炎症刺激对新生仔猪铁含量 血清生化指标及Hepcidin基因表达量的影响

挑选刚出生杜长大三元杂交仔猪10头,随机分为对照组和脂多糖(LPS)刺激组,每组5头。LPS刺激组分别于3日龄、5日龄和7日龄时腹腔注射100μg/kg·bw LPS,建立炎症刺激模型;对照组仔猪分别在相同日龄注射相同体积生理盐水。7日龄时将所有仔猪全部处死,采集血清,并分离肝脏和脾脏.。结果表明,与对照组相比,LPS刺激可显著降低仔猪肝脏铁含量(P0.05),极显著降低血清铁含量(P0.01),但对脾脏铁含量无显著影响(P0.05)。LPS刺激显著降低了仔猪血清中总蛋白、球蛋白、总胆红素和葡萄糖含量(P0.05),显著提高了肝脏中Hepcidin mRNA表达量(P0.05)。表明LPS刺激可显著增加仔猪肝脏中Hepcidin mRNA表达量,因而降低机体铁含量。     

营养素对畜禽炎症表观遗传学的调控及其机制

炎症是动物机体对病原菌、损伤组织和刺激物等产生的有害刺激做出的一种生理性应答。炎症反应可通过调节多种炎症介质及信号通路最终影响炎症因子的表达。表观遗传学涉及非DNA序列改变引起的可遗传变化，主要包括DNA甲基化、组蛋白修饰和非编码RNA表达调控。表观遗传修饰可通过影响炎症反应中相关基因的表达来调节炎症反应，饲粮中能够影响表观遗传学修饰过程的营养素可调节炎症反应。本文主要综述了营养素调控炎症的表观遗传学机制———DNA甲基化和组蛋白修饰。     

动物铁缺乏症和铁中毒的症状与防治

1铁缺乏症 铁缺乏症是由于饲草料中铁含量不足或机体铁摄入量减少，引起动物以贫血和生长受阻为主要特征的营养代谢性疾病。铁缺乏症可发生于各种动物，常见于仔猪、犊牛、羔羊、鸡等。     

猪铁缺乏在饲料中的补充

铁缺乏症又称仔猪营养性贫血或仔猪缺铁性贫血,是由于机体铁缺乏而引起猪贫血和生长受阻的营养代谢病。临床上以血红蛋白含量降低、红细胞数减少以及皮肤、粘膜苍白为主要特征。多发于2～4周龄的哺乳仔猪,集约化猪场比较     

γ-氨基丁酸对LPS介导的机体炎性反应影响的研究进展

γ-氨基丁酸(γ-aminobutyric acid,GABA)是哺乳动物体内一种重要的神经性抑制递质,主要分布在中枢神经系统,具有广泛的调控功能。GABA可通过下丘脑-垂体-肾上腺皮质(HPA)轴参与机体稳态的调节,并对外界有害刺激引起的机体炎性反应具有一定的缓解作用。机体在外界应激条件刺激下会引起血液中脂多糖(LPS)含量的升高并激活Toll样受体-4(TLR4)/NF-κB信号通路,引起肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)等的表达增多,最终导致机体产生炎症反应。GABA可在机体发生炎症反应时,通过调节相应炎性因子的表达来降低炎症反应对机体造成的损伤。作者通过对GABA生理学功能与受体类别及GABA在机体发生炎性反应时的作用进行综述,对GABA在机体发生炎性反应时的影响及其与LPS引起的机体炎性反应之间的关系进行分析,为临床上采用GABA治疗机体炎性反应提供理论依据。     

γ-氨基丁酸对LPS介导的机体炎性反应影响的研究进展

γ-氨基丁酸（γ-aminobutyric acid，GABA）是哺乳动物体内一种重要的神经性抑制递质，主要分布在中枢神经系统，具有广泛的调控功能。GABA可通过下丘脑-垂体-肾上腺皮质（HPA）轴参与机体稳态的调节，并对外界有害刺激引起的机体炎性反应具有一定的缓解作用。机体在外界应激条件刺激下会引起血液中脂多糖（LPS）含量的升高并激活Toll样受体-4（TLR4）/NF-κB信号通路，引起肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-8（IL-8）等的表达增多，最终导致机体产生炎症反应。GABA可在机体发生炎症反应时，通过调节相应炎性因子的表达来降低炎症反应对机体造成的损伤。作者通过对GABA生理学功能与受体类别及GABA在机体发生炎性反应时的作用进行综述，对GABA在机体发生炎性反应时的影响及其与LPS引起的机体炎性反应之间的关系进行分析，为临床上采用GABA治疗机体炎性反应提供理论依据。     

