Acute Toxicity of Jinchuan Formula Plum Wine Extract and Its Protective Effect on Mice with Liver Injury

[Objectives]To investigate the acute toxicity and hepatoprotective effect of Jinchuan formula plum wine extract on mice,determine its safety range,and evaluate its hepatoprotective effect.[Methods]The median lethal dose(LD_(50))was determined by acute toxicity test with the toxic reaction and mortality of mice as indexes.Sixty Kunming mice were randomly divided into 6 groups:normal control group,model group(ConA-induced liver injury model),Jinchuan formula plum wine high,medium and low dose groups(1.0,0.5,0.25 g/kg)and silybin group(0.1 g/kg).The levels of ALT,AST,LDH in serum and TG,VLDL in liver were measured.After HE staining,the pathological changes of liver tissue in mice were observed,and the liver protective effect of Jinchuan formula plum wine extract was analyzed and evaluated.[Results]LD_(50)was 11.18 g/kg,and the 95%confidence limit of LD_(50)was 10.31-12.05 g/kg.The high-dose group of Jinchuan formula plum wine extract could significantly reduce the serum ALT and AST activities of ConA-induced liver injury mice(P<0.05).[Conclusions]Jinchuan formula plum wine extract is relatively safe,and also has a protective effect on liver injury.

Protective effect of Solanum Nigrum Linn green fruit ethanolic extract on alcoholic liver injury in mice

Alcoholic liver injury is a liver disease caused by excessive alcohol consumption,which can lead to chronic liver disease death.Solanum Nigrum Linn taste bitter,cold,has the effect of clearing heat and detoxification,promoting blood and detumescence.Solanum Nigrum Linn fruit contains a variety of antioxidant enzymes,can remove the body produced by aerobic metabolism harmful substances.In this paper,a model of alcohol-induced liver injury in C57BL/6 mice was established to evaluate the protective effect of Solanum Nigrum Linn green fruit(SNGF)ethanolic extract on alcohol-induced liver injury.H&E staining and oil red O(ORO)staining showed that hepatic lobules were clearly demarcated,vacuoles were significantly reduced and lipid droplets were reduced in SNGF ethanolic extract treatment group.Serum levels of TC,TG,LDH,TBA,AKP,ALT and AST were decreased in the SNGF ethanolic extract treatment group,and SNGF ethanolic extract could clear reactive oxygen species(ROS)in time.MDA content was signifi cantly decreased after SNGF ethanolic extract treatment,while superoxide dismutase(SOD)and GSH-Px contents were increased after SNGF ethanolic extract treatment.These results suggest that SNGF ethanolic extract has a protective effect on alcohol-induced liver injury.

Protective Effect of Ethanol Extract from Sweet Potato Leaves on CCL_(4)-Induced Liver Injury in Mice

[Objectives]To investigate the protective effect of ethanol extract from sweet potato leaves on liver injury induced by CCl_(4)in mice.[Methods]25 ICR mice were randomly divided into blank group,model group,high-dose extract group(200 mg/kg),low-dose extract group(100 mg/kg)and positive control group(2 mg/kg colchicine),with 5 mice in each group.All groups except the blank group were given intraperitoneal injection of 20%CCl 4 olive oil solution(2 mL/kg),and the blank group was given the same dose of olive oil solution three times a week.After 4 weeks,each administration group was given the corresponding dose of drugs(10 mL/kg),and the blank group and model group were given the corresponding amount of normal saline for 2 weeks.After the last intragastric administration,fasting was required,but water was allowed,blood was taken from eyeballs,and upper serum was taken by static centrifugation.Serum AST,ALT,CRP,IL-6 and SOD levels were detected by the kit.[Results]Compared with the blank group,the serum AST and ALT levels in the model group were significantly increased;compared with the model group,the ethanol extract of sweet potato leaves could decrease the levels of ALT,AST,CRP,IL-6 and increase the level of SOD in serum.[Conclusions]The ethanol extract of sweet potato leaves had protective effect on the mice with liver injury induced by CCl_(4),and its mechanism may be to protect the liver by lowering enzymes,inhibiting inflammation and antioxidant stress.

