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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: models/Detail_model.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Objective: To study the effects of total flavonoids of Hippophae rhamnoides L. (TFH) on the expression of monocyte chemoattractant protein (MCP-1) in aorta of Spontaneously Hypertensive Rats (SHR) and to study the relationship of expression of MCP-1 in aorta and intimal medial thickness (IMT) of aorta.
Methods: Twelve-week-old male SHR (n=12) were randomly devided into three groups to receive TFH [30 mg/(kg x d), n=4], Enalapril [10 mg/(kg x d), n= 4] and Hydrochlorothiazide [25 mg/(kg x d), n=4] for 12 weeks, respectively. Another 4 SHR and 4 WKY which receive placebo served as positive control group and negative control group. The systolic blood pressure (SBP), intimal medial thickness and inside diameter of aorta of the rats were measured. The expression of MCP-1 in aorta was examined by real-time PCR and immunohistochemistry and the concentration of serum MCP-1 protein by ELSA.
Results: Twelve weeks later, systolic blood pressure in TFH was significantly decreased, compared with that in Enalapril and Hydrochlorothiazide without statistical differences. TFH markedly reduced the intimal medial thickness of aorta and expression of MCP-1 in aorta, similar with Enalapril, stronger than Hydrochlorothiazide.
Conclusion: TFH can markedly decrease SBP of SHR and the decrease value of the TFH group was similar with that of the Enalapril and Hydrochlorothiazide group. TFH may inhibit the expression of MCP-1 in aorta and intimal medial thickness of aorta beyond BP Lowering effect. The effect of THF on the expression of MCP-1 and intimal medial thickness of aorta was similar with Enalapril. TFH may through inhibite the expression of MCP-1 in aorta to reduce the intimal medial thickness of aorta and protect hypertensive injury in target organs.
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Metabol Open
December 2024
Post-graduate Program in Chemical Biology - Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo - UNIFESP, Diadema, Brazil.
In obesity, C-C chemokine ligand 2 (CCL2) plays a critical role in recruiting macrophages to white adipose tissue (WAT), contributing to chronic inflammation. In this study, we sought to explore the effects of fish oil (FO) on CCL2 expression and histone (H3K27)-modifying enzymes in both human model of preadipocytes and primary adipose-derived stem cells (ASCs). Present findings in preadipocytes lineage evidenced that lipopolysaccharide (LPS) increased (∼5.
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Department of Restorative Dentistry and Biomaterials Sciences, Harvard School of Dental Medicine, Boston, MA, United States.
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Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA.
Angiosarcomas are a group of vascular cancers that form malignant blood vessels. These malignancies are seemingly inflamed primarily due to their pathognomonic nature, which consists of irregular endothelium and tortuous blood channels. PIK3CA mutations are oncogenic and disrupt the PI3K pathway.
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Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
The objective of this omega-3 feeding study was to elucidate the independent effects of α-linolenic acid (ALA) versus eicosapentaenoic (EPA)/docosahexaenoic acid (DHA) on visceral adiposity and inflammatory signaling in diet-induced obese delta-6 desaturase (Fads2) knockout (KO) mice. Male wildtype (WT) and Fads2 KO mice were fed a high-fat diet (45% kcal from fat) containing either lard (no omega-3s), flaxseed (ALA), or menhaden (EPA/DHA) for 21 weeks. Epididymal white adipose tissue (eWAT) was analyzed for changes in tissue weight, adipocyte size, triacylglycerol (TAG) and fatty acid content, and inflammatory markers.
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Department of Anesthesiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-0033, Japan.
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