仔猪缺铁的原因分析及防治措施

铁缺乏症又称仔猪营养性贫血或仔猪缺铁性贫血，是由于机体铁缺乏而引起猪贫血和生长受阻的营养代谢病。临床上以血红蛋白含量降低、红细胞数减少以及皮肤、黏膜苍白为主要特征。多发于2～4周龄的哺乳仔猪，集约化猪场比较容易发生本病，以冬春季节发病率较高。     

热应激诱导畜禽氧化应激、热休克反应与免疫和炎症反应的机制及营养调控措施

热应激会引起畜禽机体代谢增强,从而引起活性氧(ROS)的过量产生而发生氧化应激;氧化应激可启动热休克反应,上调热休克蛋白(HSPs)的转录与表达;ROS和HSPs两者都可以激活核转录因子-κB(NF-κB)进而启动免疫和炎症反应。本文综述热应激引起畜禽氧化应激反应、热休克反应与免疫炎症反应的机制及三者之间的相互关系,并在此基础上总结一些营养调控缓解热应激的措施,以期认识这3种反应在畜禽热应激营养调控过程中的意义。     

仔猪贫血的原因及防治对策

<正>仔猪贫血轻则导致生长发育不良,重则形成僵猪甚至死亡。在改善仔猪贫血状况时,应合理评估补铁与血红蛋白水平、断奶后健康状况、生产力水平间的关系,二次补铁对养殖者获得最佳生产效益有至关重要的作用。仔猪贫血系铁缺乏症的晚期表现,是指仔猪体内铁的储备不能满足正常红细胞生成的需要而产生的贫血,主要与铁摄入不足、吸收减少、需求增加和利用障碍等原因有关。引起仔猪贫血的因素很多,主要有机体营养、铁储     

运动性贫血的发生机制和防治措施

贫血会导致机体生理和病理性的损伤,运动性贫血将直接影响到运动员的机体和机能水平,通常引起血液中红细胞破坏增加;影响血红蛋白的合成,严重缺铁等现象,大大影响运动员们运动水平的正常发挥,通过给运动员补充多种不同元素,会有效地预防运动性贫血的发生。     

Expression of iron regulatory proteins in full-term swine placenta

In swine, even though the pregnant sows were with iron abundance, the inborn iron reserve of piglets was compromised. This indicates the insufficiency of molecular machinery involved in local placental iron flux. Here, we investigated the expression of iron regulatory proteins like hepcidin and ferroportin and also their association with iron reserve, inflammation and oxidative stress in placenta of full-term pregnant sows (n = 6). Amplification and sequencing of placental DNA confirmed the presence of hepcidin (MN579557) and ferroportin (MN565887) sequences and their 100% identity with existing GenBank data. Real-time amplification of placental mRNA revealed significant higher expression of hepcidin (p < .05) than ferroportin. Western blot analysis of placental tissues revealed specific bands for both hepcidin (~8 kDa) and ferroportin (~62 kDa) molecules. Immunohistochemistry revealed the immunoreactivity for both proteins in the cytoplasm and membrane of trophoblastic cells of the placenta. Hepcidin and ferroportin expressions were positively associated with placental non-haem iron reserve (p < .0001; p = .033), lipid peroxidation (p = .0060; p < .0001) and reactive oxygen species level (p = .0092; p = .0292). Hepcidin expression was positively associated with interleukin – 6 (p = .0002) and interferon gamma (p < .0001) expressions but ferroportin expression was negatively associated with interleukin-6 (p = .0005), interleukin-1β (p = .0226) and interferon gamma (p = .0059) expressions. This indicates hepcidin and ferroportin may have a role in controlling the local placental iron flux by acting as a molecular bridge between iron trafficking and inflammation.     

Identification, characterization and expression analysis of hepcidin gene in sheep

Hepcidin is part of the innate immune system, and it plays a central role in the regulation of iron homeostasis. This peptide has been previously characterized in man, non-human primates, rat, mouse, dog, swine, cattle, horse, fishes, reptiles and birds but until now not in sheep. The aim of this study was to sequence, characterize and perform hepcidin expression analysis in different tissues collected from healthy sheep. The resulting open reading frame consisted of 249 bp predicted to encode an 82 aa peptide with a putative 23 aa signal peptide, a 34 aa pro-region and the 25 aa mature hepcidin. The deduced sequence of the sheep hepcidin precursor was most homologous to Bos taurus and Bubalus bubalis. Hepcidin was predominantly expressed in liver, although high expression was present in abomasum and lower level expression occurred in other tissues. These findings extend our comparative knowledge showing the relationship of sheep hepcidin to other mammalian hepcidins and will be helpful for additional studies on iron metabolism and inflammatory processes in sheep.     

