东当归对四氯化碳及乙醇性肝损伤的保护作用

研究东当归水提取物对四氯化碳及乙醇所致小鼠SGPT和SGOT活性升高的影响。在四氯化碳及乙醇所致小鼠急性肝损伤的血清中检测SGPT和SGOT值。结果表明,37．5％、75．0％和150．0％东当归水提物在体内显著抑制四氯化碳及乙醇所致小鼠SGPT值和／或SGOT值升高。东当归水提取物对小鼠四氯化碳及乙醇性肝损伤具有保护作用。     

兖州卷柏水提物对四氯化碳致小鼠肝损伤的保护作用和抗氧化活性（英文）

研究兖州卷柏对四氯化碳(CCl4)致小鼠肝损伤的保护效果。昆明小鼠随机分为6组(n=8):正常组、CCl4模型组、水飞蓟素对照组、兖州卷柏水提物(高、中、低)剂量组(400、200、100 mg/kg)。各组连续灌胃给药9d后,除正常组外,其余各组用CCl4溶液(2 m L/kg)灌胃。结果显示兖州卷柏能显著的抑制肝损伤血清中SGOT、SGPT、ALP、LDH、胆固醇和胆红素升高(P0.01)。兖州卷柏能降低损伤肝组织的脂肪含量,局灶性坏死,中心静脉充血和正弦空间拥塞。体外抗氧化实验表明兖州卷柏抗氧化活性指标T-AOC、LPO、T-SOD和NO的IC50值明显高于维生素C(P0.05)。提示兖州卷柏水提物可能通过其抗氧化活性对四氯化碳致小鼠肝损伤产生保护效果。     

茵栀黄注射液对四氯化碳和硫代乙酰胺致小鼠肝脏损伤的保护作用

目的 :研究茵栀黄注射液对四氯化碳 (CCl4 )和硫代乙酰胺 (TAA)所致小鼠肝脏损伤的保护作用。方法 :采用四氯化碳和硫代乙酰胺造成小鼠化学性损伤 ,观察茵栀黄注射液的保护作用。结果 :小鼠静脉注射茵栀黄注射液能明显降低CCl4 和TAA所致小鼠血清ALT和AST水平 ,并可显著改善小鼠肝损伤的病变程度。结论 :茵栀黄注射液对CCl4 和TAA所致小鼠肝损伤具有保护作用     

茵栀黄注射液对四氯化碳和硫化乙酰胺致小鼠肝脏损伤的保护作用

目的：研究茵栀黄注射液对四氯化碳（CCl4)和硫代乙酰胺（TAA）所致小鼠肝脏损伤的保护作用。方法：采用四氯化碳和硫代乙酰胺造成小鼠化学性损伤,观察茵栀黄注射液的保护作用,结果：小鼠静脉注射茵栀黄注射液能明显降低CCl4和TAA所致小鼠血清ALT和AST水平,并可显著改善小鼠肝损伤的病变程度,结论：茵栀黄注射液对CCl4和TAA所致小鼠肝损伤具有保护作用。     

4-羟基苯并恶唑-2-酮对四氯化碳致小鼠急性肝损伤保护作用

日的研究4一羟基苯并恶唑-2-酮（4-hydroxy-2-benzoxazolone,HBOA）对四氯化碳所致小鼠急性肝损伤的保护作用,并探讨其疗效机制。方法采用腹腔注射四氯化碳（carbonte trachloride,cch）制备小鼠急性肝损伤模型,HBOA灌胃给药,检测小鼠血清中的乳酸脱氢酶（LDH）活性以及肝组织中过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）含量,并用免疫组化法观察肿瘤坏死因子（TNF-a）的表达情况。结果HBOA能明显降低CCh致急性肝损伤小鼠血清LDH活性,同时升高肝组织中CAT、GSH-Px的活性并降低肝组织中TNF-a的表达。结论HBOA对CCh所致小鼠急性肝损伤有一定的保护作用。     

