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- 저자 : ( DA Brenner ) (검색결과 3 건)
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( DA Brenner ) 대한간학회 2007 추계 학술대회 Vol.13 No.-
Hepatic fibrosis is an outcome of many chronic liver diseases and is characterized by excessive deposition of extracellular matrix (ECM) proteins, especially collagen type I. It is initiated by a cascade of events resulting in hepatocyte damage, recruitment of inflammatory cells to the injured liver, and activation of collagen-producing cells. Hepatic stellate cells (HSC) are a major source of collagen type I. In non-injured liver HSC remain quiescent. In response to injury they undergo activation into collagen-producing myofibroblasts. Cells other than HSC are also implicated in collagen production. Therefore, myofibroblasts originating from small portal vessels proliferate in response to injury and induce synthesis collagen. Moreover, several recent studies proposed that bone marrow derived myofibroblasts and fibrocytes also contribute to ECM deposition in the course of liver fibrosis. Liver injury instigates a complex cross-talk between many hepatic and non-parenchymal cells. Hepatocyte damage often serves as a triggering event in pathogenesis of liver fibrosis. Apoptotic hepatocytes release reactive oxygen species (ROS) and cytokines inducing recruitment of inflammatory cells (lymphocytes and macrophages). Moreover, they release soluble factors (tumor necrosis factor-α [TNF-α], fibroblast growth factor [FGF]), which promote HSC activation and collagen deposition. Activated HSC, in turn, secrete proinflammatory cytokines, up-regulate adhesion molecules and further accelerate recruitment of inflammatory cells. Meanwhile, resident macrophages (Kupffer cells) not only secrete ROS, but also produce profibrogenic cytokines (transforming growth factor [TGF]-β1), which stimulate both HSC and extravasations of white blood cells. Recruitment of T cells to the injured liver shifts local cytokine production towards T helper 2 (Th2) type responses, that is associated with fibrosis.
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Gisane Biacchi Gomes,Ana Denise Zazula,Leonardo Seidi Shigueoka,Rosangela Alquieri Fedato,Ana Beatriz Brenner Affonso da Costa,Luiz Cesar Guarita-Souza,Cristina Pellegrino Baena,Marcia Olandoski,Jose´ 한국식품영양과학회 2017 Journal of medicinal food Vol.20 No.1
Consumption of food products enriched with plant sterols and the use of ezetimibe reduce cholesterol absorption in the intestine and effectively reduce low-density lipoprotein (LDL) plasma levels. We evaluated the therapeutic effect of the ezetimibe+plant sterol association in patients with coronary artery disease still not reaching recommended lipid levels despite the use of statins. We performed a prospective open-label study with 41 patients with stable coronary disease and LDL >70 mg/dL. Patients were randomized into four groups for a 6-week treatment: the control (CT) group remained on the same statin therapy, the ezetimibe (EZ) group received 10 mg/day of ezetimibe, the plant sterol (PS) group received spread enriched with 2 g of plant sterols, and the ezetimibe+PS (EZ+PS) group received 10 mg/day EZ +2 g PS. Initial mean LDL level was 97.4 ± 31.1 mg/dL in control group, 105.1 ± 23.1 mg/dL in EZ group, 95.4 ± 27.7 mg/dL in PS group, and 97.0 ± 8.3 mg/dL in EZ+PS group (P > .05). After 6 weeks of treatment, LDL of patients slightly increased in the control group (+8.9%; P > .05) and dropped in EZ group (-19.1%; P = .06), PS group (-16.6%; P = .01), and EZ+PS group (-27.3%; P < .01). Mean LDL levels after treatment were 70.5 – 17.9 mg/dL in EZ+PS group, lower than the other groups (control was 106.1 ± 34.9 mg/dL, EZ group was 85.0 ± 35.6 mg/dL, and PS was 79.6 ± 29.7 mg/dL) (P = .05 variance analysis factor [ANOVA]). Body weight, body–mass index, and glucose plasma levels did not change significantly after intervention. The combination of PS+ezetimibe was associated with lower LDL levels and suggests beneficial therapeutic effect against major cardiovascular events.
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