Studies of the pathogenesis of anemia of inflammation: mechanism of impaired erythropoiesis

Cats with induced sterile abscesses developed a hematologic disorder consistent with anemia of inflammation. Serum iron concentrations decreased while the abscess was present, but erythropoietin concentrations did not change significantly. Cobalt administration to control (healthy) cats resulted in polycythemia, reticulocytosis, and hyperferremia. Cats with abscesses responded to cobalt similarly; however, magnitudes of the polycythemia and reticulocytosis were less. Constant infusion of ferric citrate (IV) into cats with sterile abscesses maintained serum iron concentration in the normal to high range. The iron infusion did not prevent the anemia, but did enable the bone marrow to respond to the anemia.     

Hemochromatosis in Salers Cattle

Two 2-year-old Salers cattle from different herds raised on pasture were evaluated for retarded growth and diarrhea. Increase of liver enzyme activities and prolonged sulfobromophothalein (BSP) half life (T1/2) indicated liver disease with impaired liver function. Histopathologic examination of liver biopsies revealed a micronodular cirrhosis with marked deposition of hemosiderin in hepatocytes, Kupffer cells, and arterioles. Transferrin saturation (TS) and liver iron content were markedly increased, consistent with a diagnosis of hemochromatosis. Both animals were euthanatized due to deterioration in their condition. Necropsy findings included hepatomegaly and hemosiderin accumulation in the liver, lymph nodes, pancreas, spleen, thyroid, kidney, brain and other glandular tissue. Continued surveillance of the second herd (serum iron, total iron binding capacity [TIBC], unsaturated iron binding capacity [UIBC], and TS), identified a heifer as a hemochromatosis suspect in a subsequent generation. Liver biopsies from that animal revealed the same histopathologic changes as the previous 2 animals, and similar increases in liver iron content (8,700 ppm, normal range 45 to 300 ppm). The 3 affected cattle were all products of line breeding programs and shared a common ancestor. The absence of dietary iron loading in conjunction with the histopathologic and metabolic findings were consistent with a diagnosis of primary hemochromatosis. The reported disease is similar to idiopathic hemochromatosis in human beings in which there is a hereditary defect in iron metabolism.     

Anemia of inflammation in dogs infected with Ehrlichia platys

Ten adult male dogs were inoculated with Ehrlichia platys, and blood samples were collected throughout the infection to evaluate the hematologic changes with respect to serum biochemical analytes. All dogs developed a mild, normocytic, normochromic anemia by postinoculation day 7, with significantly (P less than 0.05) decreased serum iron concentration and total iron-binding capacity. Stainable bone marrow iron appeared normal or increased throughout the infection. By postinoculation day 31, the PCV was not significantly different from the pretreatment value. All dogs became hypergammaglobulinemic, leukopenic, hypoalbuminemic, and hypocalcemic during the infection. These findings were compatible with the syndrome of anemia of inflammation.     

Anemia with chronic renal disorder and disrupted metabolism of erythropoietin in ICR-derived glomerulonephritis (ICGN) mice

The ICR-derived glomerulonephritis (ICGN) mouse, a new inbred mouse strain with a hereditary nephrotic syndrome, is considered to be a good model of human idiopathic nephrotic syndrome and notably exhibits proteinuria and hypoproteinemia from the neonatal stage. In chronic renal disorder (CRD), anemia is a major subsequent symptom (renal anemia). The precise cause of renal anemia remains unclear, primarily owing to the lack of appropriate spontaneous animal models for CRD. To establish adequate animal models for anemia with CRD, we examined the hematological-biochemical properties and histopathological characteristics. With the deterioration of renal function, ICGN mice developed a normochromic and normocytic anemia, and exhibited normochromic and microcytic at the terminal stage. The expression of erythropoietin (EPO) mRNA both in the kidneys and liver and the EPO leak into the urine were observed in ICGN mice, indicating a disrupted metabolism of EPO in ICGN mice. In addition, a lack of iron induced by the hemolysis in the spleen and the leak of transferrin into urine as proteinuria aggravated the anemic condition. In conclusion, the ICGN mouse is a good model for anemia with CRD.     

Erythrocytes

Most anemias can be classified using the reticulocyte count, PCV, MCV, and MCHC. Regenerative anemias are characterized by reticulocytosis. Polychromasia and increased MCV usually are present. Hemolytic mechanisms and hemorrhage should be considered in a systemic evaluation of the blood and the patient. In animals with chronic external blood loss, a microcytic, hypochromic anemia develops secondary to iron deficiency. Nonregenerative anemias generally are characterized by normocytic, normochromic erythrocytes and the lack of reticulocytosis. Patients with nonregenerative anemia should be evaluated for chronic inflammation or neoplasia, renal disease, endocrine insufficiency, or hypoplasia of the bone marrow.