虎茵汤对小鼠急性肝损伤MDA、GSH—Px及SOD的影响

目的：观察虎茵汤对四氯化碳（CCl4）致小鼠急性肝损伤MDA、GSH－Px及SOD的变化。方法：采用腹腔注射CCl4致小鼠急性肝损伤为模型，联苯双酯作为阳性对照药物，测定高、低剂量的虎茵汤对肝损伤时MDA的含量，GSH－Px活性。结果：虎茵汤能够明显降低CCl4致小急 急怀肝损伤肝组织中MDA含量（P＜0．01），提高GSH－Px、SOD活力（P＜0．05），说明虎茵汤对肝脏损伤具有明显的保护作用。     

紫草大黄合剂对四氯化碳致小鼠急性肝损伤保护作用的观察

目的：观察不同浓度的紫草大黄合剂对四氯化碳（CCl4）致小鼠急性肝损伤的保护作用。方法：采用腹腔注射CCl4致小鼠急性肝损伤为模型，测定高低剂量的紫草大黄合剂对肝损伤ALT、AST值，同时对肝组织进行病理组织检查。结果：高剂量紫草大黄合剂同联苯双酯一样能够明显降低CCl4致小鼠肝损伤血清ALT、AST值升高（P＜0．01），减轻CCl4对肝脏细胞的病理损伤。结论：紫草大黄合剂对CCl4致急性肝损伤具有一定的保护作用。     

复方茵虎汤对实验性肝损伤的保护作用

目的：本实验研究复方茵虎汤（复方茵虎汤）对四氯化碳致小鼠肝损伤的保护作用。方法：以腹腔注射四氯化碳（CCl4）建立小鼠肝损伤模型,以复方茵虎汤作为受试药物,以联苯双酯作为阳性对照药物,以肝指数（LJI）、血清中谷氨酸氨基转移酶（ALT）、天冬氨酸转氨酶（AST）、肝组织匀浆中超氧化物歧化酶（SOD）和丙二醛（MDA）水平为检测指标,观察复方茵虎汤对肝损伤的保护作用。结果：复方茵虎汤能够明显降低CCl4致小鼠肝损伤血清中ALT和AST水平,升高肝组织中SOD水平,降低肝组织中MDA水平,减轻四氯化碳对肝脏细胞的病理损伤。结论：复方茵虎汤对CCl4致小鼠急性肝损伤有一定的保护作用。     

还原型谷胱甘肽对小鼠急性肝损伤的保护作用

目的：观察还原型谷胱甘肽对急性肝损伤的保护作用。方法：用D－氨基半乳糖及四氯化碳致小鼠急性肝损伤，还原型谷胱甘肽分别采用灌胃及腹腔注射给药，观察指标为：ALT、AST、ALP及肝脏病理形态。结果：还原型谷胱甘肽组小鼠肝细胞肿胀、胞浆疏松、炎症细胞浸润程度明显较D－氨基半乳糖组轻。结论：还原型谷胱甘肽对急性肝损伤有保护作用。     

木通皂苷D对CCl4致小鼠急性肝损伤的保护作用

目的研究木通皂苷D对CCl4致小鼠急性肝损伤的保护作用。方法采用CCl4急性肝损伤模型,小鼠ig给予不同剂量的木通皂苷D(1、0.5、0.25 g·kg-1),并以水飞蓟素(0.2 g·kg-1)为阳性对照药,采用比色法检测小鼠血清的天冬氨酸转氨酶(AST)、丙氨酸氨基转移酶(ALT)及肝脏中还原性谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物歧化酶(SOD)的含量。结果各剂量木通皂苷D能显著降低CCl4所致小鼠血清中AST、ALT的水平(P<0.01),同时升高肝脏组织中GSH、SOD的水平(P<0.05),降低肝脏组织中MDA的含量(P<0.05)。结论木通皂苷D对CCl4所致小鼠急性肝损伤具有显著的保护作用,其机制可能与抗氧化作用有关。     

Hepatoprotective effect of akebia saponin D on the acute liver injury induced by CCl4 in mice

目的 研究木通皂苷D对CCl4致小鼠急性肝损伤的保护作用.方法 采用CC14急性肝损伤模型,小鼠ig给予不同剂量的木通皂苷D(1、0.5、0.25 g·kg-1),并以水飞蓟素(0.2 g·kg-1)为阳性对照药,采用比色法检测小鼠血清的天冬氨酸转氨酶(AST)、丙氨酸氨基转移酶(ALT)及肝脏中还原性谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物歧化酶(SOD)的含量.结果 各剂量木通皂苷D能显著降低CCl4所致小鼠血清中AST、ALT的水平(P＜0.01),同时升高肝脏组织中GSH 、SOD的水平(P＜0.05),降低肝脏组织中MDA的含量(P＜0.05).结论 木通皂苷D对CCl4所致小鼠急性肝损伤具有显著的保护作用,其机制可能与抗氧化作用有关.     

