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1.
Adv Biomed Res ; 13: 16, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38525390

RESUMEN

Background: Neurons need a high amount of cholesterol to maintain the stability of their membrane-rich structures. Astrocytes synthesize and distribute cholesterol to neurons, and ABCA1 is a key mediator of cholesterol efflux to generate HDL for cholesterol transport in the brain. Several studies imply the effect of aspirin on ABCA1 expression in peripheral cells such as macrophages. Here, we compared the effect of aspirin with apoA-I on ABCA1 protein expression and cholesterol efflux in human astrocytes. Materials and Methods: Human astrocytes were cultured, and the effects of aspirin on the expression and protein levels of ABCA1 were investigated through RT-PCR and Western blot analysis. Additionally, the effect of co-treatment with apoA-I and aspirin on ABCA1 protein level and cholesterol efflux was evaluated. Results: Dose and time-course experiments showed that the maximum effect of aspirin on ABCA1 expression occurred at a concentration of 0.5 mM after 12 h of incubation. RT-PCR and western blot data showed that aspirin upregulates ABCA1 expression by up to 4.7-fold and its protein level by 67%. Additionally, co-treatment with aspirin and apoA-I increased cholesterol release from astrocytes, indicating an additive effect of aspirin on apoAI-mediated cholesterol efflux. Conclusions: The results suggest a potential role of aspirin in increasing ABCA1 expression and cholesterol efflux in astrocytes, similar to the effect of apoA-I. This indicates that aspirin could potentially regulate brain cholesterol balance and can be considered in certain neurological diseases, in particular in some neurological disorders related to cholesterol accumulation such as Alzheimer's disease.

2.
ARYA Atheroscler ; 16(4): 153-160, 2020 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-33598035

RESUMEN

BACKGROUND: Although the antioxidant properties of ginger have been revealed, there is little available information on the effectiveness of ginger on inflammatory disorders such as atherosclerosis. This study was carried out to examine the effect of ginger on improving the complication of atherosclerosis. METHODS: This study was a double-blind, placebo-controlled, randomized clinical trial conducted on patients with atherosclerosis. Participants in the ginger and control groups received 1600 mg of powdered ginger or placebo (wheat flour) in capsules daily for 8 weeks. Weight, body mass index (BMI), fasting blood sugar (FBS), cholesterol, triglyceride (TG), low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), high-density lipoprotein (HDL), lipoprotein (a) [Lp(a)], high-sensitivity C-reactive protein (hs-CRP), and total anti-oxidant capacity (TAC) were assessed before and after the intervention. RESULTS: Ginger consumption in the intervention group significantly reduced serum Lp(a) level (27.25 ± 1.30 ng/ml vs. 23.57 ± 0.97 ng/ml) (P = 0.040) and also the level of hs-CRP in the intervention group was 1.90 ± 0.33 µg/ml and 1.24 ± 0.15 µg/ml (P = 0.010) before and after intervention, respectively, but the levels of Lp(a) and hs-CRP were not decreased significantly in the placebo group. The level of TAC in the ginger group was 0.71 ± 0.05 mM and after the trial was 0.57 ± 0.04 mM (P = 0.050); no significant differences were seen in TAC when ginger was administered at 1600 mg/daily for 60 days. Also the level of Lp(a) and hs-CRP but not TAC reduced significantly in ginger group compared to placebo group after intervention. CONCLUSION: This study showed that ginger had anti-atherosclerosis and anti-glycemic properties associated through a significant decreased Lp(a) and FBS in patients with atherosclerosis supplemented with ginger.

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