美味猕猴桃根提取物保肝降酶作用的研究

目的观察美味猕猴桃根不同极性溶剂的提取物对四氯化碳(CCl4)肝损伤小鼠血浆转氨酶活性的影响。方法采用CCl4建立小鼠急性肝损伤模型,以不同的提取物和阳性对照药甘草酸二铵灌胃治疗,测定小鼠血浆中丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)活性。结果美味猕猴桃根60%乙醇提取物(C部位),经乙酸乙酯萃取,萃余物上大孔树脂60%~90%乙醇洗脱部分(A部位)60 mg/kg对CCl4造成的小鼠急性肝损伤ALT、AST活性升高具有显著的降低作用。结论美味猕猴桃根提取物部位A对肝脏损伤有保护作用。     

降肝灵对小鼠急慢性肝损伤的保护作用

目的研究中药复方降肝灵对实验性肝损伤的保护作用。方法采用CCl4所致小鼠慢性肝损伤模型和D—Gal造成的小鼠急性肝损伤模型,检测小鼠血清中Au、AST的活性,求出肝脏系数并对肝组织进行病理形态学观察。结果降肝灵对CCl。所致慢性肝损伤模型和D—Gal造成的急性肝损伤模型的血清酶活性均具有明显的抑制作用（P〈0．05,P〈0．01）;病理检查结果表明降肝灵对CCl4造成的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。结论降肝灵对小鼠的急慢性肝损伤具有一定的保护作用。     

三叶青总氨基酸对四氯化碳致小鼠肝损伤的保护作用

目的观察三叶青总氨基酸(TAART)对四氯化碳(CCl4)诱导的小鼠急性肝损伤的保护作用。方法选用CCl4致小鼠急性肝损伤模型,以测定小鼠血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)活性,肝脏系数,肝组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量及对肝组织进行病理学检查等指标观察TAART对肝损伤的保护作用。结果TAART能明显降低CCl4致小鼠肝损伤血清ALT,AST值,降低肝脏系数及肝组织中MDA的含量,增加肝组织中SOD活性,减轻CCl4对肝脏细胞的病理损伤。结论三叶青总氨基酸对CCl4致小鼠急性肝损伤具有保护作用,其机制可能与其抗氧化作用相关。     

彩虹明樱蛤多糖对小鼠急性化学性肝损伤的保护作用

目的研究彩虹明樱蛤多糖(MIP)对CCl4致小鼠急性化学性肝损伤的保护作用。方法 MIP对小鼠连续腹腔注射7 d,以0.1%CCl4橄榄油溶液经腹腔注射,建立小鼠急性化学性肝损伤模型,测定给药后模型小鼠肝指数,检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性,测定肝组织匀浆中丙二醛(MDA)含量和超氧化物歧化酶(SOD)、谷胱甘肽(GSH)的活性及观察肝脏病理学变化。结果 MIP中、高剂量组(80,160 mg/kg)均能显著降低CCl4致急性肝损伤小鼠血清ALT、AST活性(P<0.01),降低肝脏MDA含量(P<0.01),增强SOD和GSH活力(P<0.01或0.05),并能明显改善肝组织的病理学损伤,但对肝指数无明显影响。结论 MIP对CCl4致小鼠急性化学性肝损伤有保护作用。     

口服二磷酸果糖对小鼠急性肝损伤的保护作用

目的研究二磷酸果糖钠 (FDP)对CCl4 和D 氨基半乳糖两种模型引起小鼠肝损伤的保护作用 ,并分析其对肝微粒体细胞色素P45 0酶的活性影响。方法在对小鼠连续灌胃FDP 4d后 ,采用ipCCl4 和D 氨基半乳糖两种化学物质造成小鼠急性肝损害 ,研究其有无保肝作用 ;并采用Omura法测定了FDP对正常小鼠的肝细胞色素P45 0酶活力的影响。结果FDP 0 .15g/kg和 0 .30g/kg灌胃剂量下对肝损伤模型小鼠有一定的保护作用 ,并有提高正常小鼠肝微粒体P45 0酶活性的作用。结论FDP能防止化学物质造成的肝损伤 ,保护肝功能     

