HYPOTHESIS/PURPOSE: We hypothesized that LPva extracts can modulate the lipid profiles and serum antioxidant status of hypercholesterolemic rats. In the present study, we investigated the effects of aqueous and 80% ethanol extracts of LPva on atherogenic and serum antioxidant parameters as well as changes in abdominal aorta of high-cholesterol diet rats.
METHODS: The major components of the extracts, gallic acid, flavonoids and alkyl resorcinols were analyzed by using a validated reversed phase HPLC method. The rats were induced to hypercholesterolemic status with daily intake of 2% cholesterol for a duration of 8 weeks. Three different doses (100, 200 and 400mg/kg) of the extracts were administered daily on the 4th week onwards. The rats were then sacrificed and the blood was collected via abdominal aorta and serum was separated by centrifugation for biochemical analysis. Part of the aorta tissues were excised immediately for histopathological examination.
RESULTS: The serum of LPva treated rats showed significant reduction in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels and the abdominal aorta showed a significant decrease of atheroma lesions in treated rats. Serum lipid profiles of treated rats showed a decrease in total cholesterol, total triglycerides and low-density lipoprotein (LDL) levels as compared to control group. The atherogenic indices in treated rats were significantly improved along with an increasing level of serum high-density lipoprotein (HDL). The extracts also exhibited significant increase of antioxidant enzymes and decrease of MDA as a product of lipid peroxidation.
CONCLUSION: LPva extracts can reduce the risk of dyslipidemia by improving the serum lipid profiles and modulating serum antioxidants.
PURPOSE: In this study, we aimed to discover the role of oil palm phenolics (OPP) in influencing the gene expression changes caused by an atherogenic diet in mice.
METHODS: We fed mice with either a low-fat normal diet (14.6 % kcal/kcal fat) with distilled water, or a high-fat atherogenic diet (40.5 % kcal/kcal fat) containing cholesterol. The latter group was given either distilled water or OPP. We harvested major organs such as livers, spleens and hearts for microarray gene expression profiling analysis. We determined how OPP changed the gene expression profiles caused by the atherogenic diet. In addition to gene expression studies, we carried out physiological observations, blood hematology as well as clinical biochemistry, cytokine profiling and antioxidant assays on their blood sera.
RESULTS: Using Illumina microarrays, we found that the atherogenic diet caused oxidative stress, inflammation and increased turnover of metabolites and cells in the liver, spleen and heart. In contrast, OPP showed signs of attenuating these effects. The extract increased unfolded protein response in the liver, attenuated antigen presentation and processing in the spleen and up-regulated antioxidant genes in the heart. Real-time quantitative reverse transcription-polymerase chain reaction validated the microarray gene expression fold changes observed. Serum cytokine profiling showed that OPP attenuated inflammation by modulating the Th1/Th2 axis toward the latter. OPP also increased serum antioxidant activity to normal levels.
CONCLUSION: This study suggests that OPP may possibly attenuate atherosclerosis and other forms of cardiovascular disease.
OBJECTIVES: To investigate the anti-atherosclerotic activity of a C. nutans leaf methanol extract (CNME) in a type 2 diabetic (T2D) rat model induced by a high-fat diet (HFD) and low-dose streptozotocin.
MATERIALS AND METHODS: Sixty male Sprague-Dawley rats were divided into five groups: non-diabetic fed a standard diet (C), C + CNME (500 mg/kg, orally), diabetic fed an HFD (DM), DM + CNME (500 mg/kg), and DM + Metformin (DM + Met; 300 mg/kg). Treatment with oral CNME and metformin was administered for 4 weeks. Fasting blood glucose (FBG), serum lipid profile, atherogenic index (AI), aortic tissue superoxide dismutase levels (SOD), malondialdehyde (MDA), and tumour necrosis factor-alpha (TNF-α) were measured. The rats' aortas were stained for histological analysis and intima-media thickness (IMT), a marker of subclinical atherosclerosis.
RESULTS: The CNME-treated diabetic rats had reduced serum total cholesterol (43.74%; p = 0.0031), triglycerides (80.91%; p = 0.0003), low-density lipoprotein cholesterol (56.64%; p = 0.0008), AI (51.32%; p
AIM OF THE STUDY: The present study was performed to determine underlying mechanism of G. procumbens ethanol extract and its fractions such as aqueous, chloroform, ethyl acetate and hexane affect macrophage derived foam cell formation.
MATERIALS AND METHODS: Lipid droplets accumulation in treated macrophages were visualized by Oil Red O staining while the total cholesterol present in the treated macrophages were measured using Cholestryl Ester quantification assay kit. Enzyme-Linked Immunosorbent Assay (ELISA) were used to detect TNF-α and IL-1β secretion in the supernatant of treated macrophages. Gene expression of Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and ATP-binding cassette transporter A-1 (ABCA-1) in treated macrophages were analyzed using Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR).
RESULTS: G. procumbens ethanol extract and its fractions reduced lipid droplet accumulation and total cholesterol in oxLDL-treated macrophages together with significantly reduction of TNF-α and IL-1β secretions in supernatant oxLDL-treated macrophages. LOX-1 gene expression was significantly reduced when G. procumbens ethanol extract and its fractions were added in oxDL-treated macrophages. In contrast, G. procumbens ethanol extract and its fractions significantly increased the expression of ABCA-1 gene in oxLDL-treated macrophages.
CONCLUSION: In conclusion, G. procumbens ethanol extract and its fractions inhibit the formation of macrophage derived foam cell by reducing TNF-α and IL-1β expression, which usually highly expressed in atherosclerotic plaques, suppressing scavenger receptor LOX-1 gene that binds oxLDL but induced ABCA-1 gene that mediate lipid efflux from macrophages.