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《Journal of dairy science》2022,105(4):3588-3600
Fatty acid accumulation in hepatocytes induced by high concentrations of fatty acids due to lipolysis and the associated oxidative damage they cause occur most frequently after calving. Because of their role in esterification of fatty acids, diacylglycerol acyltransferase isoforms (DGAT1 and DGAT2) could play a role in the susceptibility of dairy cows to develop fatty liver. To gain mechanistic insights, we performed in vivo and in vitro analyses using liver biopsies or isolated primary hepatocytes. The in vivo study (n = 5 cows/group) involved healthy cows [average liver triacylglycerol (TAG) = 0.78%; 0.58 to 0.93%, ratio of triglyceride weight to wet liver weight] or cows diagnosed with fatty liver (average TAG = 7.60%; 5.31 to 10.54%). In vitro, hepatocytes isolated from 3 healthy female calves (1 d old, 44 to 53 kg) were challenged with (fatty acids) or without (control) a 1.2 mM mixture of fatty acids in an attempt to induce metabolic stress. Furthermore, hepatocytes were treated with DGAT1 inhibitor or DGAT2 inhibitor for 2 h followed by a challenge with (DGAT1 inhibitor + fatty acids or DGAT2 inhibitor + fatty acids) or without (DGAT1 inhibitor or DGAT2 inhibitor) the 1.2 mM mixture of fatty acids for 12 h. Data analysis of liver biopsies was compared using a 2-tailed unpaired Student's t-test. Data from calf hepatocyte treatment comparisons were assessed by one-way ANOVA, and multiplicity for each experiment was adjusted by the Holm's procedure. Data indicated that both fatty liver and in vitro challenge with fatty acids were associated with greater mRNA and protein abundance of SREBF1, FASN, DGAT1, and DGAT2. In contrast, mRNA and protein abundance of CPT1A and very low-density lipoprotein synthesis-related proteins MTTP and APOB were markedly lower. However, compared with fatty acid challenge alone, DGAT1 inhibitor + fatty acids led to greater mRNA and protein abundance of CPT1A and APOB, and greater mRNA abundance of SREBF1 and MTTP. Furthermore, this treatment led to lower mRNA abundance of FASN and DGAT2 and TAG concentrations. Compared with fatty acid challenge alone, DGAT2 inhibitor + fatty acids led to greater mRNA and protein abundance of CPT1A, MTTP, and APOB, and lower mRNA and protein abundance of SREBF1 and FASN. In addition, compared with control and fatty acids, there was greater protein abundance of GRP78 and PERK in both DGAT1 and DGAT2 inhibitor with or without fatty acids. Furthermore, compared with control and fatty acids, reactive oxygen species concentrations in the DGAT1 inhibitor with or without fatty acid group was greater. Overall, data suggested that DGAT1 is particularly relevant in the context of hepatocyte TAG synthesis from exogenous fatty acids. Disruption of both DGAT1 and DGAT2 altered lipid homeostasis, channeling fatty acids toward oxidation and generation of reactive oxygen species. Both DGAT isoforms play a role in promoting fatty acid storage into TAG and lipid droplets to protect hepatocytes from oxidative damage.  相似文献   
3.
为探讨热水处理后黄瓜果实在非低温贮藏环境放置期间果体温度及抗氧化系统的变化,该试验将热水处理(40℃、20 min)后的黄瓜果实在非低温贮藏环境[20℃,相对湿度(55±5)%]中放置不同时间(0、1、2、4、8 h),并同时测定其果体温度和抗氧化系统的变化。结果表明:热水处理后0 h黄瓜果体温度高达36.5℃,随后的0~1 h黄瓜果体温度急剧下降,1~2 h果体温度缓慢下降,2~8 h黄瓜果体温度下降并持续稳定在环境温度;同时,热水处理后在非低温贮藏环境中放置2~4 h黄瓜果实中超氧化物歧化酶、抗坏血酸过氧化物酶、过氧化氢酶的活性及抗坏血酸、谷胱甘肽的含量显著提高,而具有细胞毒性的H2O2和·O-2的含量则被显著抑制。此外,热水处理后放置2 h再进入低温贮藏环境的黄瓜果实在贮藏期间显示出低的冷害指数。因此,热水处理后应将黄瓜果实于室温下放置2 h左右,使黄瓜果实机体得以自我调节、抗氧化酶系统活性得以提高。  相似文献   
4.
过量饮酒会损害人体健康,目前酒精性肝病已经成为我国常见的肝病之一;食醋除了具有调味功能之外,前期大量的文献报道了其抑制血压升高、控制血糖、促进矿物质吸收等多种功能,但是对于其中发酵菌株的功能研究较少。最近研究报告指出,醋酸菌菌体能够作为全新的活性主体发挥新的功能,包括减轻酒精性肝损伤,对免疫调节和肠道菌群的调节等都有积极作用。该文主要对醋酸菌菌体的免疫调节、肠道菌群调节等全新保健功能及其作用机制进行综述介绍,有望为近一步探索醋酸菌保健功能、开发新型食醋产品提供理论指导。  相似文献   
5.