Protective Effect of Dimethyl-4,4'-Dimethoxy-5,6,5',6'-Dimethylene Dioxybiphenyl-2,2'-Dicarboxylate (DDB) against Carcinogen-Induced Rat Liver Nuclear DNA Damage

The protective effect of DDB against carcinogen-induced DNA damage was examined in the present investigation. Preincubation of rat liver nuclei with DDB (1 mmol.L-1) resulted in 60% inhibition of binding of 3H-benzo (a) pyrene to nuclear DNA. Unscheduled DNA synthesis (UDS) induced by aflatoxin BI (10^(-7) mol.L-1) in freshly isolated rat hepatocytes was also inhibited by DDB (10^(-6)-10^(-3)mol.L-1). Oral administration of DDB at 200 mg.kg-1 once daily for 3 d induced a significant increase of liver cytosol glutathione-S-transferase and microsomal UDPG-transferase activity in mice. These results indicate that DDB is able to directly or indirectly antagonize certain carcinogen-induced DNA damages.

The Extraction of Eucommia Ulmoides Oliv Polysaccharides and Its Protective Effect on Liver of Clophasphamidecy Injured Mice

Objective:To study the influenceof eucommia polysaccharide on the mice' liver damaged by clophasphamidecy (CY).Methods:Injecting CY build mice liver damage model,eucommia polysaccharide given different doses, measured blood serum ALT,AST and the liver's SOD,MDA. Results:After the injection CY,blood serum ALT,AST and the MDA of liver rise and the SOD of liver reduce comparedwith the blank group. The eucommia polysaccharide can improve these index.Conclusion:The Eucommia polysaccharide may protect the mice' liver damaged by CY.

Protective effects of C-phycocyanin on alcohol-induced acute liver injury in mice

Excessive alcohol consumption leads to liver disease. Extensive evidence suggests that C-phycocyanin(C-PC), a chromophore phycocyanobilin derived from Spirulina platensis, exerts protective eff ects against chemical-induced organ damage. In this study, we investigated whether C-PC could protect against ethanol-induced acute liver injury. Serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), triglyceride(TG), total cholesterol(CHOL), low-density lipoprotein(LDL), liver homogenate malondialdehyde(MDA), superoxide dismutase(SOD) content were measured, and pathological examination of liver sections were examined. C-PC showed obvious inhibitory eff ects on serum ALT, AST, TG, CHOL, LDL and MDA, and SOD content significantly increased in the liver. The structure of hepatic lobules was clear, liver sinus returned to normal, and liver cell cords were arranged in neat rows. Cloudiness, swelling, inflammatory cell infiltration and spotty necrosis of liver cells were significantly reduced. Therefore, C-PC can significantly protect against ethanol-induced acute liver injury.

Protective Effect of Mongolian Medicine Youning Bawei Powder on Liver Injury Induced by CCl4 in Mice

[Objectives]To study the protective effect of Mongolian medicine Youning Bawei Powder on liver injury induced by carbon tetrachloride(CCl_(4))in mice.[Methods]The experimental mice were divided into 5 groups:normal group,model group,positive control group,low-dose group and high-dose group of Mongolian medicine Youning Bawei Powder.The model group was induced by CCl_(4),the positive control group was treated with liver-protecting tablet,and the Mongolian medicine group was treated with Youning Bawei Powder for one month.The liver tissue injury of mice in each group was observed by HE staining,and the levels of serum ALT,AST,SOD and MDA were detected.[Results]Mongolian medicine Youning Bawei Powder significantly improved the pathological liver injury induced by CCl_(4),significantly decreased the content of ALT,AST and MDA in serum of mice with CCl_(4) liver injury,and significantly increased the activity of serum SOD.[Conclusions]Youning Bawei Powder,a Mongolian medicine,has a protective effect on liver injury induced by CCl_(4) in mice.