清肝利胆浸膏保肝、利胆的实验研究

目的：观察清肝利胆浸膏对急性肝损伤的保护作用和利胆、退黄作用。方法：用CCL4－和D－GaL致小鼠急性肝损伤，观察血清ALT和AST；用麻醉大鼠胆管收集胆汁，测定胆汁中胆固醇和总胆红素的含量；用异硫氰酸－1－萘酯造成黄疸模型，测定血液中ALT和AST、总胆红素。结果：清肝利胆浸膏能显著降低CCL4致小鼠ALT和AST升高，对D－GaL致小鼠ALT和AST升高亦有明显降低，对大鼠胆汁分泌有增加，对胆汁成份胆固醇、总胆红素升高有明显的降低。结论：清肝利胆浸膏具有一定的保肝降酶、利胆和退黄作用。     

人工发酵虫草菌粉及其提取物保肝作用的研究

目的 观察人工发酵虫草菌粉及其提取物对实验性肝损伤的保护作用。方法 分别采用D-氨基半乳糖(D—G1aN)和四氯化碳(CCl4)致小鼠急性实验性肝损伤，测定血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)的含量及肝组织切片病理观察。结果 对D—G1aN致小鼠急性肝损伤，人工发酵虫草菌粉及其提取物可使升高的ALT降低(P＜0．01)，病理检查显示有明显保肝作用，对AST作用不明显；而对CCl4致小鼠急性肝损伤，仅菌粉和其提取物高剂量组有一定的降ALT作用。结论 人工发酵虫草菌粉及其提取物有一定保肝作用。     

清开灵注射液对四氯化碳致小鼠急性肝损伤的保护机制研究

目的：观察清开灵注射液对小鼠急性肝损伤的保护作用,并阐明其可能机制.方法：建立小鼠CCl4急性肝损伤模型,观察清开灵注射液对CCl4诱导升高的小鼠血清ALT、AST活性影响,及对肝脏病理损伤的保护作用;测定肝组织中丙二醛（MDA）含量及超氧化物歧化酶（SOD）活性.结果：与阴性对照组比较,模型组小鼠ALT和AST均显著升高（P＜0.01）,MDA明显增加（P＜0.01）,SOD显著降低（P＜0.01）,组织病理损伤明显.与模型组比较,清开灵注射液中剂量组（10 ml·kg^-1）和高剂量组（20 ml·kg^-1）均能显著降低肝损伤小鼠的ALT和AST（P ＜0.05 或0.01）,并明显减轻了肝脏组织的病理损伤.清开灵注射液低剂量组（5 ml· kg^-1）、中剂量组和高剂量组的MDA均较模型组显著降低（P＜O.05或0.01）,SOD水平则显著升高（P＜0.05或0.01）.结论：清开灵注射液对小鼠CCl4致急性肝损伤的保护作用可能与其抗脂质过氧化作用有关.     

五味子藤茎中木脂素对四氯化碳致小鼠急性肝损伤的保护作用

目的：探讨五味子藤茎中木脂素对四氯化碳（CCl4）致小鼠急性肝损伤的保护作用。方法：采用CCl4致小鼠急性肝损伤模型,观察五味子藤茎中木脂素对小鼠血清ALT、AST活性及肝组织匀浆超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-Px）水平的影响,同时观察肝组织病理学改变。结果：五味子藤茎中木脂素能明显降低血清ALT、AST水平,降低肝匀浆MDA的含量,提高SOD、GSH-Px活力,肝脏病理损伤有明显改善。高剂量组抗肝损伤作用与联苯双酯阳性对照组相当。结论：五味子藤茎中木脂素对CCl4致小鼠急性肝损伤具有一定的保护作用,其作用机制与其抗氧化作用有关。     

Hepatoprotection by human epidermal growth factor (hEGF) against experimental hepatitis induced by D-galactosamine (D-galN) or D-GalN/lipopolysaccharide

The hepatoprotecive effects of recombinant human epidermal growth factor (hEGF) on chemically and immunologically induced experimental liver injury models were examined. The hEGF clearly decreased serum transaminase levels in D-galactosamine (D-GalN) and D-GalN/lipopolysaccharide (LPS)-induced liver injury models under sub-lethal conditions. However, it has not significantly changed either serum or in vitro tumor necrosis factor (TNF)-alpha production or in vitro nitric oxide (NO) production, suggesting that the hepatoprotection by EGF is not mediated by inhibiting these pathological mediators produced in D-GalN and D-GalN/LPS-induced liver injury.     

