17 publications

(17 citation statements)

References 27 publications

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“…In agreement with these findings, we revealed the sub-chronic SiNPs treatment via intratracheal instillation also aggravated the hyperlipidemia of ApoE −/− mice, characterized with the increased serum levels of TG and LDL-C. To be noted, the increase in serum LDL-C content was positively correlated with the plaque area in aortic root. Meanwhile, the AI index was increased, whilst HDL-C/LDL-C ratio was decreased in SiNPs group when compared with the control group, hinting the dyslipidemia caused by SiNPs may contribute to the progress of atherosclerotic lesions [49,50]. Coincidently, population studies have shown a highly consistent, positive correlation between blood LDL-C level and atherosclerotic CVD risk in humans [51].…”

Section: Discussionmentioning

confidence: 99%

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Amorphous silica nanoparticles accelerated atherosclerotic lesion progression in ApoE−/− mice through endoplasmic reticulum stress-mediated CD36 up-regulation in macrophage

Zhao

et al. 2020

Part Fibre Toxicol

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Background The biosafety concern of silica nanoparticles (SiNPs) is rapidly expanding alongside with its mass production and extensive applications. The cardiovascular effects of SiNPs exposure have been gradually confirmed, however, the interaction between SiNPs exposure and atherosclerosis, and the underlying mechanisms still remain unknown. Thereby, this study aimed to explore the effects of SiNPs on the progression of atherosclerosis, and to investigate related mechanisms. Results We firstly investigated the in vivo effects of SiNPs exposure on atherosclerosis via intratracheal instillation of ApoE−/− mice fed a Western diet. Ultrasound microscopy showed a significant increase of pulse wave velocity (PWV) compared to the control group, and the histopathological investigation reflected a greater plaque burden in the aortic root of SiNPs-exposed ApoE−/− mice. Compared to the control group, the serum levels of total triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) were elevated after SiNPs exposure. Moreover, intensified macrophage infiltration and endoplasmic reticulum (ER) stress was occurred in plaques after SiNPs exposure, as evidenced by the upregulated CD68 and CHOP expressions. Further in vitro, SiNPs was confirmed to activate ER stress and induce lipid accumulation in mouse macrophage, RAW264.7. Mechanistic analyses showed that 4-PBA (a classic ER stress inhibitor) pretreatment greatly alleviated SiNPs-induced macrophage lipid accumulation, and reversed the elevated CD36 expression induced by SiNPs. Conclusions Our results firstly revealed the acceleratory effect of SiNPs on the progression of atherosclerosis in ApoE−/− mice, which was related to lipid accumulation caused by ER stress-mediated upregulation of CD36 expression in macrophage. Graphical abstract

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Section: Discussionmentioning

confidence: 99%

“…The contents of TC, TG, HDL-C, and LDL-C in mice serum were measured by an automatic biochemical analyzer (HITACHI 7180) combining commercial kits (Jiancheng, Nanjing, China). The ratio of HDL-C/LDL-C was calculated, as well as AI according to the formula: AI = (TC -HDL-C)/HDL-C [49].…”

Section: Lipid Profiles Analysismentioning

confidence: 99%

Amorphous silica nanoparticles accelerated atherosclerotic lesion progression in ApoE−/− mice through endoplasmic reticulum stress-mediated CD36 up-regulation in macrophage

Zhao

et al. 2020

Part Fibre Toxicol

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“…e atherogenic effects of HDL-C are due to its role in reverse cholesterol transport and to its associated antioxidant enzymes such as paraoxonase 1 (PON1), which can degrade various proatherogenic compounds resulted from lipid oxidation [32]. Among these oxidation products, MDA, a marker of lipid oxidation and cardiovascular disease, is a toxic compound that can interact with DNA and proteins, which results in the dysfunction of the endothelium and other atherogenic events [33]. e reduction of plasma level of MDA in the hyperlipidemic hamsters receiving the T. atlanticus extracts suggests a preventive effect of these extracts against lipid oxidation and atherosclerosis development.…”

Section: Discussionmentioning

confidence: 99%

Effect of Aqueous Extract and Polyphenol Fraction Derived from Thymus atlanticus Leaves on Acute Hyperlipidemia in the Syrian Golden Hamsters