Late Protective Effects of the Anticalmodulin Drug Fluphenazine on Carbon Tetrachloride-induced Liver Necrosis

Fluphenazine (FP) treatment (50mg/kg bw, ip in saline) 30 min before or 6 or 10 h after CCl4 administration (1 ml/kg ip in olive oil) significantly prevented the liver necrosis produced by the hepatotoxin at 24 h. FP had enhancing effects on the covalent binding of CCl4 reactive metabolites to cellular constituents and on CCl4 induced lipid peroaldation.FP lowered bOdy temperature of the CCl4-poisoned animals during the 24 h observation period. The obtained results are compatible but do not prove the hypothesis that calmodulin (CaM) had participation in late occurring events preceding necrosis. FP lowering action on body temperature, however, might also play a role in the effects of this drug on the onset of CCl4 induced liver necrosis. FP levels in liver tissue as determined by gas chromatography-mass spectrometry evidenced the presence of the drug in amounts suffi cient to inhibit CaM and that suggests that not all preventive effects of FP are due to its indirect actions on the central nervous system via decreased body temperature

Protective effect of fu-qi granule on carbon tetrachloride-induced liver fibrosis in rats

AIM： To investigate the effcacy of fu-qi granule （FQG） on carbon tetrachloride （CCl4） induced liver fbrosis in rats and the underlying mechanisms. METHODS： Sixty rats were randomly divided into six groups： normal control group, CCl4 induced liver fbrosis group, AnluoHuaxianWan group and three treatment groups of FQG. Treatment of rats with intraperitoneal injection of carbon tetrachloride solution at 0.3 mL per 100 g body weigh twice a week for 8 wk. The normal control group the rats were given the media （olive oil） at the same time. In the frst 2 wk, rats were raised with feedstuff （80% corn meal, 20% lard, 0.5% cholesterol）. Serum samples were collected for alanine transaminase, aspartate aminotransferase, alkaline phosphatase, albumin, total protein assay and typical histopathological changes was observed in Hematoxylin-eosin staining sections. Smooth muscle alpha actin （α-SMA） was analyzed with immunohistochemistry. Mammalian target of rapamycin （mTOR） and hypoxia-inducible factor-1 （HIF-1α） expressions were detected by Western blot-ting. Tissue inhibitor of matrix metalloproteinases-1 （TIMP-1） and matrix metalloproteinases-9 （MMP-9） were measured with semi-quantitative reverse transcriptase-polymerase chain reaction.RESULTS： FQG significantly reduced the serum levels of alanine transaminase, aspartate aminotransferase, alkaline phosphatase and increased the serum contents of albumin, total protein in rats with liver fibrosis. Moreover, FQG promoted extracellular matrix degradation by increasing MMP-9 and inhibiting TIMP-1 and α-SMA. mTOR and HIF-1α expression in liver significantly decreased in the rats treated with FQG. CONCLUSION： The results indicated that FQG signi-fcantly reverse fbrosis induced by CCl4, which should be developed as a new and promising preparation for the prevention of liver fbrosis.

Protective Effect of Vitamin E on Liver Damage Induced by 2-Chloro-1, 3-butadiene

The present study was performed to determine the influence of lipid peroxidation and perturbance of Ca2+ homeostasis on liver damage induced by 2-chloro-1, 3-butadiene (CBD) and the protective effects of vitamin E in Wistar rats. Animals were given intraperitoneally different doses (8,40 or 200 mg·kg-1 daily) of CBD for 21 days, and the following dose-dependent events were observed: liver damage, significant increase in liver lipid peroxides, and decreases in activities of erythrocytic glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). The pretreatment of rats with vitamin E (po 150 mg·kg-1) before administering CBD (iP 60 mg·kg-1 ) daily for 21 days prevented the following CBD-induced changes, the increase in serum cholylglycine (CG), hepatic LP, hepatic mitochondrion LP, hepatic oxidized glutathione (GSSG) (while the significant increase of reduced glutathione (GSH) was not affected) and the decrease in activities of erythrocytic SOD and hepatic mitochondrial calcium sequestration. These results suggest that lipid peroxidation and perturbance of Ca2+ homeostasis appear to contribute to the hepatotoxicity of CBD, and vitamin E might prevent the liver damage induced by CBD. The decrease in activities of GSH-Px and SOD in erythrocytes might be used as biomarkers for adverse effects of CBD on defense system against lipid peroxidation.

