Protective effects of 5,4'-dihydroxy-3',5'- dimethoxy-7-O-β-D -glucopyranosyloxy-flavone on experimental hepatic injury

AIM: To investigate the pharmacological effects of rice flavone (5,4'-dihydroxy-3',5'-dimethoxy-7-0-β-D-glucopyranosyloxy-flavone, RF) separated from panicle-differentiating to flowing rice on rat experimental hepatic injury. METHODS: Models of rat acute hepatic injury induced by carbon tetrachloride (CCl4) administration, rat hepatic fibrosis induced by thioacetamide, injury of primary cultured rat hepatocytes induced by CCl4, respectively, were established. After treated with RF, content of serum alanine transaminase (ALT), aspartate aminotransferase (AST) and albumin (Alb), hyaluronic acid (HA), the activity of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and hydroxyproline (Hyp) were measured and liver tissue was observed pathologically by hematoxylin-eosin (HE) staining. Effects of RF on pathological changes, function index, enzyme of scavenging free radicals and blood rheology were evaluated. RESULTS: In model of rat acute hepatic injury induced by CCI4, RF can significantly decrease the contents of serum ALT, AST, increase the content of Alb, improve the dropsy and fat denaturalization of hepatocytes. In model of rat hepatic fibrosis induced by thioacetamide, RF can inhibit the increase of HA, Hyp and whole blood viscosity, and improve the activities of GSH-Px and SOD, and inauricular microcirculation. CONCLUSION: RF has apparent protective effects on hepatic injury by increasing activity of GSH-Px and SOD, scavenging free radicals produced by CCI4, reducing blood viscosity, and improving microcirculation and blood supply.

The new antioxidant 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2- dihydroquinoline has a protective effect against carbon tetrachloride-induced hepatic injury in rats

Liver diseases with the central pathogenetic mechanism of oxidative stress are one of the main causes of mortality worldwide.Therefore,dihydroquinoline derivatives,which are precursors of hepatoprotectors and have antioxidant activity,are of interest.We have previously found that some compounds in this class have the ability to normalize redox homeostasis under experimental conditions.Here,we initially analyzed the hepatoprotective potential of the dihydroquinoline derivative 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline(BHDQ)for carbon tetrachloride(CCl4)-induced liver injury in rats.Results suggested that BHDQ normalized the alanine aminotransferase,aspartate aminotransferase,and gamma-glutamyl transpeptidase in serum.We also observed an improvement in liver tissue morphology related to BHDQ.Animals with CCl4-induced liver injuries treated with BHDQ had less oxidative stress compared to animals with CCl4-induced liver injury.BHDQ promoted activation changes in superoxide dismutase,catalase,glutathione peroxidase,glutathione reductase,and glutathione transferase on control values in animals with CCl4-induced liver injury.BHDQ also activated gene transcription in Sod1 and Gpx1 via nuclear factor erythroid 2-related factor 2 and forkhead box protein O1 factors.Therefore,the compound of concern has a hepatoprotective effect by inhibiting the development of necrotic processes in the liver tissue,through antioxidation.

Effect of hepatocyte growth factor on inflammatory factors associated with CCL_(4)-induced hepatocyte injury

Objective:The aim of this study is to investigate the effects of Hepatocyte Growth Factor(HGF)on the expression levels of IL-8,TNF-α,IL-4,and IL-21 in mice with liver injury induced by CCL_(4).Methods:An acute liver injury mouse model was established using CCL_(4),and hepatocytes and white blood cells were separated by gradient density centrifugation.Different concentrations of HGF were added in vitro,and the expression levels of cytokines were detected using ELISA.Results:In the in vivo injury model,the hepatocyte experiment results showed that the expression level of IL-8 was reduced in the 10 ng/mL HGF group compared to the injured hepatocyte group(P<0.05),and increased in the 50 ng/mL HGF group compared to the 10 ng/mL HGF group(P<0.05).For IL-4,the expression levels were reduced in both the 25 ng/mL HGF group(P<0.05)and the 50 ng/mL HGF group(P<0.05)compared to the injured hepatocyte group.The white blood cell experiment results showed that the expression levels of TNF-αwere reduced in both the 10ng/ml HGF group(P<0.05)and the 25 ng/mL HGF group(P<0.05)compared to the injured white blood cell group.In the in vitro injury model,hepatocyte experiment results showed that the expression levels of TNF-αwere reduced in both the 25 ng/mL HGF group(P<0.05)and the 50 ng/mL HGF group(P<0.05)compared to the normal control group.For IL-4,the expression level was reduced in the 25 ng/mL HGF group compared to the normal control group(P<0.05).The white blood cell experiment results showed that the expression level of TNF-αwas increased in the 50 ng/mL HGF group compared to the 10 ng/mL HGF group(P<0.001);for IL-21,the expression levels were reduced in the CCL_(4) model group(P<0.05),10 ng/mL HGF group(P<0.05),25 ng/mL HGF group(P<0.05),and 50 ng/mL HGF group(P<0.05)compared to the normal control group.Conclusion:when the liver of mice is acutely damaged by CCL_(4),HGF can reduce the expression levels of inflammatory cytokines IL-8,TNF-α,IL-4 in hepatocytes,and TNF-αin liver white blood cells.

