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脂肪变性

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MethodsThe samples were pretreated utilizing the denaturalization of protein when heated, and the agglomerate of it in low temperature.

方法利用蛋白加热变性和低温凝聚的原理对样品进行预处理,分离样品中的蛋白质、脂肪。

The fat existence had the protective function to the protein denaturation.

脂肪的存在对蛋白质的变性具有保护作用。

Four detergents above mentioned didn't denature P450 of microsomes in midgut and fatbody at concentration of 0.5%.

在0.5%浓度下,四种去垢剂均未使中肠和脂肪体微粒体P450变性。

Objective:To detect the rat model of non-alcohol fatty liver disease the effect of medical intervention Methods: The Wistar rats were fed with high fatty chow for 12 weeks to induce NAFLD.And then,these rats were fed the low fatty chow,and separately intervened by Rhizoma polygoni cuspidate,Polyene phosphatidylcholine and metformin hydrychloride or controlled by distill water for 4 weeks.The total RNA of adipose tissue was extracted and reversely translated into cDNA.

Non-alcohol fatty liver disease;Intervention;Rhizoma polygoni cuspidatei;Polyene phosphatidylcholine;Metformin hydrychloride非酒精性脂肪肝病(Non-alcohol fatty liver disease,NAFLD)是无过量饮酒史的肝实质细胞脂肪积贮和变性的病理综合症,是由于肝脏本身和各种肝外因素引起的肝脏脂肪代谢功能障碍,导致肝细胞内脂类物质蓄积过多的一种病理变化,常见原因有营养缺乏、肥胖、糖尿病、妊娠、糖皮质激素、肝炎及药物或毒物的损伤等[1],发病机理尚未完全清楚。

The findings of the newly identified goose paramyxovirus strain GPMV/HBexperimental infection were as follows: The challenge caused high morbidity and highmortality.The clinical signs included severe depression, decreased appetite or anorexia,white,yellow and green diarrhea, with neural symptoms;pathological changes showed thathaemorrhage and ulceration of intestine mucosa, necrosis of spleen and pancreas,andedema of liver and kidney, uratic deposition in kidney.Eosinophilic inclusion bodies werefound in the cytoplasm of pancreas and a large quantities of fiber protein were found inintestine. Lots of hemosidefin was found in some area of liver and kidney. A number ofT、B lymphocytes reduced sharply in spleen,lymph nodes in dead geese. Transmissionalelectron microscope showed that some cells had the morphological characteristics ofmitochondria swelling, morphological changes were condensation of nuclear chromatininto dense masses,followed by its marginating against the nuclear envelope, andespecially concentration of cytoplasm association with lots of lipid droplet.

人工感染雏鹅实验中,雏鹅临床表现为高发病率和高死亡率,食欲和饮水减少,拉白色、黄绿色稀粪,伴有神经症状;常规组织学观察,脾脏和胰腺肿大,有白色坏死斑点,肠道出血和坏死,肝脏肿大变性,肾脏肿大变性有尿酸盐沉着等;用特殊染色和组织化学方法首次对人工感染鹅副粘病毒的雏鹅的重要脏器进行研究,结果表明:胰腺中发现病毒包涵体,肠道中大量纤维素以及胶原纤维增生,肾脏、肺脏大量含铁血黄素沉着,免疫器官如脾脏和淋巴结中T、B淋巴细胞大量减少;电镜下多种细胞呈现线粒体水肿,多种实质细胞的染色质固缩,染色质边集,特别是细胞内容物如脂肪滴增多的病理变化特征。

Results Model group rats had marked increase in ALT levels compared with normal group, and their liver tissue showed hepatocytes fatty degeneration,focal necrosis and inflammatory cells infiltration.

结果模型组大鼠血清ALT水平与正常对照组相比,显著升高,并且肝组织表现肝细胞中度脂肪变性,点状坏死,炎性细胞浸润。

Pathological observation showed that fatty degeneration and liver cell swelling were relieved in all the dosage groups, and were close to the normal level.

病理观察显示,番茄红素各剂量组脂肪变性及肝细胞肿胀程度减轻,接近正常水平。

Lobules of liver in the rats of model group was disorder with a pile of deposition of fibrous tissue, inflammatory cell infiltration and fatty degeneration of hepatocytes.

模型组大鼠肝小叶结构紊乱,有大量纤维组织沉积,炎症细胞浸润,肝细胞脂肪变性

There were many acidophil corpuscles in hepatic sinus.

Subacute severe hepatitis 1 肝细胞水肿,肝细胞亚大块坏死,纤维组织紊乱,肝窦内见许多嗜酸性小体,肝细胞及毛细胆管淤胆明显,肝细胞部分脂肪变性,汇管区充血,有炎症细胞浸润

There were many acidophil corpuscles in hepatic sinus.

Subacute severe hepatitis 1 肝细胞水肿,肝细胞亚大块坏死,纤维组织紊乱,肝窦内见许多嗜酸性小体,肝细胞及毛细胆管淤胆明显,肝细胞部分脂肪变性,汇管区充血,有炎症颈椎病细胞浸润

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