Antioxidant activity and hepatoprotective effect of 10 medicinal herbs on CCl4-induced liver injury in mice

BACKGROUND Many natural products confer health benefits against diverse diseases through their antioxidant activities.Carbon tetrachloride(CCl4)is often used in animal experiments to study the effects of substances on liver injury and the related mechanisms of action,among which oxidative stress is a major pathogenic factor.AIM To compare antioxidant and hepatoprotective activities of ten herbs and identify and quantify phytochemicals for the one with strongest hepatoprotection.METHODS The antioxidant activity of ten medicinal herbs was determined by both ferricreducing antioxidant power and Trolox equivalent antioxidant capacity assays.The total phenolic and flavonoid contents were determined by Folin–Ciocalteu method and aluminum chloride colorimetry,respectively.Their effects on CCl4-induced oxidative liver injury were evaluated and compared in a mouse model by administrating each water extract(0.15 g/mL,10 mL/kg)once per day for seven consecutive days and a dose of CCl4 solution in olive oil(8%,v/v,10 mL/kg).The herb with the strongest hepatoprotective performance was analyzed for the detailed bioactive components by using high-performance liquid chromatography-electrospray ionization source-ion trap tandem mass spectrometry.RESULTS The results revealed that all tested herbs attenuated CCl4-induced oxidative liver injury;each resulted in significant decreases in levels of serum alanine transaminase,aspartate transaminase,alkaline phosphatase,and triacylglycerols.In addition,most herbs restored hepatic superoxide dismutase and catalase activities,glutathione levels,and reduced malondialdehyde levels.Sanguisorba officinalis(S.officinalis)L.,Coptis chinensis Franch.,and Pueraria lobata(Willd.)Ohwi root were the three most effective herbs,and S.officinalis L.exhibited the strongest hepatoprotective effect.Nine active components were identified in S.officinalis L.Gallic acid and(+)-catechin were quantified(7.86±0.45 mg/g and 8.19±0.57 mg/g dried weight,respectively).Furthermore,the tested herbs displayed a range of in vitro antioxidant activities proportional to their phenolic content;the strongest activities were also found for S.officinalis L.CONCLUSION This study is of value to assist the selection of more effective natural products for direct consumption and the development of nutraceuticals or therapeutics to manage oxidative stress-related diseases.

Protective effects of NYG-1 on CCl4-induced acute liver injury in rats

OBJECTIVE To study the protection effects and mechanisms of NYG-1 on CCl4-induced acute liver injury.METHODS Acute liver injury model of rats was established by using CCl4.48 male SPF SD rats were weighed and randomly divided into six groups with 8 in each group,normal group,model group,positive control group(silibinin),low-,medium-and high-dose NYG-1 group.Silibinin was given orally to rats in the positive control group,NYG-1(high-,medium-and low-dose)was given orally in the high-,medium-and low-dose NYG-1group,respectively.Those rats were administered appropriately according to the group once daily for seven consecutive days.On the seventh day,rats were treated with 10% CCl4(10mL·kg-1 of0.1% CCl4 solution in olive oil)intraperitoneally injecting(ip)to induce acute liver injury,except the normal group.At 16 h after CCl4 treatment,rats were weighed,then anaesthed with ether,the blood and liver were collected.Serum ALT,AST,LDH and ALP were measured.MDA content and SOD activity in liver homogenate were detected.The histopathological changes of liver were observed by H&E staining.RESULTS Acute liver injury model was established successfully in rats by intraperitoneally injecting CCl4.Pretreatment with medium and high dose NYG-1 decreased the increase of ALT,AST and MDA induced by CCl4,but it had no influence on serum LDH,ALP level and SOD activity in the liver homogenate.CONCLUSION The obtained results suggest that oral administration of NYG-1 hasve the protective effects against CCl4-induced acute hepatic injury in rats,Its mechanism may be related to antioxidant-like action.