基于TGF-β1/Smads信号通路探讨2-十二烷基-6-甲氧基-2,5-二烯-1,4-环己二酮抗肝纤维化的作用机制

目的探讨2-十二烷基-6-甲氧基-2,5-二烯-1,4-环己二酮(2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione,DMDD)对CCl_(4)致大鼠肝纤维化的影响及潜在作用机制。方法采用50%CCl_(4)复制肝纤维化模型,检测血液中门冬氨酸转移酶(aspartate transferase,AST)、丙氨酸转移酶(alanine transferase,ALT)、白蛋白/球蛋白(albumin/globulin,A/G)、总蛋白(total protein,TP)、总胆红素(total bilirubin,T-BIL)、大鼠透明质酸(hyaluronic acid,HA)、层黏连蛋白(laminin,LN)、Ⅲ型胶原(collagen typeⅢ,ColⅢ)和Ⅳ型胶原(collagen typeⅣ,ColⅣ)。HE和Masson染色观察肝脏组织病变和纤维形成情况。免疫组织化学法检测肝脏组织中α平滑肌肌动蛋白(αsmooth muscle actin,α-SMA)、Ⅰ型胶原(collagen typeⅠ,ColI)、转化生长因子β1(transformed growth factor-β1,TGF-β1)、Smad2、Smad7蛋白表达水平。RT-PCR法检测肝脏组织中α-SMA、ColI、TGF-β1、Smad7mRNA水平。Western blot法检测肝脏组织中TGF-β1、Smad4、Smad7蛋白表达水平。结果与正常对照组相比,模型组血清AST、ALT、TP、T-BIL、HA、LN、ColⅢ、ColⅣ水平明显升高,A/G水平明显降低,肝脏HE和Masson染色显示有大量纤维形成,说明造模成功。与模型组相比,DMDD给药组大鼠AST、ALT、TP、T-BIL、HA、LN、ColⅢ、ColⅣ含量和α-SMA、ColI、TGF-β1、Smad2、Smad4mRNA及蛋白水平显著下调,A/G、Smad7水平上调。肝脏HE和Masson染色结果显示纤维增生明显减少。结论DMDD对CCl_(4)诱导的肝纤维化具有保护作用,其机制可能与TGF-β1/Smads信号通路有关。

鲨肝刺激物质类似物对CCl_4致小鼠急性肝损伤的保护作用

目的:探讨重组鲨肝刺激物质类似物(r-sHSA)对CCl4致小鼠急性肝损伤的保护作用及其作用机制.方法:利用腹腔注射CCl4制备小鼠急性肝损伤动物模型,以血清转氨酶活性以及组织病理变化为指标判断r-sHSA对化学性肝损伤的保护作用,并通过定量RT-PCR方法测定肝组织中相关细胞因子表达量的变化.结果:8～200μg/kg r-sHSA均可显著降低损伤小鼠血清转氨酶的活性,明显减轻肝细胞肿胀,减少中性粒细胞浸润,具有显著的肝保护作用,其机制可能与r-sHSA诱导TNF-a和肝细胞生长因子(HGF)表达,并下调TGF-β1的表达有关.结论:r-sHSA对CCl4致小鼠急性肝损伤具有明显的保护作用,其机制可能与细胞因子的表达调控有关.

