Association between Mediterranean-dietary approaches to stop hypertension intervention for neurodegenerative delay diet and biomarkers of oxidative stress, metabolic factors, disease severity, and odds of disease in rheumatoid arthritis patients.

This research aimed to examine the association between the following Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) dietary pattern and oxidative stress indicators, metabolic factors, disease activity, and the odds of disease in patients with rheumatoid arthritis (RA). In this cross-sectional study, we included 101 patients with RA and 101 healthy individuals. The MIND diet score was measured using a semi-quantitative Food Frequency Questionnaire (FFQ) with 147 food items. Total capacity antioxidant (TCA), superoxide dismutase (SOD), glutathione peroxidase (GPX), and malondialdehyde (MDA) serum concentrations were evaluated by ELISA, and the disease severity was measured regarding the disease activity score 28 (DAS-28) criteria. The average score of the MIND diet was substantially lower in the RA subjects than in the healthy people (p < .001). Individuals with a higher MIND diet score had lower odds of RA than those with a low score (p < .001). There was no remarkable link between the MIND diet and oxidative stress factors (p > .05). A reverse association was found between the MIND diet score and disease activity (p < .05). The MIND diet was significantly and negatively correlated with triglycerides, low-density lipoprotein cholesterol, total cholesterol, fasting blood glucose, and hemoglobin A1C. There was a positive association between the diet and high-density lipoprotein cholesterol. The findings indicate that following the MIND diet may decrease disease activity and the odds of RA. Also, high adherence to the MIND diet may improve the lipid profile and blood glucose status in RA patients.

Development of a novel method for the purification of C-phycocyanin pigment from a local cyanobacterial strain Limnothrix sp. NS01 and evaluation of its anticancer properties.

C-phycocyanin (C-PC) pigment, as a natural blue dye, has particular applications in various fields. It is a water-soluble protein which has anticancer, antioxidant and anti-inflammatory properties. Here, we introduce an efficient procedure for the purification of C-PC pigment, followed by conducting a comprehensive investigation of its cytotoxic effects on human breast cancer (MCF-7) cells and the underlying mechanisms. A novel four-step purification procedure including the adsorption of impurities with chitosan, activated charcoal, ammonium sulfate precipitation, and ion exchange chromatography was employed, achieving a high purity form of C-PC with purity index (PI) of 5.26. SDS-PAGE analysis showed the purified C-PC with two discrete bands, subunit α (17 kD) and ß (20 kD), as confirmed its identity by Native-PAGE. A highly purified C-PC was employed to evaluate its anticancer activity and underlying molecular mechanisms of action. The inhibitory effects of highly purified C-PC on the proliferation of human breast cancer cells (MCF-7) have detected by MTT assay. The IC50 values for 24, 48, and 72 hours of exposure to C-PC were determined to be 5.92, 5.66, and 4.52 µg/µl, respectively. Flow cytometric analysis of cells treated with C-PC, by Annexin V/PI double staining, demonstrated to induce MCF-7 cells apoptosis. Also, the results obtained from propidium iodide (PI) staining showed that MCF-7 cells treated with 5.92 µg/µl C-PC for 24 h would arrest at the G2 phase and 5.66 and 4.52 µg/µl C-PC for 48 and 72 h could induce cell cycle arrest at both G2 and S phases. The oxidative damage and mitochondrial dysfunction were evaluated to determine the possible pathways involved in C-PC-induced apoptosis in MCF-7 cells. Our findings clearly indicated that the treatment of MCF-7 cells with C-PC (IC50 for 24 h) increased the production of reactive oxygen species (ROS). Consequently, an increase in the lipid peroxidation (LPO) level and a reduction in the ATP level, mitochondrial membrane potential (MMP), glutathione (GSH) and its oxidized form (GSSG), occurred over time. The reduced expression levels of anti-apoptotic proteins, Bcl2 and Stat3, plus cell cycle regulator protein, Cyclin D1, using Real-Time PCR confirm that the C-PC-induced death of MCF-7 human breast cancer cells occurred through the mitochondrial pathway of apoptosis. Collectively, the analyses presented here suggest that C-PC has the potential so that to develop it as a chemotherapeutic anticancer drug.