以天麻为主要原料配以西洋参、枸杞子制备天麻酒。采用天麻素、对羟基苯甲醇、人参皂苷Re、人参皂苷Rb1的溶出率之和为评价指标,在单因素试验的基础上,通过响应面试验设计探讨原料粒径、浸泡时间、料液比对天麻酒渗漉工艺的影响,并采用小鼠模型分析天麻酒对小鼠肝组织的影响。结果表明,天麻酒最佳渗漉工艺为:原料粒径50目、浸泡时间6 h、料液比1∶9(g∶mL)。在此优化条件下,4种功能成分的溶出率之和为3.59 mg/g。动物实验结果显示,天麻酒与普通酒相比能显著降低肝组织中的谷丙转氨酶、谷草转氨酶、丙二醛、白细胞介素-4、白细胞介素-6、肿瘤坏死因子-α和前列腺素E2,提高超氧化物歧化酶的活性(P<0.05),对因酒精摄入导致的肝损伤有减缓作用。  相似文献   
6.
研究了葛根枳椇子植物饮料对小鼠急性酒精性肝损伤的保护作用。采用一次性灌胃50%酒精的方法建立急性酒精性肝损伤模型,检测相关生化指标及肝组织形态,评价葛根枳椇子植物饮料的肝保护作用。与模型组比较,葛根枳椇子植物饮料中剂量组的小鼠血清中谷草转氨酶、谷丙转氨酶、总胆固醇、甘油三酯以及低密度脂蛋白水平显著降低至(19.17±6.22)U/L、(14.81± 4.61)U/L、(4.77±0.33)mmol/L、(1.92±0.24)mmol//L、(0.22±0.09)mmol/L,肝脏超氧化物歧化酶、谷胱甘肽过氧化物酶以及还原型谷胱甘肽的活性明显升高,丙二醇含量显著降低至(0.80±0.09)nmol/mg pro。葛根枳椇子植物饮料在一定程度上改善肝组织的病理变化,减轻脂肪变性及炎性细胞浸润。结果表明,葛根枳椇子植物饮料对小鼠急性酒精暴露后的肝组织具有一定的保护作用。  相似文献   
7.
《Journal of dairy science》2022,105(6):5420-5434
High circulating concentrations of fatty acids cause triacylglycerol (TAG) accumulation in hepatocytes of dairy cows, a common metabolic disorder after calving. Low secretion of apolipoprotein B (APOB) and very low density lipoprotein (VLDL) are thought to be the major factors for TAG accumulation in hepatocytes. Recent data in nonruminant models revealed that sortilin 1 (SORT1) is a key regulator of VLDL secretion in part due to its ability to bind APOB. Thus, SORT1 could play a role in the susceptibility of dairy cows to develop fatty liver. To gain mechanistic insights in vivo and in vitro, we performed experiments using liver biopsies or isolated primary hepatocytes. For the in vivo study, blood and liver samples were collected from healthy multiparous dairy cows (n = 6; 9.0 ± 2.1 d in milk) and cows with fatty liver (n = 6; 9.7 ± 2.2 d in milk). In vitro, hepatocytes isolated from 4 healthy female calves (1 d old, 42–51 kg) were challenged with (fatty acids) or without (control) a 1.2 mM mixture of fatty acids in an attempt to induce metabolic stress. Furthermore, hepatocytes were treated with empty adenovirus vectors (Ad-GFP) or SORT1 overexpressing adenovirus (Ad-SORT1) for 6 h, or SORT1 inhibitor for 2 h followed by a challenge with (Ad-GFP + fatty acids, Ad-SORT1 + fatty acids, or SORT1 inhibitor + fatty acids) or without (Ad-GFP, Ad-SORT1, or SORT1 inhibitor) the 1.2 mM mixture of fatty acids for 12 h. Data from liver biopsies were compared using a 2-tailed unpaired Student's t-test. Data from calf hepatocytes were analyzed by one-way ANOVA. Data revealed that both fatty liver and in vitro challenge with fatty acids were associated with greater concentrations of TAG and mRNA and protein abundance of SORT1, SREBF1, FASN, and ACACA. In contrast, mRNA and protein abundance of CPT1A and APOB, and mRNA abundance of MTTP were markedly lower. Compared with fatty acid challenge alone, SORT1 overexpression led to greater concentration of TAG and mRNA abundance of SREBF1, FASN, ACACA, DGAT1, and DGAT2, and protein abundance of SREBF1, FASN, and ACACA. In contrast, concentration of secreted VLDL-APOB and mRNA abundance of APOB and MTTP, and protein abundance of CPT1A, APOB, and MTTP were lower. Compared with fatty acid challenge alone, SORT1 inhibitor + fatty acids led to lower concentrations of TAG and mRNA abundance of SREBF1, FASN, and DGAT2, and protein abundance of FASN, ACACA, and DGAT1. Concentrations of secreted VLDL-APOB and mRNA abundance of CPT1A and protein abundance of CPT1A and APOB were greater. Overall, in vitro data suggested that greater SORT1 abundance induced by exogenous fatty acids caused a reduction in VLDL-APOB secretion and increased hepatocyte TAG synthesis. Such mechanism was also apparent in tissue from cows with fatty liver. Thus, targeted downregulation of hepatic SORT1 could represent a viable mechanism to unload lipid during conditions where the influx of fatty acids increases markedly.  相似文献   
8.