空心莲子草醇提物抗CCl_4肝损伤的实验研究

目的 :观察空心莲子草醇提物对CCl4 肝损伤的保护作用。方法 :给小鼠腹腔注射CCl4 制成肝损伤模型 ,分为 3组 ,每组 10只。分别经口给予生理盐水、空心莲子草醇提物 (0 0 2g g)和联苯双酯 (0 2mg g)。连续用药6天后 ,第 7天将小鼠断头处死 ,取血和肝脏 ,分别测定空白对照组、空心莲子草组和联苯双酯组小白鼠的血清ALT和血清AST、肝指数及肝细胞镜检 ,并进行比较。结果 :空心莲子草组能明显对抗CCl4 引起的血清ALT和血清AST增高 ,减轻CCl4 对肝细胞的损伤。空白对照组与联苯双酯组和空心莲子草组比较均有显著性差异 (P <0 0 1)。结论 :空心莲子草醇提物对CCl4

脂糖舒对CCl_4所致大鼠肝损伤的保护作用

目的探讨脂糖舒对实验性损伤的保护作用。方法建立大鼠CCL4 肝损伤模型 ,将大鼠随机分为正常组、模型组、治疗组。治疗组于建模后灌胃施药。检测丙氨酸转氨酶 (ALT) ,观察肝脏病理学变化。结果脂糖舒可以抑制CCl4 导致的大鼠血清ALT升高 ,使肝细胞变性、坏死得到明显的改善和恢复。

In vitro and in vivo protective effects of proteoglycan isolated from mycelia of Ganoderma lucidum on carbon tetrachlorideinduced liver injury

AIM： To investigate the possible mechanism of the protective effects of a bioactive fraction, Ganoderma lucidum proteoglycan （GLPG）isolated from Ganoderma luddum mycelia, against carbon tetrachloride-induced liver injury. METHODS： A liver injury model was induced by carbon tetrachloride. Cytotoxicity was measured by MTY assay. The activities of alanine aminotransferase （ALT） and aspartate aminotransferase （AST） were determined with an automatic multifunction-biochemical analyzer and the levels of superoxide dismutase （SOD） and TNF-α were determined following the instructions of SOD kit and TNF radioimmunoassay kit. Uver sections were stained with hematoxylin and eosin （H＆E） for histological evaluation and examined under light microscope. RESULTS： We found that GLPG can alleviate the L-02 liver cells injury induced by carbon tetrachloride （CCh） through the measurements of ALT and AST activities and the administration of GLPG to L-02 cells did not display any toxicity. Furthermore, histological analysis of mice liver injury induced by CCh with or without GLPG pretreatment indicated that GLPG can significantly suppress the toxicity induced by CCh in mice liver. We also found that GLPG reduced TNF-α level induced by CCh in the plasma of mice, whereas increased SOD activity in the rat serum. CONCLUSION： GLPG has hepatic protective activity against CCl4 induced injury both in vitro and in vivo. The possible antihepatotoxic mechanisms may be related to the suppression of TNF-α level and the free radical scavenging activity.

Protective Effects of Flavonoids from Pteridium aquilinum on CCl_(4)-induced Acute Liver Injury in Mice

[Objectives]To explore the protective effects of flavonoids from Pteridium aquilinum(PAFL)on carbon tetracholoride(CCl_(4))-induced acute liver injury in mice and its potential mechanism.[Methods]All mice were randomly divided into four groups(n=10 in each),normal group,CCl_(4)group,CCl_(4)+PAFL groups[treated with PAFL(50 or 200 mg/kg)].Animal treatment was continued for 7 consecutive days.The blood was collected after injection of CCl_(4)for 24 h,and the liver tissue was removed from the mice and stored at-80℃.[Results]The PAFL(50 and 200 mg/kg)significantly inhibited the increase of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)levels in serum caused by CCl_(4)treatment.PAFL administration not only increased the activity of antioxidant enzymes superoxide dismutase(SOD),Glutathione(GSH)and catalase(CAT)in mice,but also reduced the level of malondialdehyde(MDA).Meanwhile,PAFL administration decreased the expression of nuclear factor-kappa B(NF-κB)and Cyclooxygenase-2(COX-2)proteins and inhibited the release of pro-inflammatory factors tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin 6(IL-6).In addition,PAFL(200 mg/kg)treatment down-regulated extracellular regulated protein kinases(ERK)and c-Jun N-terminal kinase(JNK)protein levels in liver tissue.[Conclusions]These findings clearly indicate that the protective effects of PAFL on CCl_(4)-induced acute liver injury is related to its antioxidant and anti-inflammatory activity,which may be mediated by NF-κB and MAPKs signaling pathways.