Protective effect of hydrogen-rich saline on liver ischemia-reperfusion injury in mice

Objective To explore protective effect of hydrogen - rich saline on liver ischemia reperfusion ( IR) in mice and possible mechanisms. Methods Twenty - four C57BL /6 mice were randomly divided into 3 groups: sham - operated group,control group ( mice were injec-

枸杞多糖对肝内胆汁淤积模型大鼠肝脏预防保护作用的研究

目的 探讨枸杞多糖(LBP)对肝内胆汁淤积模型大鼠肝脏损伤的预防保护作用。方法 SPF级雄性SD幼龄大鼠,设阴性对照组、模型组、LBP 50、150、450 mg/kg剂量组,以及阳性对照组,每组各10只。构建大鼠肝内胆汁淤积模型,模型组、LBP各剂量组及阳性对照组,予60mg/kg α-萘异硫氰酸酯,每隔1天给药一次,第2周开始改为每隔3天给药一次,持续6周。第2周起,各剂量组每天予不同剂量的LBP,阳性对照组予熊去氧胆酸,模型组大鼠予蒸馏水。6周后采集血液及肝组织样本,测定血清生化指标、凝血功能指标及白细胞分类计数指标,检测肝组织中的炎症因子含量以及Toll样受体4(TLR4)、核因子κB(NF-κB)、核转录因子(pNF-κB)及髓分化因子88(MyD88)蛋白的表达量,观察大鼠肝脏的病变情况。结果 与阴性对照比较,模型组大鼠血清γ-谷氨酰转移酶(γ-GGT)、碱性磷酸酶(ALP)、总胆汁酸(TBA)、总血红素(TBiL)、胆固醇(CHOL)、丙氨酸氨基转移酶(ALT)及天冬氨酸氨基转移酶(AST)水平,血液白细胞(WBC)、淋巴细胞(LYMP)、中性粒细胞(NEUT)、单核细胞(MONO)及嗜酸性粒细胞(EO)计数,纤维蛋白原(FIB)含量均升高(均P <0.05),肝组织中炎症因子肿瘤坏死因子(TNF-α)、白介素1β(IL-1β)、白介素6及巨噬细胞炎性蛋白2(MIP-2)含量增加,TLR4、pNF-κB、MyD88蛋白表达水平上调(均P <0.05)。肝脏可见多量炎症细胞浸润、胆管增生、纤维组织增生等病理性改变,组织形态学观察评分上升(均P <0.05);与模型组比较,LBP450mg/kg组大鼠血清γ-GGT、TBA、TBiL、ALT水平,血液WBC、LYMP、NEUT计数,FIB含量均下降(均P<0.05),肝组织中炎症因子TNF-α、IL-1β、MIP-2含量降低,TLR4、pNF-κB、MyD88蛋白的表达水平下调(均P<0.05),肝脏组织形态学观察评分下降(均P <0.05),肝脏损伤减轻,LBP 150 mg/kg组大鼠血液FIB含量均下降,TLR4蛋白的表达水平下调(均P<0.05)。结论 LBP对肝内胆汁淤积模型大鼠肝脏损伤有缓解和保护功效,其作用机制可能与下调TLR4/MyD88/NF-κB信号通路相关蛋白的表达,抑制过度炎症反应有关。