This study aimed to determine the main bioactive components of Cornus officinalis vinegar (COV) and assess the effects of COV on the body weight (BW) and hepatic steatosis in a nonalcoholic fatty liver disease (NAFLD) mouse model. Seven-week-old KM female mice were divided into five treatment groups: (1) Normal control (NC) group, (2) high fat diet (HFD) group, (3) low concentration treatment group (3.5% COV), (4) medium concentration treatment group (5.0% COV), and (5) high concentration treatment group (6.5% COV). Mice in the NC group were fed with a normal chow diet, and those in the other four groups were fed with a HFD known for causing obesity for 10 weeks. Then, mice in the three COV treatment groups were orally administered with COV once a day for 6 weeks. Results showed that the contents of loganin and morroniside in COV reached 16.82 and 51.17 µg/ml, respectively, and COV also contained multiple organic acids. COV significantly reduced BW, abdominal fat weight, liver weight, and the levels of glucose, triglyceride, and low-density lipoprotein cholesterol of serum and increased the levels of high-density lipoprotein cholesterol of serum (< 0.05). COV also improved the liver function and anti-oxidant activity of liver (< 0.05). COV treatments increased the interleukin-10 expression and reduced the tumor necrosis factor-α expression in the liver tissue of NAFLD mice (< 0.05). Histopathological observation revealed that COV suppressed hepatic lipid accumulation and steatosis. The results suggest that COV may contribute to the alleviation of NAFLD and obesity.  相似文献   
9.
目的:探究骆驼乳对慢性酒精性肝损伤小鼠肠道菌群多样性及结构的影响。将雄性C57BL/6NCr小鼠随机分为4组:对照组(Con,n=6)、模型组(Et,n=6)、骆驼乳剂量组(EtCM,n=6)和牛乳剂量组(EtNM,n=6);实验期为8周,前4周饲喂Lieber-DeCarli液体饲料(含对照),后4周在饲喂Lieber-DeCarli液体饲料的基础上,灌胃相应的乳或生理盐水。灌胃结束后,按照5 g/kg剂量一次性灌胃31.5%酒精溶液,建立NIAAA模型。检测血清LPS含量,并在无菌条件下取小鼠结肠粪便,进行16S rRNA测序,分析肠道菌群α多样性、β多样性及基于门、属水平的物种结构。血清指标结果显示,EtCM组和EtNM组小鼠血清LPS显著降低(P<0.01)。16S r RNA测序结果表明,骆驼乳和牛乳能显著提高ALD小鼠结肠肠道菌群的丰度和均匀度,更好地调整肠道菌群结构,其中骆驼乳较牛乳显示出更好的α多样性。在门水平上,骆驼乳和牛乳显著提高拟杆菌门的丰度,降低厚壁菌门的丰度。在属水平上,骆驼乳和牛乳显著提高副拟杆菌属、拟杆菌属、阿克曼菌属的丰度,降低瘤胃菌科下的未知属RuminococcaceaeUCG-013丰度。其中,骆驼乳的有益菌丰度较牛乳高出9%。结论:骆驼乳通过改变ALD小鼠肠道菌群环境,来调节肠道菌群结构,可作为调节肠道菌群的功能性乳制品,可预防慢性ALD引起的肠道屏障功能障碍。  相似文献   
10.
蔡卫超  曹卫红 《辐射防护》2022,42(2):111-118
机体受到意外照射或在接受放射治疗时会引起放射性皮肤损伤,皮肤组织中最先发生水分解而产生活性氧,其次呼吸链及炎症过程也会产生大量活性氧。活性氧作为信号分子在调控生理生化过程中起到了不可替代的作用。本文就辐射刺激后皮肤内活性氧变化、活性氧干预放射性皮肤损伤的机制以及活性氧消除调控放射性损伤等三个方面的研究进展进行综述,旨在联系活性氧代谢与放射性损伤的生理病理反应,为相关研究及临床治疗提供便利。  相似文献   
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