肝细胞生长因子对CCl_(4)致肝细胞损伤相关炎性因子的影响

目的:探究肝细胞生长因子(hepatocyte growth factor,HGF)对CCl_(4)所致小鼠肝脏损伤IL⁃8、TNF⁃α、IL⁃4、IL⁃21表达水平的影响。方法:建立CCl_(4)急性肝损伤小鼠模型,通过梯度密度离心分离肝实质细胞及白细胞,体外加入不同浓度HGF,ELISA检测细胞因子表达水平。结果:体内损伤模型中,肝实质细胞实验结果显示,10 ng/mL HGF组与损伤肝细胞组相比IL⁃8表达水平降低(P<0.05),50 ng/mL HGF组与10 ng/mL HGF组相比IL⁃8表达水平升高(P<0.05);与损伤肝细胞组相比,25 ng/mL HGF组(P<0.05),50 ng/mL HGF组(P<0.05)IL⁃4表达水平均降低。白细胞实验结果显示,与损伤白细胞组相比,10 ng/mL HGF组(P<0.05)、25 ng/mL HGF组(P<0.05)TNF⁃α表达水平均降低。体外损伤模型中,肝实质细胞实验结果显示,与正常对照组相比,25 ng/mL HGF组(P<0.05)、50 ng/mL HGF组(P<0.05)TNF⁃α表达水平均降低;25 ng/mL HGF组与正常对照组相比IL⁃4表达水平降低(P<0.05)。白细胞实验结果显示,50 ng/mL HGF组与10 ng/mL HGF组相比TNF⁃α表达水平升高(P<0.001);与正常对照组相比CCl_(4)模型组(P<0.05)、10 ng/mL HGF组(P<0.05)、25 ng/mL HGF组(P<0.05)、50 ng/mL HGF组(P<0.05)IL⁃21表达水平均降低。结论:CCl_(4)致小鼠肝脏急性受损时,HGF可降低肝实质细胞分泌炎性因子IL⁃8,TNF⁃α,IL⁃4以及肝脏白细胞TNF⁃α的表达水平。