当归及其炮制品水提物体外抗脂质过氧化作用

为了研究当归及其不同炮制品水提物抗脂质过氧化的作用。采用体外小鼠肝组织自发性脂质过氧化、H2O2诱导的红细胞膜脂质过氧化和溶血反应,评价了当归及其炮制品水提物对脂质过氧化的抑制作用。结果表明当归及其不同炮制品水提物体外对肝组织自发性脂质过氧化的抑制能力为当归碳酒当归生当归油当归土当归;对H2O2诱导的红细胞膜脂质过氧化的抑制能力为当归碳土当归生当归酒当归油当归;对H2O2诱导的溶血作用的抑制能力为酒当归当归碳土当归油当归生当归,且抑制效果均呈现良好的剂量依赖关系。说明当归及其不同炮制品水提物体外都具有一定的抗脂质过氧化的作用,其中抗肝组织自发性脂质过氧化和H2O2诱导的红细胞膜脂质过氧化的能力以当归碳最好,而抗H2O2诱导的溶血作用以酒当归最好。     

当归水提液和醇提液体外抗脂质过氧化和红细胞溶血作用

研究当归水提液和醇提液对小鼠肝组织自发性过氧化酯质分解产物丙二醛（malondialdehyde,MDA）的生成和对红细胞膜脂质过氧化及红细胞溶血作用的影响。采用TBA比色法测定肝组织匀浆MDA生成,分光光度法测定过氧化氢诱导红细胞膜脂质过氧化和溶血。实验分为空白组、对照组、加药组。加药组分为25、50、100和200mg/mL四个浓度组。当归水提液和醇提液均在25～200mg／mL的浓度范围内,能够明显抑制小鼠肝组织匀浆自发性MDA的生成,具有抑制过氧化氢诱导红细胞膜脂质过氧化和溶血的作用,抑制效果随当归水提液和醇提液浓度的增大而逐渐增强,抑制率与药物浓度成良好的量效关系。当归水提液和醇提液具有抗脂质过氧化和红细胞溶血的作用。     

基于仿生技术对不同产地当归阿魏酸含量与滋味的关联性研究

目的：比较45个产地当归的滋味及阿魏酸含量差异,探讨滋味与阿魏酸含量的相关性,从而评价不同产地当归品质的优劣。方法：运用电子舌技术测定甘肃省45个县市当归样品的9种滋味,HPLC法测定阿魏酸含量,采用95%可信区间重叠法进行统计分析与比较味觉及阿魏酸差异,并将9种滋味与阿魏酸含量进行相关性研究,为当归药材的品质评价提供参考。结果：GS19（西宁县）阿魏酸含量最高（0.29%）,GS37（西当县）甜味值最高,GS38（高台县）苦味值最高,GS14（合水县）鲜味值最高。当归滋味与其品质相关,阿魏酸与鲜味值呈显著正相关（R=0.508,P=0.000,n=45）,与苦味、涩味、甜味、咸味、苦味回味、鲜味回味值无显著相关性。结论：不同产地当归的鲜味值差异反映阿魏酸含量的高低,故可用电子舌技术评价及快速鉴别药材的品质。     

当归栽培的研究现状

当归为我国常用大宗药材,目前商品当归大多是栽培品。根据近年来有关栽培当归的研究报道,我们归纳、总结了当归种子质量、种苗大小及不同栽培方式与当归药材产量和质量的相关性,阐述了当归栽培过程中难以彻底解决的有关早期抽薹问题和麻口病问题的研究现状及生产实践中采取的主要防控措施。本综述可为当归的可持续开发利用提供科学依据。     

当归浸提物对四种药用种子萌发及幼苗的影响

目的：通过研究当归根水浸液对膜荚黄芪、板蓝根、党参和王不留行的种子萌发及幼苗生长的影响，选择当归的适宜倒茬品种。方法：采用生物测定法，研究不同浓度梯度当归根浸提液对四种药材种子萌发及幼苗生长的影响。结果：当归根水浸液对四种药材呈现“低促高抑”效应，且对发芽整齐度的影响大于发芽率，对根长的影响大于苗高，化感效应与处理浓度呈正相关。四种药材的化感物质的敏感性为：党参>黄芪>板蓝根>王不留行。结论：在选择当归倒茬品种时，应优先选择王不留行和板蓝根。     

Protective effect of L-theanine on carbon tetrachloride-induced acute liver injury in mice