陈皮复合固体饮料制备工艺及其对急性酒精性肝损伤小鼠的保护作用

[目的]以药食同源的陈皮、山楂、葛根为主要原料,开发一种具有解酒功能的固体饮料,并探究其对急性酒精性肝损伤小鼠的保护作用。[方法]以浸膏得率和总黄酮含量为标准,采用正交试验选取最佳提取工艺;以感官评价、成型率、溶化性的综合评分为指标,采用单因素试验优化成型工艺。采用52%酒精灌胃的方法建立急性酒精性肝损伤小鼠模型,检测陈皮复合固体饮料对模型小鼠肝脏指数,血清中谷草转氨酶(AST)、谷丙转氨酶(ALT),肝组织中总胆固醇(TC)、甘油三酯(TG)、超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)及炎症因子白细胞介素-1β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子-α(TNF-α)的影响,苏木素—伊红(HE)染色分析各组肝脏病理变化。[结果]陈皮复合固体饮料最佳制备工艺:3味药材浸泡30 min后提取2次,第一次料液比1∶12(g/mL)、提取时间2.0 h,第二次料液比1∶10(g/mL)、提取时间1.5 h;经浓缩、干燥、粉碎后得到干膏粉;干膏粉与麦芽糊精1∶1混合,加入1.0%的罗汉果甜苷,并以90%乙醇作为润湿剂进行湿法制粒。动物试验表明:与模型组相比,陈皮复合固体饮料组的AST、ALT、TG、TC、MDA、IL-1β、IL-6、TNF-α水平降低(P<0.01或P<0.05),GSH、SOD含量增加(P<0.01或P<0.05),且肝组织病理切片显示给药组小鼠肝损伤程度均有显著改善。[结论]陈皮复合固体饮料色泽均匀、溶解性好、甜度适中、口感细腻,对急性酒精性肝损伤具有良好的保护作用。

姜黄素对镉染毒大鼠肝脏功能的保护作用

目的研究姜黄素对镉染毒大鼠肝脏功能的保护作用。方法选取64只SPF级雄性SD大鼠随机分成8组,分别是对照组、染镉(Ⅰ-Ⅴ)组、姜黄素组、镉+姜黄素组,按照不同干预方式连续灌胃90 d。期间观察大鼠的行为表现,并记录体重。造模完成后处死大鼠,收集大鼠肝组织及血液,计算肝指数,并检测大鼠的肝功能、血脂及肝组织中氧化损伤相关指标。结果与对照组相比,染镉Ⅲ、Ⅳ、Ⅴ组大鼠肝指数增高;染镉Ⅳ组大鼠血清甘油三酯(triglyceride,TG)、总胆固醇(total cholesterol,T-CHO)水平增加;染镉Ⅳ、Ⅴ组大鼠血清丙氨酸氨基转移酶(alanine aminotransferase,ALT)、碱性磷酸酶(alkaline phosphatase,ALP)和总胆汁酸(total bile acid,TBA)均明显增高,天冬氨酸氨基转移酶/丙氨酸氨基转移酶(aspartate aminotransferase/alanine aminotransferase,AST/ALT)降低;染镉Ⅲ、Ⅳ、Ⅴ组大鼠肝组织中黄嘌呤氧化酶(xanthine oxidase,XOD)活力及丙二醛(malondialdehyde,MDA)含量明显增加,超氧化物歧化酶(superoxide dismutase,SOD)活力明显降低,差异均具有统计学意义(P<0.05)。与染镉Ⅲ组相比,镉+姜黄素组大鼠的肝指数、血清ALT均降低,差异有统计学意义(P<0.05);血清TG及肝组织MDA含量呈下降趋势,SOD活力增加。结论姜黄素可发挥抗氧化及调节脂代谢作用,能对镉染毒大鼠的肝脏功能起到保护作用。该研究为姜黄素治疗镉导致的肝损伤提供了基础理论依据。

基于网络药理学和体内实验探讨茯苓多糖抗对乙酰氨基酚致肝损伤的作用机制

目的利用网络药理学和体内实验,探讨茯苓多糖(PCP)抗对乙酰氨基酚(APAP)致肝损伤的作用靶点。方法通过SwissTargetPrediction数据库、SuperPred数据库和Pharmmapper数据库获取PCP的作用靶点,利用OMIM数据库、GeneCards数据库查找APAP致肝损伤相关作用靶点,使用String数据库构建蛋白互作网络(PPI)并筛选核心靶点。利用R软件进行基因本体(GO)和京都基因与基因组百科全书(KEGG)通路分析,通过AutoDuck vina软件对茯苓多糖和核心靶点进行分子对接。最后,用HE染色评估小鼠肝组织损伤情况,并且通过RT-PCR和免疫组化染色法(IHC)检测核心靶点的表达情况。结果共获得26个核心靶点,GO富集分析显示细胞凋亡、细胞周期、免疫等生物过程可能参与PCP抗APAP致肝损伤的进程。KEGG富集分析显示茯苓多糖抗APAP致肝损伤的信号通路主要集中在p53信号通路(p53 signaling pathway)、NOD样受体信号通路(NOD-like receptor signaling pathway)、TNF信号通路(TNF signaling pathway)等。分子对接结果显示,PCP与等核心靶点具有较好的结合能力。HE染色显示,APAP组小鼠肝组织形态结构出现异常,表现为细胞大面积坏死,而PCP干预后可以减轻肝组织损伤。RT-PCR和IHC结果表明,PCP通过逆转APAP暴露引起的CDK2、TNF、BCL2L1及MAOA水平升高来缓解小鼠肝损伤。结论通过网络药理学和体内实验找到了PCP抗APAP致肝损伤的可能潜在靶点,其作用机制可能与调节细胞周期、免疫反应、凋亡和药物代谢有关。