Ablation of apoptosis-stimulating of p53 protein 1 protects mice from acute hepatic injury and dysfunction via NF-κB pathway in CCl4-induced hepatotoxicity

Acute liver injury(ALI)is characterized by apoptosis,inflammation,and oxidative stress,and pathogenic mechanism of ALI is poorly understood.Apoptosis-stimulating of p53 protein 1(ASPP1)is involved in environmental responses,tumor growth,and NF-κB activity,which is of critical importance to ALI.However,the role of ASPP1 in ALI remains largely unexplored.The current study aimed to determine the role of ASPP1 in ALI induced by CCl4 and the underlying mechanism.ASPP1 expression was detected in wild type(WT)mice with ALI induced by CCl4.The function of ASPP1 in ALI induced by CCl4 was investigated using conventional knockout ASPP1 mice.ASPP1 expression significantly increased in ALI mice at 24 hours after CCl4 injection.Deletion of ASSP1 ameliorated apoptosis,inflammation,and necrosis in ALI relative to WT mice.In addition,deficiency of ASPP1 improved liver flood flow as well as ALT and AST levels.The levels of phosphorylated p65 and phosphorylated IκBαwere lower in ASPP1-/-mice than in WT mice with ALI.These results implicate that deletion of ASPP1 may act via inhibition of the NF-кB pathway and protect mice from ALI,which may be a new potential therapeutic target for the treatment of ALI.

CCL 4与BDL致大鼠肝损伤中α-SMA、Hab18G/CD147表达的差异

探究CCL 4腹腔注射和胆总管结扎(Bile Duct Ligation,BDL)致大鼠肝损伤中α-SMA、Hab18G/CD147表达的差异,为法医学鉴定药物性肝损伤提供科学参考。选取雄性SD大鼠60只,随机分为CCL 4对照组(N)、BDL对照组(S)、CCL 4肝损伤组(C)、BDL肝损伤组(B),每组各15只。各组分别在实验1 w、3 w、5 w时断颈处死5只大鼠,采血检测谷丙转氨酶(Glutamic pyruvic transaminase,ALT)、谷草转氨酶(Aspertate aminotransferase,AST),总胆红素(Total bilirubin,TBIL)、直接胆红素(Direct bilirubin,DBIL),检测α-SMA、Hab18G/CD147mRNA的表达情况。qRT-PCR检测结果显示,C组α-SMAmRNA、Hab18G/CD147mRNA的表达量在1 w、3 w、5 w同时间段相比均高于B组(P<0.05)。与对照组相比较,C组、B组血清中ALT、AST、DBIL、TBIL含量均增加,说明大鼠肝脏均有不同程度的损伤;CCL 4与BDL肝损伤有不同特点,在肝损伤过程中α-SMA、Hab18G/CD147mRNA的表达随着损伤时间的延长表达量逐渐增加。

Protective Effect and Action Mechanism of Modified Ershiwuwei Songshi Pills on Chronic Liver Injury Induced by CCL4

[Objectives]To study the protective effect of Ershiwuwei Songshi Pills on chronic liver injury induced by carbon tetrachloride(CCL4)in rats before and after the modification conforming to the compatibility theory of Tibetan medicine,and to explore its action mechanism.[Methods]Male Wistar rats were randomly divided into the blank control group,model group,Hugan tablets group(0.490 g/kg),Ershiwuwei Songshi Pills group(0.117 g/kg),and Modified Ershiwuwei Songshi Pills group(removing cinnabaris,Aristolochia contorta,and Aconitum naviculare,0.105 g/kg).Except the blank group,the remaining groups were injected subcutaneously with 20%carbon tetrachloride olive oil solution every 3 d,and modeled for 6 weeks.During this time,intragastrically administered corresponding drugs.Six weeks later,blood was taken from the femoral artery,and the rats were killed through dislocating the cervical spine,the liver was taken,and the content of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)was determined.Then,liver fibrosis indicators tumor necrosis factor-α(TNF-α),nuclear factor-κB(NF-κB),interleukin-6(IL-6)and interleukin-1β(IL-1β)were detected by immunohistochemical method.[Results]Compared with the model group,the pathological map of the liver section showed that liver injury was improved in each administration group.The serum ALT and AST contents in rats of each administration group were significantly reduced(P<0.05),and the protein expressions of NF-κB,TNF-α,IL-1βand IL-6 in liver tissue were also reduced by varying degrees(P<0.05).[Conclusions]Ershiwuwei Songshi Pills and its modification group have a protective effect on liver injury induced by carbon tetrachloride.The modified prescription conforms to the compatibility rules of Tibetan medicine.The mechanism may be related to reducing the damage caused by inflammatory factors through regulating the role of inflammatory signaling pathway.Thus,it can be used as a reference for future optimization proposals.