We studied effects of L-theanine, a unique amino acid in tea, on carbon tetrachloride (CCl(4))-induced liver injury in mice. The mice were pre-treated orally with L-theanine (50, 100 or 200 mg/kg) once daily for seven days before CCl(4) (10 ml/kg of 0.2% CCl(4) solution in olive oil) injection. L-theanine dose-dependently suppressed the increase of serum activity of ALT and AST and bilirubin level as well as liver histopathological changes induced by CCl(4) in mice. L-theanine significantly prevented CCl(4)-induced production of lipid peroxidation and decrease of hepatic GSH content and antioxidant enzymes activities. Our further studies demonstrated that L-theanine inhibited metabolic activation of CCl(4) through down-regulating cytochrome P450 2E1 (CYP2E1). As a consequence, L-theanine inhibited oxidative stress-mediated inflammatory response which included the increase of TNF-α and IL-1β in sera, and expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in livers. CCl(4)-induced activation of apoptotic related proteins including caspase-3 and PARP in mouse livers was also prevented by L-theanine treatment. In summary, L-theanine protects mice against CCl(4)-induced acute liver injury through inhibiting metabolic activation of CCl(4) and preventing CCl(4)-induced reduction of anti-oxidant capacity in mouse livers to relieve inflammatory response and hepatocyte apoptosis.     

Transgene expression of human PON1 Q in mice protected the liver against CCl4-induced injury

BACKGROUND: Oxidative stress, often in association with decreased antioxidant defenses, plays a pathogenetic role in both initiation and progression of liver injuries, leading to almost all clinical and experimental conditions of chronic liver diseases. Human paraoxonase 1 (hPON1) is a liver-synthesized enzyme possessing antioxidant properties. Here, we investigate the effects of transgene-expressed hPON1 Q on alleviating lipid peroxidation and preventing liver injury in a mouse model. METHODS: The hPON1 Q gene was cloned into pcDNA3.0 plasmid and electro-transferred into mouse skeletal muscle. After CCl4 had been administrated to induce liver injury, mice were monitored for serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malonyldialdehyde (MDA). The extent of CCl4-induced liver injury was also analyzed through histopathological observations. RESULTS: After gene delivery, hPON1 mRNA expression was detected in mouse muscle and serum PON1 activity was 1.5 times higher than that of the control counterpart. In the PON1 Q gene transferred mice, protection against CCl4-induced liver injury was reflected by significantly decreased serum ALT, AST and MDA levels compared to those in control mice (P < 0.01). Histological observations also revealed that hepatocyte necrosis, hemorrhage, vacuolar change and hydropic degeneration were apparent in control mice after CCl4 administration. In contrast, the damage was significantly prevented (P < 0.01) in the hPON1 Q transferred mice. CONCLUSIONS: Intramuscular electro-transfer of the hPON1 Q gene led to efficient expression of hPON1 in mice. Elevated levels of PON1, by virtue of its potency to alleviate oxidative stress, could protect mice from suffering CCl4-induced liver damage.     

Hepatoprotective effect of Hibiscus hispidissimus Griffith, ethanolic extract in paracetamol and CCl4 induced hepatotoxicity in Wistar rats

Hibiscus hispidissimus Griff. is used in tribal medicine of Kerala, the southern most state of India, to treat liver diseases. In the present study, the effect of the ethanolic extract of Hibiscus hispidissimus whole plant on paracetamol (PCM)-induced and carbon tetrachloride (CCl4)-induced liver damage in healthy Wistar albino rats was studied. The results showed that significant hepatoprotective effects were obtained against liver damage induced by PCM and CCl4 as evidenced by decreased levels of serum enzymes, glutamate oxaloacetate transaminase (SGOT), glutamate pyruvate transaminase (SGPT), serum alkaline phosphatase (SAKP), serum bilirubin (SB) and an almost normal histological architecture of the liver of the treated groups compared to the toxin controls. The extract also showed significant antilipid peroxidant effects in vitro, besides exhibiting significant activity in quenching 1, 1-diphenyl-2-picryl hydrazyl (DPPH) radical, indicating its potent antioxidant effects.     