爬岩红提取物对化学性肝损伤小鼠的保护作用

分别用体积分数0.5%CCl_(4)、50%乙醇溶液建立小鼠急性肝损伤模型,研究爬岩红水提物、醇提物对CCl_(4)和酒精所致的肝损伤小鼠的保护作用。结果显示,爬岩红水提物、醇提物均能降低CCl_(4)肝损伤小鼠血清ALT活性、肝组织MDA水平,升高肝组织GSH-PX、T-SOD、CAT、白蛋白水平,减轻CCl4肝损伤小鼠肝组织的病理变化程度,且二者的保肝作用无显著差异(P>0.05);爬岩红水提物、醇提物均能降低酒精性肝损伤小鼠血清ALT活性、肝组织MDA和TG水平,升高肝组织GSH、T-SOD水平,减轻酒精性肝损伤小鼠肝组织的病理变化程度,且水提物的效果更为显著(P<0.05)。爬岩红水提取物、醇提取物对CCl_(4)和酒精所致的肝损伤小鼠均有保护作用,水提物对酒精性肝损伤的保护作用更好。

早期免疫生态肠内营养对重症急性胰腺炎大鼠肝功能的保护作用

目的探讨早期免疫生态肠内营养对重症急性胰腺炎(SAP)大鼠肝功能的保护作用。方法选取健康雄性SD大鼠120只随机分为假手术对照组(SO组),重症急性胰腺炎模型组(SAP组),早期肠内营养组(EEN),早期生态免疫营养组(EIN)4组。将每组分为12、24、48 h三个亚组(n=10)。除假手术对照组外,其余各组大鼠采用逆行胰胆管注射5%牛磺胆酸钠制备SAP模型。采集大鼠腹主动脉血检测血清淀粉酶(AMY)、脂肪酶(LPS)、丙氨酸氨基转氨酶(ALT)、天门冬氨酸氨基转移酶(AST)水平;采用酶联免疫吸附剂测定(ELISA)法检测细胞因子白介素-10(IL-10)、白介素-6(IL-6)及肿瘤坏死因子(TNF-α)水平;取肝脏组织进行HE染色,观察组织病理改变;通过蛋白质印迹法(western blot,WB)方法观察肝脏组织内p-STAT3及cleaved caspase-3蛋白表达。结果EEN组、EIN组制模后各时间点血清AMY、LPS和ALT和AST水平均低于同期SAP组,P<0.05。各时间点EIN组与同时间点EEN组相比血清TNF-α、IL-6水平下降,IL-10水平升高,P<0.05。与同期EEN组、SAP组相比,EIN组肝脏p-STAT3及cleaved caspase-3蛋白表达明显减弱(P<0.05)。结论早期免疫生态肠内营养改善SAP大鼠肝脏组织病理损伤,抑制肝脏组织p-STAT3激活,抑制cleaved caspase-3蛋白表达,具有肝功能保护作用。

