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Non-alcoholic fatty liver disease (NAFLD) is the emerging cause of chronic liver disease globally and lack of approved therapies. Here, we investigated the feasibility of combinatorial effects of low molecular weight fucoidan and high stability fucoxanthin (LMF-HSFx) as a therapeutic approach against NAFLD. We evaluated the inhibitory effects of LMF-HSFx or placebo in 42 NAFLD patients for 24 weeks and related mechanism in high fat diet (HFD) mice model and HepaRGTM cell line. We found that LMF-HSFx reduces the relative values of alanine aminotransferase, aspartate aminotransferase, total cholesterol, triglyceride, fasting blood glucose and hemoglobin A1c in NAFLD patients. For lipid metabolism, LMF-HSFx reduces the scores of controlled attenuation parameter (CAP) and increases adiponectin and leptin expression. Interestingly, it reduces liver fibrosis in NAFLD patients, either. The proinflammatory cytokines interleukin (IL)-6 and interferon-γ are reduced in LMF-HSFx group. In HFD mice, LMF-HSFx attenuates hepatic lipotoxicity and modulates adipogenesis. Additionally, LMF-HSFx modulates SIRI-PGC-1 pathway in HepaRG cells under palmitic acid-induced lipotoxicity environment. Here, we describe that LMF-HSFx ameliorated hepatic steatosis, inflammation, fibrosis and insulin resistance in NAFLD patients. LMF-HSFx may modulate leptin-adiponectin axis in adipocytes and hepatocytes, then regulate lipid and glycogen metabolism, decrease insulin resistance and is against NAFLD.  相似文献   
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蛹虫草是一种食药用真菌,具有重要的药用价值,已经成为近年来研究的热点。非酒精性脂肪肝(NAFLD)发病率随着人们生活水平的提高而逐年上升,人们不断寻求NAFLD的预防和治疗手段。已有研究报道,将蛹虫草用于NAFLD的治疗取得了很好的临床效果。从AMPK信号通路、固醇调节元件结合蛋白和炎症因子3个方面,概述蛹虫草活性成分在NAFLD治疗中发挥的作用机制,为蛹虫草资源的开发提供参考。  相似文献   
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Ecklonia cava (E. cava; CA) is an edible brown alga with beneficial effects in diabetes via regulation of various metabolic processes such as lipogenesis, lipolysis, inflammation, and the antioxidant defense system in liver and adipose tissue. We investigated the effect of the polyphenol-rich fraction of E. cava produced from Gijang (G-CA) on nonalcoholic fatty liver disease (NAFLD) in high-fat diet (HFD)-fed mice. C57BL6 mice were fed a HFD for six weeks and then the HFD group was administered 300 mg/kg of G-CA extracts by oral intubation for 10 weeks. Body weight, fat mass, and serum biochemical parameters were reduced by G-CA extract treatment. MRI/MRS analysis showed that liver fat and liver volume in HFD-induced obese mice were reduced by G-CA extract treatment. Further, we analyzed hepatic gene expression related to inflammation and lipid metabolism. The mRNA expression levels of inflammatory cytokines and hepatic lipogenesis-related genes were decreased in G-CA-treated HFD mice. The mRNA expression levels of cholesterol 7 alpha-hydroxylase 1 (CYP7A1), the key enzyme in bile acid synthesis, were dramatically increased by G-CA treatment in HFD mice. We suggest that G-CA treatment ameliorated hepatic steatosis by inhibiting inflammation and improving lipid metabolism.  相似文献   
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研究了普洱茶调控非酒精性脂肪肝大鼠肠道对长链脂肪酸的吸收,并探讨了其可能机制。将36只SD大鼠随机分成正常对照组、脂肪肝模型组和普洱茶干预组,每组12只。实验第8周末处死所有大鼠,测定大鼠体质量、肝指数及血清血脂水平;采用定量PCR测定大鼠肠道黏膜脂质吸收相关蛋白细胞分化抗原36(Cluster of differentiation 36,CD36)、紧密连接相关蛋白如闭锁蛋白(Occludin)、紧密连接蛋白(Zonula occludens 1,ZO-1)和肿瘤坏死因子α(Tumor necrosis factor-α,TNF-α)基因表达水平。研究结果表明,与模型组相比,普洱茶组大鼠体质量和血清LDL-C水平分别下降了16.12%和42.59%;此外,普洱茶组大鼠小肠组织CD36、TNF-α表达水平明显降低,而Occludin、ZO-1表达水平明显升高。研究发现,普洱茶对NAFLD大鼠肠道长链脂肪酸吸收及肠道紧密连接蛋白有一定程度的调控作用,尤其是对NAFLD早期发生发展中游离脂肪酸过度沉积的"第一次打击"有防治价值。  相似文献   