Rho-kinase inhibitor prevents hepatocyte damage in acute liver injury induced by carbon tetrachloride in rats

A protective effect of Rho-kinase inhibitor on various organ injuries is gaining attention. Regarding liver injury, Rho-kinase inhibitor is reported to prevent carbon tetrachloride (CCl4)- or dimethylnitrosamine-induced liver fibrosis and hepatic ischemia-reperfusion injury in rats. Because Rho-kinase inhibitor not only improved liver fibrosis but also reduced serum alanine aminotransferase (ALT) level in CCl4-induced liver fibrosis, we wondered whether Rho-kinase inhibitor might exert a direct hepatocyte-protective effect. We examined this possibility in acute CCl4 intoxication in rats. Rho-kinase inhibitor, HA-1077, reduced serum alanine ALT level in rats with acute liver injury induced by CCl4 with the improvement of histological damage and the reduction of the number of apoptotic cells. In cultured rat hepatocytes in serum-free condition, HA-1077 reduced apoptosis evaluated by quantitative determination of cytoplasmic histone-associated DNA oligonucleosome fragments with the reduction of caspase-3 activity and the enhancement of Bcl-2 expression. HA-1077 stimulated phosphorylation of Akt, and wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3-kinase)/Akt pathway, abrogated the reduction of hepatocyte apoptosis by HA-1077 in vitro. Furthermore, wortmannin abrogated the reduction of serum ALT level by HA-1077 in rats with acute liver injury induced by CCl4, suggesting that the activation of PI3-kinase/Akt pathway may be involved in the hepatocyte-protective effect by Rho-kinase inhibitor in vivo. In conclusion, Rho-kinase inhibitor prevented hepatocyte damage in acute liver injury induced by CCl4 in rats and merits consideration as a hepatocyte-protective agent in liver injury, considering its direct antiapoptotic effect on hepatocytes in vitro.     

Hepatoprotective and antioxidant effect of tender coconut water on carbon tetrachloride induced liver injury in rats

Hepatoprotective and antioxidant effects of tender coconut water (TCW) were investigated in carbon tetrachloride (CCl4)-intoxicated female rats. Liver damage was evidenced by the increased levels of serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) and decreased levels of serum proteins and by histopathological studies in CCl4-intoxicated rats. Increased lipid peroxidation was evidenced by elevated levels of thiobarbituric acid reactive substance (TBARS) viz, malondialdehyde (MDA), hydroperoxides (HP) and conjugated dienes (CD), and also by significant decrease in antioxidant enzymes activities, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (Gpx) and glutathione reductase (GR) and also reduced glutathione (GSH) content in liver. On the other hand, CCl4-intoxicated rats treated with TCW retained almost normal levels of these constituents. Decreased activities of antioxidant enzymes in CCl4-intoxicated rats and their reversal of antioxidant enzyme activities in TCW treated rats, shows the effectiveness of TCW in combating CCl4-induced oxidative stress. Hepatoprotective effect of TCW is also evidenced from the histopathological studies of liver, which did not show any fatty infiltration or necrosis, as observed in CCl4-intoxicated rats.     

Garlic oil and DDB, comprised in a pharmaceutical composition for the treatment of patients with viral hepatitis, prevents acute liver injuries potentiated by glutathione deficiency in rats

A pharmaceutical composition PENNEL comprising garlic oil (GO) and dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylene dioxybiphenyl-2,2'-dicarboxylate (DDB) as ingredients active for phase II enzyme induction and liver protection, respectively, has been used as a curative preparation for patients with acute or chronic viral hepatitis. In spite of the wide clinical use of PENNEL in Asian and Middle Eastern countries, whether GO+DDB treatment synergistically protects the liver from injuries potentiated by GSH deficiency compared to the individual treatment has not been determined. This study investigated the effects of GO+DDB in comparison with each ingredient alone on chemical-induced liver injury potentiated by a GSH depleting agent. Rats that had been daily pretreated with GO+DDB, GO, DDB, ursodesoxycholic acid or silymarin for 6 days were exposed to buthionine sulfoximine (BSO) and then injected with a single dose of CCl4. The effects of the agents on acute liver toxicities induced by BSO, CCl4 or BSO+CCl4 were assessed by blood biochemistry and histopathology. GO+DDB pretreatment effectively prevented increases in plasma aminotransferases or lactate dehydrogenase activities in rats exposed to BSO+CCl4, compared to GO or DDB treatment alone. Whereas BSO potentiated CCl4-induced liver injuries as evidenced by elevations in central necrosis, hepatocyte degeneration and inflammation, pretreatment with GO+DDB abrogated BSO+CCl4-induced liver injuries more efficaciously than did that with GO or DDB. The hepatoprotective effect of GO+DDB was superior to that of ursodesoxycholic acid or silymarin. Also, blood biochemistry indicated that GO+DDB pretreatment prevented increases in plasma triglyceride contents in rats insulted with CCl4 or BSO+CCl4. The present study demonstrated that GO+DDB, when daily pretreated for six consecutive days, exerted synergistic protection of the liver from chemical-induced injury potentiated by the condition of GSH deficiency, and has additional advantages in lowering the plasma lipids.     