发酵前后粉葛提取物对酒精性肝损伤大鼠的解酒护肝作用

为研究发酵前后粉葛提取物的解酒护肝作用,该试验建立56%vol白酒灌胃大鼠致酒精性肝损伤模型(13 mL/kg),设置空白组、模型组、阳性组(0.945 g/kg)、发酵前提取物组(1.6 g/kg)、发酵后提取物组(1.6 g/kg),按组别灌胃给药,考察发酵前后粉葛提取物对大鼠酒精耐受、睡眠和醒酒时间的影响,对大鼠血清中谷丙氨酸氨基转移酶(alanine aminotransferase,ALT)、谷草氨酸氨基转移酶(aspartate aminotransferase,AST)、甘油三酯(triglycerides,TG)水平,以及乙醇脱氢酶(alcohol dehydroge-nase,ADH)、超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活性及丙二醛(malondialdehyde,MDA)水平的影响,并通过组织切片苏木精-伊红(hematoxylin-eosin,HE)染色观察其肝脏状态变化。结果显示,与模型组相比,发酵前后粉葛提取物组均有解酒护肝作用,且与发酵前粉葛提取物组相比,发酵后粉葛提取物组延长大鼠酒精耐受时间,缩短睡眠、醒酒时间(P<0.05);降低大鼠血清AST、ALT和TG水平(P<0.001),增强肝组织中ADH、SOD、GSH-Px活性(P<0.01),降低MDA水平(P<0.01)的效果更明显;HE染色结果显示,发酵后粉葛提取物组比发酵前粉葛提取物组肝细胞脂肪变性程度低。粉葛提取物均具有防醉酒和解酒护肝作用,发酵后粉葛提取物效果优于发酵前粉葛提取物。

葛根素对小鼠非酒精性脂肪肝保护作用的研究

目前,非酒精性脂肪肝病已成为肝脏相关疾病的重要研究对象,我国非酒精性脂肪肝患病率也呈逐年上升趋势。然而,非酒精性脂肪肝的治疗方案比较局限,其中中药在其治疗中发挥了优势。将40只健康雄性小鼠随机分成5组:正常组、模型组、低剂量组、中剂量组、高剂量组,每组8只。除正常组外,其他组按照改良的造模方法高脂喂食35 d制备非酒精性脂肪肝模型(nonalcoholic fatty liver disease,NAFLD)。从第36天起低剂量组、中剂量组和高剂量组(60、80、100 mg·kg-1)将葛根素溶解在生理盐水中进行灌胃,其余组小鼠按照灌胃体积公式灌胃生理盐水。给药16 d后对小鼠血清中甘油三酯(triglyceride,TG)、胆固醇(total cholesterol,TC)、高密度脂蛋白(high-density lipoprotein,HDL)、低密度脂蛋白(low-density lipoproteins,LDL)指标进行检测,并取出小鼠的肝脏制备病理切片染色。研究结果显示,中、高剂量的葛根素对NAFLD模型小鼠的血脂相关指标(TC、TG、LDL)有较显著的降低作用,且高剂量的葛根素降低TG的效果最明显(P<0.01)。研究结果表明葛根素对小鼠非酒精性脂肪肝可能有一定的保护作用。

解酒护肝胶囊对大鼠酒精性肝损伤保护作用研究

目的评价解酒护肝胶囊对酒精性肝损伤的防治作用以及增强酒精代谢功效研究。方法各实验组灌胃给予不同浓度受试样品后,建立酒精性肝损伤及急性酒精中毒模型。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)、谷氨酰氨基转移酶(GGT)、乙醇和乙醛含量;检测肝脏中三酰甘油(TG)、超氧化物歧化酶(SOD)水平;HE染色观察肝脏和胃组织的病理变化。结果与模型组比较,解酒护肝胶囊中剂量组能显著降低血清中ALT含量(P<0.05),中、高剂量组能显著降低AST和GGT含量(P<0.01),低、中、高剂量组均能显著降低肝脏组织中TG含量(P<0.01),高剂量组显著提高SOD水平(P<0.01)。肝脏组织病理切片显示,模型组大鼠肝细胞大小不均,肝索排列紊乱,有较多小泡性脂肪空泡,同时伴有炎症浸润、细胞坏死,各剂量给药组均可不同程度改善大鼠肝脏组织病变情况;与模型组比较,解酒护肝胶囊高剂量组在醉酒后8 h内乙醇和乙醛含量均显著下降(P<0.01)。解酒护肝胶囊低、高剂量组肝脏和胃组织的病变情况均有所缓解。结论解酒护肝胶囊可抑制氧化应激反应,降低脂质过氧化,加速酒精代谢,对肝组织和胃黏膜具有一定的保护作用。