肝细胞坏死

  • 网络Hepatocellular necrosis;necrosis;necrosis of hepatocytes;hepatic cell necrosis
肝细胞坏死肝细胞坏死
  1. IL-6可以反映肝细胞坏死程度,可以作为判断肝功能的又一实验室指标。

    IL-6 level can reflect the hepatocellular necrosis degree and can be used as a laboratory marker to determine the liver function .

  2. 结果A组注药后48h血清天冬氨酸氨基转移酶、总胆红素、血氨和凝血酶原时间达最高峰,1周年生存率为17%,肝脏病理检查显示大量肝细胞坏死伴出血。

    Results In group A , the level of aspartate transaminase , total bilirubin , ammonia and prothrombin time reached to peak at 48h , and the 7-day survival rate was only 17 % . The postmortem liver specimens showed a severe hepatocellular necrosis with hemorrhage .

  3. 结果:B、C组再灌注后均无肝细胞坏死。

    Results No hepatocyte necrosis was found in groups B and C.

  4. C组肝细胞坏死较明显,D组上述改变明显减轻;

    These changes were markedly alleviated in group D with urinastatin treatment ( P < 0.05 , compared to groupC ) .

  5. 重型乙型病毒性肝炎患者血清IL-1、IL-6、TNF-α水平与肝细胞坏死程度密切相关,检测血清中IL-1、IL-6、TNF-α对判断病情危重程度和预后有重要意义。

    Detect serum IL-1 , IL-6 and TNF - α is helpful for judging the degree hepatitis and its prognosis .

  6. 结论TNFα、IL6和NO水平与肝细胞坏死程度、内毒素血症和自发性细菌性腹膜炎肾损害(SBPRI)密切相关。

    Conclusion The results showed TNF - α, IL-6 and NO were closely associated with the degree of hepatocyte necrosis , endotoxemia and SBP-RI .

  7. 光镜下检查显示,BDL组及PTX组均可见肝细胞坏死及增生,汇管区可见胆管扩张、胆汁淤积,肝坏死程度以BDL组为重。

    Microscope examination showed that liver cell necrosis was heavier in BDL group than that in PTX group . Bile was filled up in bile duck in both group .

  8. 乙型肝炎病毒(HBV)所致的肝细胞坏死,被认为是与人类白细胞抗原(HLA)有关的MHC限制的T细胞为主的免疫应答的结果。

    Hepatocellular injury during hepatitis B virus ( HBV ) infection is postulated ^ to result from an human leucocyte antigen ( HLA ) restricted T-cell host immune response against HBV antigens . However , it is not known if HBV itself can induce HLA expression on infected hepatocytes .

  9. 结论五灵胶囊能有效地对抗由CCl4的脂质过氧化作用所致的肝细胞坏死,能显著阻滞DGlaN诱导小鼠慢性肝损伤,明显地降低DGlaN、LPS诱导损伤原代大鼠肝细胞。

    Conclusion Wuling capsule could effectively restore necrotic liver cells induced by lipid-peroxide of CCl_4 , block chronic liver trauma in mice caused by D-GlaN , and restore the lesion of prototype hepatic cells induced by D-GlaN or LPS .

  10. 体外大鼠肝细胞坏死性损伤模型的建立

    Establishment of necrotic injured models of primary hepatocytes from rats

  11. 并可出现灶性肝细胞坏死和炎细胞浸润。

    Necrosis of focal hepatocytes and infiltration of inflammatory cells were also found .

  12. 肝细胞坏死、萎缩等是肝脏细粒棘球蚴病肝脏损伤的重要基础。

    These changes seem to be the major hepatic lesion in cystic echinococcosis .

  13. 各种病因引起的慢性肝炎,都具有肝细胞坏死、炎症及纤维化的病理特征。

    Kinds of chronic hepatitis have the symptom of liver cell putrescence , inflammation and fibrosis .

  14. 形态学观察显示柴胡合剂治疗组的肝细胞坏死及肝纤维化程度明显为轻,且脾脏结构破坏也较轻。

    Morphological study reveled that damage and fibrosis of the liver and spleen were slight in group C.

  15. 肝硬化是肝细胞坏死后,肝纤维化和肝细胞再生所致。

    Ongoing liver damage with liver cell necrosis followed by fibrosis and hepatocyte regeneration results in cirrhosis .

  16. 然而,肝细胞坏死和纤维化征象预示预后较差。

    Nevertheless , necrosis of liver cells and signs of fibrosis seem to indicate a serious prognosis .

  17. 肝脏组织HE染色及网状纤维染色提示单抗干预组小鼠肝细胞坏死程度及纤维化程度较轻。

    Milder liver necrosis and fibrosis was detected in treatment group by means of HE staining and reticular fiber staining .