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通过肠道菌群改变研究青砖茶(GBT)对小鼠非酒精性脂肪肝(NAFLD)的预防作用.C57BL/6小鼠随机分为5组,即正常对照组(NC),模型对照组(MC),阳性药物对照组(PC)以及青砖茶低剂量组(LD)、高剂量组(HD),高脂饲料喂养小鼠建立NAFLD模型,同时预防性给予低、高剂量青砖茶水提取物和阳性药物血脂康,分别...  相似文献   
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为探讨茯砖茶对高脂诱导的非酒精性脂肪肝病(Non-alcoholic fatty liver disease,NAFLD)大鼠肠黏膜屏障及肝损伤的保护作用,将SD雄性大鼠随机分为正常组、NAFLD组、茯砖茶低、高剂量组,每组8只。通过分析大鼠的采食量、体重变化、血脂指标、肝脏指标及病理切片来评估NAFLD大鼠模型的构建情况及茯砖茶的干预作用。通过分析空肠与结肠病理及PAS染色切片、绒毛高度/隐窝深度值(V/C值)、血清二胺氧化酶(DAO)和脂多糖(LPS)活力评估肠道完整性和通透性;通过分析空肠上皮间淋巴细胞(JIL)数量和血清肿瘤坏死因子(TNF-α)活力评估肠道相关炎症。结果表明,茯砖茶能减少NAFLD大鼠的采食量和体重,降低血脂水平,减少血清中谷草转氨酶(AST)和谷丙转氨酶(ALT)活力,并抑制肝脏的脂质聚集和炎细胞浸润。茯砖茶还降低了血清炎症因子TNF-α和血清LPS的水平,并使血清DAO活力上升。同时,茯砖茶抑制了NAFLD大鼠空肠和结肠绒毛中发生的炎细胞浸润现象,减少了空肠绒毛脱落、断裂、稀疏和紊乱现象,增加了空肠绒毛V/C值,降低了空肠上皮间淋巴细胞数量,增加了空肠和结肠的杯状细胞数量。这些结果说明,茯砖茶能够有效的改善高脂饮食诱导的肠道黏膜屏障及肝损伤,起到防治NAFLD的作用。  相似文献   
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非酒精性脂肪肝是以肝实质细胞发生脂肪堆积和脂肪变性为主要特征,并伴随机体脂质代谢紊乱的一种获得性代谢疾病。以高脂饲料喂养大鼠,建立非酒精性脂肪肝大鼠模型;以低、中、高剂量(10、50、100 mg·kg-1)表没食子儿茶素没食子酸酯(EGCG)分别灌胃模型大鼠,探讨茶叶中EGCG对非酒精性脂肪肝大鼠的调脂保肝作用。结果表明,与模型组相比,EGCG能显著降低血清中甘油三酯(TG)、总胆固醇(TC)和低密度脂蛋白-胆固醇(LDL-C)含量,降低丙氨酸氨基转移酶(ALT)和天冬氨酸转氨酶(AST)活性水平,提高高密度脂蛋白-胆固醇(HDL-C)的含量,改善大鼠肝脏氧化应激状态。此外,肝脏病理切片显示,EGCG能减少肝细胞中脂滴的形成,同时脂质代谢相关基因表达量分析显示,EGCG能调理肝脏的脂质代谢。综合以上实验结果表明,EGCG能显著改善非酒精性脂肪肝大鼠的脂质代谢紊乱和脂肪性肝损伤。  相似文献   
8.
Fucoxanthin, a xanthophyll carotenoid abundant in brown algae, is reported to have several biological functions, such as antioxidant, anti-inflammatory, and anti-tumor activities, in mice. We investigated the effects and mechanisms of fucoxanthin in the mixture oleate/palmitate = 2/1(FFA)-induced nonalcoholic fatty liver disease (NAFLD) cell model in this study. The results showed that the content of superoxide dismutase in the FFA group was 9.8 ± 1.0 U/mgprot, while that in the fucoxanthin high-dose (H-Fx) group (2 μg/mL) increased to 22.9 ± 0.6 U/mgprot. The content of interleukin-1β in the FFA group was 89.3 ± 3.6 ng/mL, while that in the H-Fx group was reduced to 53.8 ± 2.8 ng/mL. The above results indicate that fucoxanthin could alleviate the FFA-induced oxidative stress and inflammatory levels in the liver cells. Oil red-O staining revealed visible protrusions and a significant decrease in the number of lipid droplets in the cytoplasm of cells in the fucoxanthin group. These findings on the mechanisms of action suggest that fucoxanthin can repair FFA-induced NAFLD via the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway and nuclear factor erythroid-2-related factor 2-mediated (Nrf2) signaling pathway, as well as by downregulating the expression of the Toll-like receptor 4-mediated (TLR4) signaling pathway. Fucoxanthin exhibited alleviating effects in the FFA-induced NAFLD model and could be explored as a potential anti-NAFLD substance.  相似文献   
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旨在初步分析血管紧张素转换酶2(ACE2)的激活剂二乙酰胺三氮脒(DIZE)对高脂饮食诱导大鼠非酒精性脂肪肝病(NAFLD)的保护作用。利用高脂饮食诱导建立大鼠NAFLD模型,分为空白组、模型组、DIZE和阳性药物(洛伐他汀LOV)组,观察记录其生长状况。试验至第10周,剖检所有大鼠,采血测定血浆生化指标,取其肝脏观制作切片察病理变化。结果显示:1)第4周起模型组大鼠体重显著高于空白组(P0.05),且血糖调节能力减弱,灌胃DIZE和LOV后大鼠增重得到控制,糖耐量有所恢复。2)与空白组相比,模型组大鼠血浆中甘油三酯(TG)、总胆固醇(TC)、总胆汁酸(TBA)含量和谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(AKP)和乳酸脱氢酶(LDH)活性极显著上升(P0.01),游离脂肪酸(NEFA)含量显著下降(P0.05)。灌胃DIZE和LOV后,TG、TC、AKP、LDH和TBA均极显著(P0.01)下降,ALT和AST活性显著下降(P0.05)。3)模型组大鼠肝组织中有大量脂肪滴,肝细胞发生脂肪变性,肝指数极显著高于空白组(P0.01);灌胃DIZE后,肝指数减小,肝脏病理损伤有所缓解。综上,DIZE对高脂饮食诱导的NAFLD大鼠有保护作用,可显著降低大鼠血脂水平,改善血糖调节能力,缓解肝脏脂肪蓄积和脂肪变性,但其相关机制有待进一步研究,为DIZE成为新的NAFLD治疗药物的开发提供了理论依据。  相似文献   
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