合生元对CCl_(4)诱发小鼠急性化学性肝损伤的改善作用及其机制

目的探讨不同组合的合生元对CCl_(4)所致急性化学性肝损伤小鼠的肝脏保护作用,及其机制是否与肠—肝轴有关。方法将72只SPF级ICR雄性小鼠随机分12组,每组6只。将含量为5%、15%和20%的麦麸膳食纤维饲料分别记为A1、A2、A3,灌胃剂量为10、20、30 mL/kg的益生菌酸奶分别记为B1、B2、B3,对A1B1组、A1B2组、A1B3组、A2B1组、A2B2组、A2B3组、A3B1组、A3B2组、A3B3组分别进行不同组成合生元干预,阳性对照组、模型组和空白对照组给予普通饲料,阳性对照组同时灌胃复方鳖甲软肝片溶液;30 d后,除空白对照组外的其余各组小鼠灌胃给予1%的CCl_(4)油溶液5 mL/kg,空白对照组灌胃给予等体积玉米油溶液。24 h后,全部小鼠摘眼球取血并分离血清,采用ELISA法检测血清超氧化物歧化酶(SOD)、丙二醛(MDA)水平;取肝脏、结肠、回肠,计算肝脏指数和结肠指数,同时对肝脏和回肠进行HE染色后观察病理改变;收集A1B1组、阳性对照组、模型组和空白对照组小鼠粪便,采用16S rDNA高通量测序法检测肠道菌群情况(Chao、Ace、Shannon、Simpson指数及门水平、属水平上的肠道菌群丰度)。结果模型组肝脏指数及血清MDA水平均高于空白对照组(P均<0.05)。A1B1、A1B2、A2B1和A3B1组小鼠肝脏指数均低于模型组,A1B1、A2B1组小鼠肝脏指数均低于阳性对照组(P均<0.05)。各组小鼠结肠指数比较差异无统计学意义(P>0.05)。A2B1、A2B3组小鼠血清SOD水平均低于模型组、阳性对照组,A1B1、A1B2、A2B3、A3B1和A3B2组小鼠血清MDA水平均低于模型组(P均<0.05);除A1B2组外,其余合生元组小鼠血清MDA水平均高于阳性对照组(P均<0.05)。肝脏病理观察结果:空白对照组小鼠肝组织细胞排列紧密且形态正常,细胞结构清晰且完整,未见炎症细胞浸润和坏死细胞;模型组小鼠肝索、肝小叶结构严重紊乱,细胞肿胀、细胞内存在大量未代谢的CCl_(4);阳性对照组肝细胞形态正常,仅有少量未代谢的CCl_(4);与模型组比较,A1B1组肝小叶结构完整、仅有少量炎症细胞浸润,A2B2组、A3B3组肝小叶严重受损、有大量炎症细胞浸润,A3B1组和A3B3组可见大量未代谢的CCl_(4)。回肠病理观察结果:空白对照组小鼠回肠绒毛较长,绒毛结构完整,肠内皮结构较厚;模型组小鼠回肠结构破坏,肠腔内可见大量黑色物质;阳性对照组绒毛结构较为完整,肠腔内有少量黑色物质;与空白对照组相比,其他合生元组均存在绒毛结构破坏,以A1B1组小鼠绒毛结构完整度最高。模型组小鼠Chao、Ace、Shannon指数均低于空白对照组及A1B1组,Simpson指数高于空白对照组及A1B1组;阳性对照组Shannon指数高于模型组,Simpson指数低于模型组(P均<0.05)。门水平上:与空白对照组比较,模型组小鼠拟杆菌门和变形菌门相对丰度升高,而厚壁菌门相对丰度降低;与模型组比较,A1B1组小鼠厚壁菌门和变形菌门相对丰度均升高,拟杆菌门相对丰度均降低;与阳性对照组比较,A1B1组疣微菌门相对丰度降低(P均<0.05)。属水平上:模型组有10种菌属的相对丰度低于空白对照组,A1B1组7种菌属的相对丰度高于模型组(P均<0.05)。结论合生元对CCl_(4)所致急性化学性肝损伤小鼠具有一定的肝脏保护作用,以5%麦麸膳食纤维联合10 mL/kg益生菌酸奶的合生元组合的肝脏保护效果更好,其机制可能与调节肠—肝轴有关。

蝙蝠草醇提物对四氯化碳所致大鼠急性肝损伤的影响

研究蝙蝠草醇提物对四氯化碳(CCl_(4))所致大鼠急性肝损伤的保护作用及其机制。40只雄性SD大鼠随机分为5组,包括正常组、模型组、水飞蓟素组(120 mg/kg)、蝙蝠草醇提物组(260和520 mg/kg),连续灌胃给药15 d。于第14天,除正常组外,其余大鼠腹腔注射12%CCl_(4)(5 mL/kg)建立急性肝损伤模型。造模24 h后,采血剖检大鼠,并计算肝指数,检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)水平,检测肝组织白介素-1β(IL-1β)、IL-6、肿瘤坏死因子α(TNF-α)、超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽(GSH)水平,HE染色观察肝组织病理学改变。结果显示,蝙蝠草醇提物各剂量组均可降低肝指数(P<0.05),降低血清AST、ALT和肝组织IL-1β、IL-6、TNF-α和MDA水平(P<0.05),升高肝组织SOD、GSH水平(P<0.05),明显改善肝组织病理学损伤。认为,蝙蝠草醇提物对CCl_(4)所致急性肝损伤具有良好的保护作用,可减轻肝损伤,其机制可能与增强肝功能,促进组织修复,降低促炎因子水平和增强机体抗氧化损伤能力有关。

GPX4 Promoter Hypermethylation Induced by Ischemia/Reperfusion Injury Regulates Hepatocytic Ferroptosis