  18. 研究背景重型肝炎发病率高,患者肝细胞坏死严重,预后差。

    Background Patients with severe hepatitis suffer from serious hepatocytes necrosis , high incidence and poor prognosis [ 4,27 ] .

  19. 结果:造模12周时,酒精组大鼠肝脏呈现重度脂肪变性,点片状肝细胞坏死及炎性细胞浸润,纤维条索形成;

    Results : Up to 12 weeks , marked hepatic fatty changes , inflammation , necrosis and fibrosis were observed in ethanol-fed rats .

  20. 其特征是血清谷丙转氨酶水平迅速升高,血清中含有大量细胞因子,肝脏出现白细胞浸润,肝细胞坏死和凋亡。

    Characterized by the rapid serum alanine aminotransferase levels increased and serum contains large amounts of cytokines , leukocyte infiltration in the liver , liver cell necrosis and apoptosis .

  21. 结果表明,海参脑苷脂可以明显降低血清转氨酶活性,有效调节大鼠肝脏氧化应激状态,显著改善肝细胞坏死,显示出良好的肝损伤保护作用。

    The results turns out that CSCC can attenuate liver damage in rats by reduction of the activities of serum aminotransferase , amelioration of hepatocyte necrosis and regulation of hepatic oxidative stress .

  22. 肝脏组织病理切片显示,模型组有炎细胞浸润,肝细胞坏死,与模型组相比,rhKD/APP小、中、大剂量组肝组织损伤程度较轻,且随着rhKD/APP剂量增加肝组织损伤程度逐渐减轻。

    The pathological results showed that there were inflammatory cells and hepatocellular necrosis in model group , the protective effects of rhKD / APP on hepatic injury showed linear relation to the drug dose .

  23. 随着肝脏病变的发展,肝细胞坏死,肝实质弥漫性结节再生,胶原纤维大量沉积,最终导致肝组织结构改变,发展为不可逆转的肝硬化。

    With the development of liver disease , liver cell necrosis , diffuse nodular regeneration of liver parenchyma and deposition of collagen fibers which ultimately caused the liver structural changes , eventually lead to cirrhosis .

  24. 对照组肝细胞坏死明显,肝细胞索排列紊乱,零星肝细胞间大量纤维母细胞增生,小胆管增生明显。

    The necrosis of liver cells of the matched group was obvious , the cords of liver cells were disorder . There were sporadic liver cells in hyperplasia of fibroblast , proliferation of the small bile duct was obvious .

  25. 注毒后小鼠行动迟缓,严重者死亡,解剖观察,发现肝脏无色泽,甚至有白色斑点,中毒导致肝细胞坏死。

    After toxin injection , the action of mice is slow , the severe cases even dead , anatomical observation found that liver became pale colored , even with white spots , indicating that poisoning can cause liver cell necrosis . 2 .

  26. 电镜检查结果显示,大蒜素11mg/kg组肝细胞坏死、自溶较模型组明显减轻,大蒜素22mg/kg组肝细胞接近正常。

    Electronic microscope examination showed that in garlicin 11 mg / kg group the liver necrosis and isophagy were less severe than that in the model group . The hepatic cells in garlicin 22 mg / kg group were as normal as that in negative control group .

  27. 结论:肝组织细胞坏死和凋亡在T1WI和T2WI上有明显的信号差异表现。

    Conclusion : There were significant different signal changes on conventional T1WI and T2WI on the groups of necrosis and apoptosis .

  28. 6周模型组肝细胞大量坏死,中央静脉及汇管区纤维隔形成,与4周模型组相比IL-1β及IL-1βR阳性细胞明显减少(P<0.01);

    In 6 week group the necrosis of hepatocytes was serious and the fibrotic septa formed around central vein and portal area . The positive cells of IL-1_ β and IL-1_ β R decreased obviously compared with that of 4 week group ( P < 0.01 ) .

  29. 结果:随着CHB肝细胞变性坏死及肝血管病变加重,bFGF在肝血管及肝窦壁表达强阳性率逐渐上升(P<001),部分固缩性肝细胞也示强阳性显色。

    Results The strongly positive rate of the expression of bFGF on hepatic vessels and hepatic sinusoidal walls increased accompanied with the exacerbation of degeneration , necrosis of hepatocytes and hepatic vascular diseases ( P < 0 01 ), and partial shrunken hepatocytes also showed strongly positive .

  30. 慢性乙型肝炎以肝细胞变性坏死明显;

    Chronic hepatitis B was marked by degenerative and necrotic liver cell .