The Protective Effect of Arabinose + Mannose on Mice with Acute Liver Injury Induced by CCl_4 and Its Mechanism

[Objectives] Taking mice with acute liver injury induced by CCl_4 as the model,the effect of arabinose + mannose( w/w = 1∶ 1) on mice with acute liver injury induced by CCl_4 was studied. [Methods]60 experimental mice were selected and then randomly divided into normal control,model group and positive group( bifendate 120 mg/kg),high-dose arabinose + mannose group( 800 mg/kg),middle-dose arabinose + mannose group( 400 mg/kg) and low-dose arabinose + mannose group( 200 mg/kg),each group had 10 mice,which were fed adaptively for 1 week. Except normal control group and model group,each treatment group was given medicine by gavage once a day and lasted for7 days according to the dosage of 20 ml/kg. After the last drug,except normal control group,the mice of other groups were injected 10 ml/kg0. 12% CC14 peanut oil through enterocoelia,thereby establishing acute liver injury model. The mice were fasted but not water for 24 h,after that,blood was sampled from mice eyes,then dissected rapidly. The activities of ALT and AST in the serum were determined,the expression levels of TNF-α,IL-1β and IL-6 from the hepatic tissues were detected by enzyme-linked immunosorbent assay( ELISA); then after HE dye,the changes of liver histopathology were observed. [Results]Compared with CCl_4 model,the activities of ALT and AST from the serum of mice from high-dose and middle dose groups decreased significantly( P < 0. 01); the contents of TNF-α,IL-1β and IL-6 from the hepatic tissues of mice decreased significantly( P < 0. 01); the pathological section showed that the liver injury of mice from the combined drug groups showed alleviating trend to varying degrees,in which the liver injury of mice from the high-dose group was the best. [Conclusions] Arabinose + mannose has an obvious protective effect on mice with acute liver injury induced by CCl_4,and its mechanism may relate to anti-inflammatory.

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.

小分子多肽LK-5对CCl4致急性肝损伤小鼠的保护作用研究

【目的】研究小分子多肽LK-5(氨基酸序列为LHMFK)对CCl4致急性肝损伤模型小鼠的保护作用,探讨其作用机制。【方法】72只小鼠随机分为正常组、模型组、联苯双酯组(150 mg/kg)及LK-5低、中、高剂量组(30、60、120 mg/kg),每组12只。连续给药10 d, 1次/d,每次10 mL/kg。末次给药2 h后,各组(除正常组外)腹腔注射0.1%CCl4花生油溶液,建立CCl4致小鼠急性肝损伤模型,16 h后,按照试剂盒方法,检测小鼠血清天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、总胆汁酸(TBA)和碱性磷酸酶(AKP)水平,检测肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、肿瘤坏死因子(TNF-α)、白细胞介素-6(IL-6)、IL-10、血管紧张素1-7(Ang 1-7)和血管紧张素Ⅱ(AngⅡ)水平。制作肝脏病理组织切片,苏木精-伊红染色(HE)后观察肝脏组织病理学变化。【结果】与正常组比较,模型组小鼠肝细胞有明显的脂肪变性,炎细胞分散分布于肝小叶血管周围和肝实质内,血清ALT、AST、AKP活性和TBA水平均显著上升,肝组织SOD、GSH-Px活性显著下降,MDA水平显著上升(P<0.05),说明成功建立急性肝损伤模型,TNF-α、IL-6、AngⅡ水平显著升高(P<0.05)。与模型组比较,LK-5中、高剂量组能够显著降低血清ALT、AST活性(P<0.05),各剂量组均可降低血清TBA水平和AKP活性(P<0.05),LK-5高剂量组能够显著提高小鼠肝组织SOD、GSH-Px活性(P<0.05),LK-5中、高剂量组能够显著降低肝组织MDA水平(P<0.05),LK-5高剂量组TNF-α水平显著降低(P<0.05),各剂量组能够显著降低肝组织IL-6、AngⅡ水平(P<0.05)。病理切片结果显示,LK-5各剂量组炎细胞均有不同程度减少,LK-5高剂量组肝小叶血管周围和肝实质内无炎细胞浸润。【结论】LK-5各剂量组对CCl4致急性肝损伤小鼠具有保护作用,其中60、120 mg/kg LK-5效果更为明显,其作用机制可能与抗氧化、抗炎及对肾素-血管紧张素系统(RAS)的调控有关。