Background and Aims:Glutathione peroxidase 4(GPX4)is a key factor in ferroptosis,which is involved in ischemia-rep-erfusion injury.However,little is known about its role in he-patic ischemia-reperfusion injury(HIRI).This study aimed to investigate the role of GPX4 methylation in ferroptosis during HIRI.Methods:For the in vitro experiments,an oxygen and glucose deprivation cell model was established.For the in vivo experiments,an ischemia-reperfusion model was created by subjecting mice to simulated HIRI.Ferroptosis occurrence,GPX4 promoter methylation,and global methylation levels were then assessed.Results:Ferroptosis was observed in oxygen and glucose deprivation,characterized by a signifi-cant decrease in cellular viability(P<0.05),an increase in lipid peroxidation(P<0.01),iron overload(P<0.05),and down-regulation of GPX4(P<0.05).This ferroptosis was ex-acerbated by GPX4 knockdown(P<0.01)and mitigated by exogenous glutathione(P<0.01).Similarly,ferroptosis was evident in mice subjected to HIRI,with a down-regulation of GPX4 mRNA and protein expression(all P<0.01),and an upregulation of acyl-CoA synthetase long-chain family mem-ber 4 mRNA and protein(all P<0.01),as well as prostaglan-din-endoperoxide synthase 2 mRNA and protein expression(all P<0.05).Methylation levels increased,evidenced by upregulation of DNA methylation transferase expression(P<0.05)and down-regulation of Ten-eleven translocation fam-ily demethylases(P<0.01),along with an upregulation of GPX4 promoter methylation.Conclusions:Ferroptosis may be the primary mode of cell death in hepatocytes following ischemia-reperfusion injury.The methylation of the GPX4 promoter and elevated levels of global hepatic methylation are involved in the regulation of ferroptosis.

肝勃宁对四氯化碳致大鼠慢性肝损害的保护作用

四氯化碳（ＣＣｌ４）致大鼠慢性肝损害，用肝勃宁（ＧＢＮ）２．３１，０．７７，０．２６ｇ／ｋｇ分别给大鼠每天１次ｉｇ，连续４５天。经病理学检查显示能减轻肝纤维化程度，肝脂肪变、嗜酸性坏死发生率明显减少；血清总蛋白量增高，ＳＧＰＴ、ＳＧＯＴ、唾液酸浓度、羟脯氨酸含量下降。结果表明ＧＢＮ对ＣＣｌ４致大鼠慢性肝损害有一定保护作用。

岩黄连总碱提取物对小鼠免疫性肝损伤的改善作用

目的探讨岩黄连总碱提取物(CTFTAE)对小鼠免疫性肝损伤的改善作用及其可能机制。方法小鼠尾静脉iv给予卡介苗和脂多糖制备免疫性肝损伤小鼠模型。注射卡介苗当天ip给予CTFTAE0.26,0.78和2.34mg·kg-1,每天1次,共12d。末次给药后尾静脉iv给予脂多糖(7.5μg),16h后检测小鼠血清谷丙转氨酶(GPT)和谷草转氨酶(GOT)活性;HE染色,光镜下观察肝组织病理变化;ELISA法检测血清干扰素γ(IFN-γ)和白细胞介素4(IL-4)的含量。[3H]TdR掺入法测定CTFTAE体外对小鼠脾淋巴细胞增殖反应的影响。结果模型组小鼠血清GPT和GOT活性较正常对照组明显升高;CTFTAE0.26,0.78和2.34mg·kg-1剂量组血清GPT活性较模型组明显降低,GOT活性无明显变化。模型组可见明显的肝细胞溶解坏死,而CTFTAE0.78和2.34mg·L-1组肝细胞变性、坏死及炎症细胞浸润均明显减轻。模型组小鼠血清IFN-γ和IL-4含量升高,IL-4升高较明显,IFN-γ/IL-4比值降低;CTFTAE0.26,0.78和2.34mg·kg-1组IL-4含量降低,IFN-γ/IL-4比值升高。CTFTAE15～1500mg·L-1体外单独应用可增强小鼠脾脏淋巴细胞增殖反应,亦可增强刀豆蛋白A诱导的脾淋巴细胞增殖反应。结论CTFTAE对免疫性肝损伤具有改善作用,其机制可能与其调节辅助性T细胞(Th)1/Th2平衡有关。