茵栀黄颗粒的急性毒性和保肝作用研究

目的　检测茵栀黄颗粒的急性毒性和保肝作用。方法　采用灌胃给药观察茵栀黄颗粒对四氯化碳 (CCl4)所引起的小鼠急性肝损伤的影响及其急性毒性 ,给药后观察动物摄食、活动、中毒症状并记录死亡动物数。结果小鼠一次性灌胃给药 ,茵栀黄颗粒的最大耐受量为 32 g·kg-1。茵栀黄颗粒能明显降低CCl4和D -氨基半乳糖 (D -GalN)所致肝损伤小鼠血清ALT、AST。结论　茵栀黄颗粒为低毒药物 ,对CCl4和D -GalN所致肝损伤具有保护作用     

Immunomodulatory activity of TNF-alpha during acute liver injury induced by D-galactosamine and its protection by PGE1 in rats

Tumour necrosis factor-alpha (TNF-alpha) mediates hepatocyte cell death by D-galactosamine (D-GalN) and its protection by prostaglandin E(1) (PGE(1)). The activation of immune system plays an important role in the development of liver injury. TNF-alpha and PGE(1) regulate the activity and cytokine release of different inflammatory cells. The present study was undertaken to determine if the noxious or hepatic protective properties of TNF-alpha during D-GalN-induced liver injury was related to an alteration by PGE(1) of the immunoregulatory activity of TNF-alpha. The role of TNF-alpha was assessed by anti-TNF-alpha antibodies to D-GalN-treated rats in the presence or absence of PGE(1). D-GalN enhanced the percentage of monocytes and T lymphocytes in the total peripheral blood mononuclear cells (PBMCs). D-GalN enhanced the activation degree of monocytes, but reduced that of T lymphocytes. D-GalN also enhanced TNF-alpha, IL-1alpha, IL-6 and IFN-gamma concentrations in blood. Anti-TNF-alpha antibodies abolished all immunological changes and greatly reduced liver damage induced by D-GalN. The protection by PGE(1) against D-GalN liver injury was associated with an increase in TNF-alpha concentration and a reduction of IL-1alpha and IL-6. These changes were associated with a reduction of monocyte activation degree and a recovery of that of T lymphocytes. Although anti-TNF-alpha antibodies abolished the protection by PGE(1) against D-GalN-liver injury, they did not essentially counteract the effect of the prostanoid in all immunological parameters studied. The present study showed that the protection against D-GalN liver damage by PGE(1) or anti-TNF-alpha was associated with similar effects on the inflammatory parameters studied. Nevertheless, the abolishment of liver protection by PGE(1) with anti-TNF-alpha in D-GalN-treated rats in the presence of a protective cytokine profile suggests that the release of TNF-alpha induced by PGE(1) pre-administration was exerting a direct protective effect on hepatocytes against D-GalN injury. Consequently, the effect of PGE(1) on inflammatory parameters studied during liver injury was unrelated to TNF-alpha.     

6,7-二乙酰黄芩素对四氯化碳和D-氨基半乳糖所致的急性肝损伤的保护作用

目的:研究6,7-二乙酰黄芩素对四氯化碳(CCl4)和D-氨基半乳糖(D-GalN)所致急性肝损伤的保护作用。方法:分别用CCl4和D-GalN诱导化学性急性肝损伤模型,测定血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)水平;并用苏木素-伊红(HE)染色处理肝脏组织切片,光镜观察病理学改变;用试剂盒测定肝线粒体中AST,SOD和GSH-PX的活性及脂质过氧化产物MDA含量。结果:在CCl4和D-GalN诱导和的小鼠肝急性损伤模型中,6,7-二乙酰黄芩素给药(50,100 mg.kg-1,ig)明显降低血清ALT,AST水平;明显改善肝脏病理组织状况;6,7-二乙酰黄芩素给药(25,50,100 mg.kg-1,ig)明显降低CCl4诱导的肝急性损伤小鼠的肝线粒体中AST活性和MDA的含量,显著增加SOD和GSH-PX的活性。结论:6,7-二乙酰黄芩对CCl4和D-GalN诱导和的小鼠肝急性损伤均具有保护作用,该作用与其增加线粒体中抗氧化酶的酶的活性、降低脂质过氧化水平有关。     

Protective effect of baicalin against lipopolysaccharide/D-galactosamine-induced liver injury in mice by up-regulation of heme oxygenase-1