Portulaca oleracea alleviates CCl4-induced acute liver injury by regulating hepatic S100A8 and S100A9

Objective: Acute liver injury(ALF) is a potential factor of many serious hepatopathies. Carbon tetrachloride(CCl4) is a possible environmental toxicant that can induce ALF. Portulaca oleracea(PO) is one of the most popular edible herbs and has several biological activities such as antioxidant, antimicrobial, antiinflammatory effects. We explored the significance of PO in regulating inflammatory function in animal models and cultured hepatocytes during liver damage caused by CCl4.Methods: The effect of PO on ALF was evaluated by CCl4-induced mice models in vivo. Hepatic levels of transaminase activities and inflammatory factors were examined. The gene and protein expression of S100A8 and S100A9 were measured by RT-PCR and Western blot analysis. Meanwhile, the efficacy of PO was certified by HepG2 cells in vitro. The transaminase activities, inflammatory factors, and the protein expression of S100A8 and S100A9 were also detected.Results: Animal tests showed that pretreatment with PO reduced the liver pathological tissue damage and the serum levels of ALT, AST, ALT and LDH, as well as reducing the pro-inflammatory cytokines(IL-1β, IL-6, TNF-a) secretion in CCl4-induced liver injury mice. Simultaneously, Hep G2 cells pretreated with PO exhibited a significant decrease in the activities of ALT and AST. Moreover, PO resulted in a significant downregulation of the pro-inflammatory markers S100A8, S100A9 gene and protein expression on CCl4induced acute liver injury was demonstrated entirely in vivo and vitro experiments.Conclusion: PO may down-regulate S100A8 and S100A9 and inhibit pro-inflammatory cytokines’ release,indicating a potential clinical effect for controlling the disease.

黄芩苷镁盐对CCl4诱导的SD大鼠急性肝损伤的影响

目的探讨黄芩苷镁盐对四氯化碳(CCl4)诱导的SD大鼠急性肝损伤的影响及有效的治疗浓度。方法80只SD大鼠,随机分为正常对照组、模型组、阳性对照组〔异甘草酸镁,18mg/(kg·d)〕及黄芩苷镁盐Ⅰ〔12.5mg/(kg·d)〕、Ⅱ〔25.0mg/(kg·d)〕、Ⅲ〔50.0mg/(kg·d)〕、Ⅳ〔100.0mg/(kg·d)〕、Ⅴ〔200.0mg(kg·d)〕组。连续尾静脉注射1w。末次给药2h,除正常对照组外,其余组腹腔注射1ml/kg50%CCl4橄榄油溶液造模。采用苏木素-伊红(HE)染色观察肝组织病理改变,全自动生化检测各组血清中天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)的变化情况,丙二醛(MDA)测定试剂盒检测各组MDA的水平变化。结果模型组肝细胞结构破坏明显,各组黄芩苷镁盐肝细胞结构较模型组有所改善,尤以黄芩苷镁盐Ⅲ、Ⅳ、Ⅴ组肝细胞改善明显。模型组ALT、AST水平显著高于正常对照组(P<0.01)。黄芩苷镁盐Ⅲ、Ⅳ、Ⅴ组ALT、AST水平均显著低于模型组(P<0.05)。与阳性对照组相比,黄芩苷镁盐Ⅲ、Ⅳ、Ⅴ组ALT水平均显著性降低(P<0.05),但AST两者无显著区别(P>0.05)。模型组MDA水平显著高于正常对照组(P<0.01)。黄芩苷镁盐Ⅲ、Ⅳ、Ⅴ组均可显著降低肝组织MDA水平(P<0.05)。与阳性对照组相比,黄芩苷镁盐Ⅳ、Ⅴ组MDA降低水平无显著区别(P>0.05)。结论黄芩苷镁盐可减轻CCl4对SD大鼠造成的急性肝损伤,100.0mg/(kg·d)的给药剂量效果较好。