Kupffer cells inhibition prevents hepatic lipid peroxidation and damage induced by carbon tetrachloride

The aim of this work was to determine if the action mechanism of gadolinium on CCl(4)-induced liver damage is by preventing lipid peroxidation (that may be induced by Kupffer cells) and its effects on liver carbohydrate metabolism. Four groups of rats were treated with CCl(4), CCl(4)+GdCl(3), GdCl(3), and vehicles. CCl(4) was given orally (0.4 g 100 g(-1) body wt.) and GdCl(3) (0.20 g 100 g(-1) body wt.) was administered i.p. All the animals were killed 24 h after treatment with CCl(4) or vehicle. Glycogen and lipid peroxidation were measured in liver. Alkaline phosphatase, gamma-glutamyl transpeptidase, alanine amino transferase activities and bilirubins were measured in rat serum. A liver histological analysis was performed. CCl(4) induced significant elevations on enzyme activities and bilirubins; GdCl(3) completely prevented this effect. Liver lipid peroxidation increased 2.5-fold by CCl(4) treatment; this effect was also prevented by GdCl(3). Glycogen stores were depleted by acute intoxication with CCl(4). However, GdCl(3) did not prevent this effect. The present study shows that Kupffer cells may be responsible for liver damage induced by carbon tetrachloride and that lipid peroxidation is produced or stimulated by Kupffer cells, since their inhibition with GdCl(3) prevented both lipid peroxidation and CCl(4)-induced liver injury.     

Protective effects of melatonin against carbon tetrachloride hepatotoxicity in rats

Melatonin is an indolamine, mainly secreted by the pineal gland into the blood of mammalian species. The potential for protective effects of melatonin on carbon tetrachloride (CCl(4))-induced acute liver injury in rats was investigated in this work. CCl(4) exerts its toxic effects by generation of free radicals; it was intragastrically administered to male Wistar rats (4 g kg(-1) body weight) at 20 h before the animals were decapitated. Melatonin (15 mg kg(-1) body weight) was administered intraperitoneally three times: 30 min before and at 2 and 4 h after CCl(4) injection. Rats injected with CCl(4) alone showed significant lipid and hydropic dystrophy of the liver, massive necrosis of hepatocytes, marked increases in free and conjugated bilirubin levels, elevation of hepatic enzymes (alanine aminotransferase and aspartate aminotransferase) in plasma, as well as NO accumulation in liver and in blood. Melatonin administered at a pharmacological dose diminished the toxic effects of CCl(4). Thus it decreased both the structural and functional injury of hepatocytes and clearly exerted hepatoprotective effects. Melatonin administration also reduced CCl(4)-induced NO generation. These findings suggest that the effect of melatonin on CCl(4)-induced acute liver injury depends on the antioxidant action of melatonin.     

Lipid peroxidation in purified plasma membrane fractions of rat liver in relation to the hepatoxicity of carbon tetrachloride

Preparations of rat liver sinusoidal plasma membrane have been tested for their ability to metabolize the hepatotoxin carbon tetrachloride (CCl4) to reactive free radicals in vitro and compared in this respect with standard preparations of rat liver microsomes. The sinusoidal plasma membranes were relatively free of endoplasmic reticulum-associated activities such as the enzymes of the cytochrome P450 system and glucose-6-phosphatase. CCl4 metabolism was measured as (i) covalent binding of [14C]-CCl4 to membrane protein, (ii) electron spin resonance spin-trapping of CCl3. radicals and (iii) CCl4-induced lipid peroxidation. By all of these tests, purified sinusoidal plasma membranes were found unable to metabolize CCl4. The fatty acid composition of the plasma membranes was almost identical to that of the microsomal preparation and both membrane fractions exhibited similar rates of the lipid peroxidation that was stimulated non-enzymically by gamma-radiation or incubation with ascorbate and iron. The absence of CCl4-induced lipid peroxidation in the plasma membranes seems to be due, therefore, to an absence of CCl4 activation rather than an inherent resistance to lipid peroxidation. We conclude that damage to the hepatocyte plasma membrane during CCl4 intoxication is not due to a significant local activation of CCl4 to CCl3. within that membrane.