Baicalin, a traditional anti-inflammatory drug, has been found to protect against liver injury in several experimental animal hepatitis models; however, the mechanisms underlying the hepatoprotective properties of baicalin are poorly understood. In the present study,we investigated the effects of baicalin on the acute liver injury in mice induced by Lipopolysaccharide/D-galactosamine (LPS/D-GalN). Baicalin (50, 150, and 300 mg/kg) was pretreated intraperitoneally (i.p.) at 2, 24, and 48 h respectively before LPS/D-GalN injected in mice.The mortality, hepatic tissue histology, hepatic tissue Tumor necrosis factor-alpha (TNF-alpha) and myeloperoxidase (MPO), plasma levels of TNF-alpha and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed. Besides, western blotting analyses of nuclear factor kappa B (NF-kappaB) translocation and Heme oxygenase-1(HO-1) protein expression, as well as HO-1 activity were determined. The results showed that baicalin protected against LPS/D-GalN-induced liver injury, including dose-dependent alleviation of mortality and hepatic pathological damage, decrease of ALT/AST release and the rise of MPO. Baicalin reduced nuclear translocation of NF-kappa B, TNF-alpha mRNA and protein levels in hepatic tissues and plasma levels of TNF-alpha induced by LPS/D-GalN. Moreover, baicalin dose-dependently increased HO-1 protein expression and activity. Further, inhibition of HO-1 activity significantly reversed the protective effect of baicalin against LPS/D-GalN-induced liver injury. These results suggest that baicalin can effectively prevent LPS/D-GalN-induced liver injury by inhibition of NF-kappa B activity to reduce TNF-alpha production and the underlying mechanism may be related to up-regulation of HO-1 protein and activity.     

异甘草酸镁对D-氨基半乳糖急性肝损伤模型小鼠的保护作用研究

目的研究异甘草酸镁对D-氨基半乳糖急性肝损伤模型小鼠的保护作用。方法以D-氨基半乳糖建立小鼠急性肝损伤模型,分别设正常对照组、病理模型组、异甘草酸镁高、低剂量组以及美能组、易善复组、凯西莱组,测定各组小鼠血清中丙氨酸氨基转移酶(ALT)、天门冬酸氨基转移酶(AST)活性及肝组织中丙二醛(MDA)、黄嘌呤氧化酶(XOD)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、总抗氧化能力(T-AOC)、一氧化氮(NO)、一氧化氮合成酶(NOS)、诱生型一氧化氮合酶(iNOS)含量。另以HE染色,采用光镜对各组小鼠肝脏作病理检查。结果异甘草酸镁可明显降低ALT、AST的活性(P<0.01)及肝组织中MDA、XOD、NO、NOS、iNOS的含量;升高肝组织中SOD、GSH-PX、T-AOC的含量。光镜下可观察到异甘草酸镁能减轻小鼠肝脏坏死性病理改变。结论异甘草酸镁对D-氨基半乳糖诱导的小鼠急性肝损伤具有良好的保护作用。     

乙酸钠对D-GalN/LPS所致内毒素休克的保护作用

目的研究乙酸钠(NaAc)对小鼠急性肝损伤的保护作用及药理机制。方法分别用不同剂量的NaAc 2.50、2.30、2.00、1.75 g/kg对受试动物预处理30 min,然后腹腔注射D-氨基半乳糖/脂多糖(D-GalN/LPS)诱导小鼠急性肝衰竭,观察肝脏组织结构的变化,测定血清ALT活性及一氧化氮(NO)的含量。结果 NaAc预处理可显著降低动物死亡率,明显抑制血清ALT活性,降低NO的产生,减轻肝组织损伤。结论 NaAc对D-GalN/LPS诱导的急性肝损伤具有显著的保护作用。     

护肝降酶口服液对小鼠急性肝损伤的保护作用

目的：探讨护肝降酶口服液(HGJMKFY)对小鼠急性肝损伤的保护作用。方法：采用四氯化碳(carbontetrachloride,CCl4)、D-半乳糖胺(D-galactosamine,D-GaIN)复制小鼠急性肝损模型。给予护肝降酶口服液(分大、小剂量组),并设联苯双酯阳性对照及空白对照组。测定血清中丙氨酸氨基转移酶(alanineaminotransferase,ALT)、天门冬氨酸氨基转移酶(aspartate aminotransferase,AST)的水平。结果：护肝降酶口服液36g/kg剂量组对CCl4所致的小鼠急性肝损ALT和AST升高有明显降低作用;其36g/kg和18g/kg剂量组对D-半乳糖胺所致的小鼠急性肝损血清ALT和AST的升高均有明显降低作用。结论：护肝降酶口服液对CCl4、D-GaIN所致小鼠急性肝损伤有一定保护作用。     

鹅不食草煎液对小鼠肝损伤的保护作用

目的:观察鹅不食草煎液对小鼠3种肝损伤模型的保护作用.方法:采用四氯化碳(CCl4)、对乙酰氨基酚(APAP)、D-氨基半乳糖 脂多糖(D-GalN LPS)致3种小鼠肝损伤模型,测定血清谷丙转氨酶(ALT).结果:鹅不食草煎液能明显降低CCl4,APAP,D-GalN LPS引起的肝损伤后小鼠血清中升高的ALT水平.结论:鹅不食草煎液对实验性肝损伤有明显的保护作用.