Ramchoun

Khouya

Harnafi

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Thymus atlanticus, an endemic plant of Morocco, is traditionally used as a liniment or a drink to treat various diseases. However, there are few available scientific data regarding its biological effects. In this connection, the present study aimed to investigate the hypolipidemic and antioxidant effects of aqueous extract and polyphenol fraction of Thymus atlanticus in Syrian golden hamsters treated with Triton WR-1339 (triton, 20 mg/100 g body weight). The hamsters orally received the extracts (400 mg/kg), and blood samples were collected after 24 h of treatment to determine plasma lipid, insulin, and fasting blood glucose levels. Plasma malondialdehyde level and plasma total antioxidant (TAS) were also evaluated. The T. atlanticus extracts significantly decreased triglycerides, total cholesterol, VLDL-C, and LDL-C and increased HDL-C when compared with the hyperlipidemic group. Both extracts suppressed the effect of the triton injection on TAS and reduced the level of plasma malondialdehyde. The extracts produced no significant change in the blood glucose level but effectively prevented the mild hyperinsulinemia induced by triton. These findings suggest that T. atlanticus may be a useful alternative treatment for the control of hyperlipidemia and its related diseases.

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“…In agreement with these ndings, we revealed the sub-chronic SiNPs treatment via intratracheal instillation also aggravated the hyperlipidemia of ApoE -/mice, characterized with the increased serum levels of TG and LDL-C. To be noted, the increase in serum LDL-C content was positively correlated with the plaque area in aortic root. Meanwhile, the AI index was increased, whilst HDL-C/LDL-C ratio was decreased in SiNPs group when compared with the control group, hinting the dyslipidemia caused by SiNPs may contribute to the progress of atherosclerotic lesions [50,51]. Coincidently, population studies have shown a highly consistent, positive correlation between blood LDL-C level and atherosclerotic CVD risk in humans [52].…”

Section: Discussionmentioning

confidence: 99%

Section: Lipid Pro Les Analysismentioning

confidence: 99%

Amorphous silica nanoparticles accelerated atherosclerotic lesion progression in ApoE-/- mice through endoplasmic reticulum stress-mediated CD36 up-regulation in macrophage

Zhao

et al. 2020

Preprint

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Abstract Background: The biosafety concern of silica nanoparticles (SiNPs) is rapidly expanding alongside with its mass production and extensive applications. The cardiovascular effects of SiNPs exposure have been confirmed. However, the interaction between SiNPs exposure and atherosclerosis, and the underlying mechanisms still remain unknown. Thereby, this study aimed to explore the effects of SiNPs on the progression of atherosclerosis, and to investigate related mechanisms. Results: We firstly investigated the in vivo effects of SiNPs exposure on atherosclerosis via intratracheal instillation of ApoE -/- mice fed a Western diet. Ultrasound microscopy showed a significant increase of pulse wave velocity (PWV) compared to the control group. Histopathological investigation reflected a greater plaque burden in the aortic root of SiNPs-exposed ApoE -/- mice. When compared to the control, serum levels of total triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) were elevated after SiNPs exposure. Moreover, intensified macrophage infiltration and endoplasmic reticulum (ER) stress was occurred in plaques after SiNPs exposure, as evidenced by the upregulated CD68 and CHOP expressions. Further in vitro , SiNPs was confirmed to activate ER stress and induce lipid accumulation in mouse macrophage, RAW264.7. Mechanistic analyses showed that 4-PBA (a classic ER stress inhibitor) pretreatment greatly alleviated SiNPs-induced macrophage lipid accumulation, and reversed the elevated CD36 expression by SiNPs. Conclusions: Our results firstly revealed the acceleratory effect of SiNPs on the progression of atherosclerosis in ApoE -/- mice, which was related to lipid accumulation caused by ER stress-mediated upregulation of CD36 expression in macrophage.

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Malondialdehyde, lipoprotein-a, lipoprotein ratios, comprehensive lipid tetrad index and atherogenic index as surrogate markers for cardiovascular disease in patients with psoriasis: a case–control study

Cited by 17 publications

References 27 publications

Amorphous silica nanoparticles accelerated atherosclerotic lesion progression in ApoE−/− mice through endoplasmic reticulum stress-mediated CD36 up-regulation in macrophage

Amorphous silica nanoparticles accelerated atherosclerotic lesion progression in ApoE−/− mice through endoplasmic reticulum stress-mediated CD36 up-regulation in macrophage

Effect of Aqueous Extract and Polyphenol Fraction Derived from Thymus atlanticus Leaves on Acute Hyperlipidemia in the Syrian Golden Hamsters

Amorphous silica nanoparticles accelerated atherosclerotic lesion progression in ApoE-/- mice through endoplasmic reticulum stress-mediated CD36 up-regulation in macrophage

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