山荷降脂方对CCl_4诱导的小鼠急性肝损伤的保护作用

目的 :探讨山荷降脂方对CCl4 诱导的小鼠急性肝损伤的保护作用。方法 :用腹腔注射CCl4 法制作小鼠肝损伤模型。实验动物随机分为①正常对照组 ;②假肝损伤组 ;③肝损伤组 ;④生理盐水 +肝损伤组 ;⑤山荷降脂方 (低剂量 ) +肝损伤组 ;⑥山荷降脂方 (中剂量 ) +肝损伤组 ;⑦山荷降脂方 (高剂量 ) +肝损伤组。末次给药后 0 .5～ 1h ,腹腔注射质量分数为 0 .12 %的CCl4 花生油溶液(剂量为 0 .0 1mL/g) ,禁食 16h后处死。取肝脏 ,进行HE染色 ;球后取血 ,离心血清 ,测谷丙转氨酶、谷草转氨酶活性。结果 :(1)谷丙转氨酶、谷草转氨酶活性 :⑤、⑥、⑦组与③组比较有显著性差异 (P=0 .0 0 0 1) ,⑤、⑥、⑦组两两之间也有显著性差异 (P =0 .0 0 0 1)。 (2 )HE染色 ,光镜下观察肝脏组织病理学变化 ,⑥、⑦组肝损伤程度与③组比较 ,有显著性差异 (P <0 .0 1;P <0 .0 0 1) ,⑤、⑥组与⑦组也有显著性差异 (P <0 .0 0 1,P <0 .0 5 )。结论 :山荷降脂方对急性肝损伤具有呈量效关系的保护作用。

秃疮花有效成分对小鼠CCL_4肝损伤的保护作用

目的 探讨不同剂量的DLF对小鼠肝脏的保护作用。方法 先用DLF预防给药 ,再采用CCL4 制作小鼠急性化学性肝损伤模型 ,以BDD为阳性对照。采用全自动生化分析仪测定血清ALT、ALP、AST和LDH的含量 ;联苯三酚自氧化法测定血清SOD含量 ;TBA显色法测定肝匀浆中的MDA含量 ;肝组织常规制片 ,组织学观察。结果 不同剂量的DLF组血清ALT、ALP、AST、LDH和肝组织中MDA含量明显低于CCL4 组 ,血清SOD组明显高于CCL4 组 ;镜下病理显示 ,DLF对由CCL4 引起的小鼠急性化学性肝损伤造成的肝细胞变性、坏死有一定的保护作用。结论 DLF对由CCL4 引起的小鼠急性化学性肝损伤有保护作用 ,其作用机制可能与其抗自由基有关。

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

Experimental Study of Pratia Extact on Acute Liver Injury in Mice

[Objectives] This study was conducted to observe the protective effect of Pratia extract on acute liver injury in mice.[Methods] Mice were randomly divided into 6 groups according to body weight,10 in each group: normal control group,ethanol-induced/CCl4 liver injury model,low-dose,middle-dose and high-dose Pratia extract groups,and bifendatatum group.Except the blank group,other groups were given 50% ethanol intragastrically at a dose of 12 ml/kg to cause acute alcoholic liver injury,or intraperitoneally injected with 10% CCl4 soybean oil solution to cause acute CCl4 liver injury.The serum ALT and AST activity were measured as well as liver SOD and MDA concentrations.[Results] Pratia extract effectively reduced serum ALT and AST,decreased MDA content and increased liver tissue SOD activity.[Conclusions] Pratia extract has certain protective effect on acute liver injury.