儿茶素类化合物对四氯化碳致大鼠慢性肝损伤的保护作用

目的 观察儿茶素类化合物保肝降酶的作用。方法 制备大鼠的四氯化碳 (CCl4)慢性肝损伤模型 ,观察儿茶素类化合物对肝损伤大鼠血清丙氨酸转氨酶 (ALT)、天冬氨酸转氨酶 (AST)、丙二醛 (MDA)等的影响 ,以及肝组织羟脯氨酸含量和肝脏组织结构的变化。结果 儿茶素类化合物给药 2个月后 ,中、高剂量给药组 (10 0 ,2 0 0mg/kg)均能降低血清ALT的活力以及脂质过氧化产物MDA和肝组织羟脯氨酸的含量 (P <0 0 1或P <0 0 5 ) ,其降低肝组织羟脯氨酸含量的作用与联苯双酯相当。肝组织的病理改善情况两药相似 ,而抗膜脂质过氧化作用优于联苯双酯。结论 儿茶素类化合物具有保护化学性肝损伤作用 ,有降低转氨酶活力。

委陵菜对四氯化碳致小鼠肝损伤保护作用

目的 :研究委陵菜对四氯化碳 (CCl4)致小鼠急性肝损伤的保护作用。方法 :用委陵菜给小鼠灌胃 7天 ,观察对四氯化碳致小鼠肝损伤所引起血清谷丙转氨酶和谷草转免酶升高、肝脂质过氧化物含量的影响。结果 :委陵菜能明显降低模型组的血清转氨酶、肝脂质过氧化物含量。结论

鲨肝活性肽S-8300对小鼠急性肝损伤的保护作用

目的 :研究鲨肝活性肽S 830 0对四氯化碳 (CCl4 )小鼠肝损伤的保护作用。方法 :采用CCl4 致小鼠肝损伤 ,观察肝组织切片 ;测定生化指标 ,检测小鼠腹腔注射S 830 0后血清谷丙转氨酶 (sGPT)、血清谷草转氨酶 (sGOT)和乳酸脱氢酶 (LDH)活性 ,肝脏超氧化物歧化酶 (SOD)活性与丙二醛 (MDA)和谷胱甘肽 (GSH)含量。结果 :S 830 0能明显减轻CCl4 所致小鼠急性肝损伤 ;降低血清GPT、GOT、LDH活性及降低肝组织MDA含量 ,增加肝组织GSH含量和提高SOD活性。结论 :鲨肝活性肽S 830

三叶委陵菜对四氯化碳致小鼠肝损伤保护作用

目的 :研究三叶委陵菜对四氯化碳 (CCl4)致小鼠急性肝损伤的保护作用。方法 :用三叶委陵菜给小鼠灌胃 7d,观察对四氯化碳致小鼠肝损伤所引起血清谷丙转氨酶和谷草转氨酶升高、肝线粒体脂质过氧化物含量的影响。结果 :三叶委陵菜能明显降低模型组的血清转氨酶、肝线粒体脂质过氧化物含量。结论

内毒素预处理对内毒素血症大鼠肝TLR-4、NF-κB和ICAM-1表达的影响

目的观察内毒素预处理对内毒素血症大鼠肝Toll样受体4(TLR-4)、核因子-κB(NF-κB)和白细胞间粘附分子-1(ICAM-1)表达的影响,探讨内毒素预处理对内毒素血症肝损伤的保护作用及机制。方法采用直接注射内毒素脂多糖(LPS,10mg/kg体重)的方法建立大鼠急性内毒素血症模型,实验动物随机分成3组:生理盐水对照组(N组);内毒素脂多糖(LPS)组(L组)和LPS预处理组(P组),其中P组在制模前分别经腹腔注射LPS 0.25、0.50mg/kg体重。逆转录聚合酶链反应(RT-PCR)检测肝组织TLR-4mRNA表达,免疫印迹法(Western blot)检测肝组织NF-κB表达,免疫组化法检测肝组织ICAM-1表达,取肝脏(肝左上叶)用10%的中性甲醛固定观察肝脏病理形态。结果内毒素血症时,肝脏组织TLR-4、NF-κB和ICAM-1水平明显增加,显著高于N组(P<0.05),而经内毒素预处理的模型动物肝脏组织TLR-4、NF-κB和ICAM-1水平明显降低(P<0.05),P组肝脏组织病理学改变较L组减轻。结论内毒素预处理能够减轻内毒素血症导致的肝损伤,其机制可能与抑制TLR-4信号传导通路及减少单核巨噬细胞内NF-κB和ICAM-1的表达有关。