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1.
Semin Arthritis Rheum ; 50(4): 769-775, 2020 08.
Article in English | MEDLINE | ID: mdl-32531506

ABSTRACT

Systemic lupus erythematosus (SLE) is a heterogeneous disease which is characterized with excessive inflammation and autoantibodies, macrophage and complement activation, and subsequently immunologically mediated tissue damage. In spite of improved treatments of SLE, these patients experience premature atherosclerosis and the rate of mortality among them remains high. Autoantibodies and circulating immune complexes might contribute to the pathogenesis of atherosclerosis by injuring the endothelium, as well as inducing pro-inflammatory and pro-adhesive endothelial cell phenotypes, as well as altering the metabolism of lipoproteins involved in atherogenesis. Hence, high levels of atherogenic lipoproteins (like low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL)) and low levels of high-density lipoprotein (HDL-C) are important risk factors for atherosclerotic cardiovascular complications in SLE patients but these traditional risk factors fail to fully explain the increased risk of cardiovascular disease (CVD) in these patients. The exact mechanism by which inflammation decreases HDL levels is not defined, but decreases in apoA-I production and lecithin cholesterol acyltransferase (LCAT) activity, as well as increased serum amyloid A (SAA), endothelial lipase and secretory phospholipase A2 activity (PLA2) could all contribute. In addition, during inflammation multiple changes in HDL structure occur, leading to alterations in HDL function which may be implicated in the CVD complications of SLE. Therefore, this review will aim to identify the mechanisms implicated in HDL dysfunction which occurs in SLE patients.


Subject(s)
Lipoproteins, HDL/blood , Lupus Erythematosus, Systemic/blood , Animals , Apolipoprotein A-I/blood , Atherosclerosis/blood , Atherosclerosis/complications , Atherosclerosis/immunology , Autoantibodies/blood , Humans , Inflammation , Lupus Erythematosus, Systemic/complications , Mice , Risk Factors
2.
Article in English | MEDLINE | ID: mdl-31538907

ABSTRACT

BACKGROUND: Inflammation has been shown to accompany Metabolic Syndrome (MetS) and its features. Cathepsin D is one of a proinflammatory mediator. In the current study, we aimed to investigate the effect of curcumin supplementation on serum cathepsin D levels in patients with MetS. METHODS: The current study was conducted on 18-65 years old individuals with MetS diagnosed according to the International Diabetes Federation guidelines. A total of 80 participants were randomly divided into treatment and control groups. The first group (n=40) was given 2 capsules containing 500 mg of phosphatidylcholine complex of curcumin, and the other group (n=40) was given two 500 mg placebo capsules for 6 weeks. Before (week 0) and after (week 6) the intervention, anthropometric indices and blood pressure were measured and blood samples were taken. Serum cathepsin D was measured using an ELISA kit. RESULTS: There was no significant difference between treatment and control groups in terms of weight, body mass index, waist circumference and serum cathepsin D levels before and after the intervention. In addition, there was no significant difference between pre- and post-trial values of serum cathepsin D. CONCLUSION: The present results do not suggest any effect of curcumin on cathepsin D levels in patients with MetS.


Subject(s)
Cathepsin D/blood , Curcumin/therapeutic use , Metabolic Syndrome/drug therapy , Adolescent , Adult , Aged , Curcumin/pharmacology , Female , Humans , Male , Middle Aged , Young Adult
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