大豆、枸杞子、山楂复合提取物对小鼠化学性肝损伤的保护作用

目的 : 研究大豆、枸杞子、山楂复合提取物对小鼠化学性肝损伤的保护作用。方法 : 设立空白对照、肝损伤对照和 0 .0 6、0 .2 0、0 .60 g/( kg· bw)复合提取物五组 ,分别建立小鼠CCl4 肝损伤模型和乙醇肝损伤模型 ,4w后 ,前者测定血清中丙氨酸氨基转移酶 ( ALT)及天门冬氨酸氨基转移酶 ( AST)活性 ,同时观察肝脏组织病理 ;后者测定肝匀浆中丙二醛 ( MDA)、谷胱甘肽( GSH)和甘油三酯 ( TG)含量 ,同时观察肝脏病理。结果 : CCl4 肝损伤模型 :复合提取物中剂量组的血清 ALT及中、高剂量组的血清 AST水平均较 CCl4 对照组降低 ,低剂量组发生肝细胞坏死和中、高剂量组发生炎症细胞浸润的程度明显较 CCl4 对照组轻。乙醇肝损伤模型 :低、高剂量组MDA和各剂量组 TG含量以及低、中剂量组脂肪变性评分均明显低于乙醇对照组。结论 : 大豆、枸杞子、山楂复合提取物对 CCl4 和乙醇诱导的小鼠化学性肝损伤有保护作用。

正交试验法优选小鼠四氯化碳肝损伤模型

目的 采用正交试验法优选小鼠四氯化碳肝损伤最佳模型制作条件。方法 选择对小鼠血清转氨酶 (ALT)有影响的四个因素 (1)四氯化碳浓度 ;(2 )肝毒剂中毒剂量 ;(3)中毒次数 ;(4)中毒途径 ,每个因素取 3个水平 ,按L9(34 )正交试验表安排试验 ,以阳性药联苯双酯对小鼠四氯化碳肝损伤改善率为考察指标 ,评定四氯化碳中毒方案的优劣。结果 采用 0 .1% (v/v)的四氯化碳 ,按每 10g小鼠 0 .2ml剂量腹腔一次注射的给药方案为佳。

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

枸杞粗多糖对化学性肝损伤保护作用

目的 探讨服用枸杞粗多糖对小鼠肝损伤的保护作用。方法 采用卫生部的《保健食品检验与评价技术规范》(2 0 0 3年版 ) [1] 。结果 枸杞粗多糖可明显抑制CCl4 引起小鼠血清谷丙转氨酶(ALT)和谷草转氨酶 (AST)的升高 ,并能改善和恢复各病理指标。结论 枸杞粗多糖对肝脏有较好的保护作用。

疏肝胶囊对实验性肝损伤的保护作用

采用四氯化碳和D 氨基半乳糖诱导的大鼠实验性肝损伤动物模型研究疏肝胶囊的护肝效应 ,疏肝胶囊 1 2 5、2 5和5 0 g/kg显著抑制四氯化碳肝损伤大鼠血清中丙氨酸转移酶、门冬氨酸转移酶活性 ,5 0 g/kg明显抑制D 氨基半乳糖肝损伤大鼠血清丙氨酸转移酶、门冬氨酸转移酶活性 ,降低总胆红素含量 。

丙肝宁对动物实验性肝损伤的保护作用

目的 研究中药复方丙肝宁的保肝作用。方法 采用D Gal造成大鼠的急性肝损伤模型和CCl4 所致慢性肝损伤模型。结果 丙肝宁 2个剂量组对D Gal造成大鼠的急性肝损伤模型和CCl4 所致慢性肝损伤模型的血清酶活性均具有明显的抑制作用 (P <0 .0 5 ,P <0 .0 1) ,病理检查结果表明 ,丙肝宁 2个剂量组对D Gal造成大鼠的急性肝损伤模型和CCl4 所致慢性肝损伤模型的肝脏病理形态的改变具有明显的改善作用。