羧甲基壳聚糖钙对小鼠CCl_4造成的急性肝损伤的保护作用

目的观察羧甲基壳聚糖钙对CCl4损伤小鼠丙氨酸转氨酶(ALT)和天门冬氨酸转氨酶(AST)活性及肝脏抗氧化能力的影响。方法将小鼠分为正常对照组、CCl4肝损伤模型组、羧甲基壳聚糖钙低、中、高剂量实验组,灌胃给予受试物。连续20 d后腹腔注射CCl4,24 h后采血测ALT、AST活性,同时取肝脏制匀浆,用试剂盒测定丙二醛(MDA)、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)值。结果羧甲基壳聚糖钙能显著降低ALT和AST活性,抑制脂类过氧化,提升SOD活性和T-AOC水平,对GSH-Px无显著影响。结论羧甲基壳聚糖钙对CCl4引起的急性肝损伤小鼠具有一定的抗氧化能力和肝保护作用。     

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-8300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-8300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-8300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-8300对急性肝损伤有明显的保护作用。     

恩施富硒藤茶水提液对四氯化碳致急性肝损伤小鼠的保护作用

目的 观察恩施富硒藤茶水提液对四氯化碳（CCl4）诱导的小鼠急性肝损伤的影响。方法用腹腔注射CCl4致小鼠急性肝损伤模型,测定不同剂量的恩施富硒藤茶水提液对肝损伤血清丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）活性、肝中超氧化物歧化酶（SOD）活性、肝中丙二醛（MDA）含量的影响。结果恩施富硒藤茶水提液具有剂量依赖性地降低CCl4致小鼠肝损伤血清ALT、AST值升高,降低肝组织匀浆中MDA的含量,增强SOD的活性（P〈0．01或P〈0．05）。结论恩施富硒藤茶水提液对CCl4致小鼠急性肝损伤具有一定的保护作用。     

来氟米特对急性化学性肝损伤的治疗作用

目的：观察来氟米特对急性化学性肝损伤的治疗作用。方法：分别利用CCl4和D－Gal诱导化学性肝损伤。血浆中ALT,AST和肝组织中MDA水平用紫外分光光度法检测。结果：Lef(4、12、36mg.kg^1)明显降低CCl4和D－Gal诱导的化学性肝损伤小鼠血浆ALT、AST活性和肝匀浆DNA水平的上升,结论：来氟米特对急性化学性肝损伤有治疗作用。     

口服鲨鱼肝再生因子脂质体对小鼠急性肝损伤的保护作用

为研究口服鲨鱼肝再生因子脂质体对四氯化碳(CCl4)和硫代乙酰胺(TAA)对小鼠急性肝损伤的保护作用,采用CCl4和TAA致小鼠肝损伤,观察肝组织切片,测定生化指标,检测小鼠给药后血清谷丙转氨酶(ALT)、血清谷草转氨酶(AST)活力。结果口服鲨鱼肝再生因子脂质体能明显减轻CCl4和TAA所致小鼠急性肝损伤模型的肝组织损伤作用,降低ALT、AST活力。因此口服鲨鱼肝再生因子脂质体对急性肝损伤也有明显的保护作用。     

Protective effect of Mentha piperita against arsenic-induced toxicity in liver of Swiss albino mice

The protective role of leaves of Mentha piperita Linn (Mint) was studied in adult Swiss albino mice against arsenic-induced hepatopathy. The animals were divided into four groups. Group I: only vehicle (0.9% NaCl) was administered. Group II: the animals received Mentha leaf extract (1 g/kg body weight per day) orally for 30 days. Group III: animals were treated with sodium arsenite (4 mg/kg body weight) intraperitoneally in 0.9% NaCl. Group IV: animals were given Mentha extract for 10 consecutive days prior to sodium arsenite treatment and continuously for 30 days after sodium arsenite treatment. The animals from the above groups were killed at various time-points, and body weight and liver weight were measured. The biochemical estimation of lipid peroxidation (LPO), reduced glutathione (GSH), lactate dehydrogenase (LDH), acid phosphatase (ACP), and alkaline phosphatase (ALP) in liver and serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) in serum were done. In the arsenic-treated group there was a significant increase in ACP, ALP, SGOT, SGPT and LPO content, whereas a significant decrease was recorded in body weight, liver weight, GSH and LDH activity in liver. Pre- and post-treatment of Mentha with arsenic significantly alters the biochemical parameters in liver. A significant decline in ACP, ALP, SGOT, SGPT and LPO content was observed. However, a significant increase in body weight, liver weight, GSH content and LDH activity in liver was estimated. The results indicate that the Mentha extract may be useful in reducing the side effects of arsenic-induced hepatopathy.     

Relationship between hepatotoxicity and induction of replicative DNA synthesis following single or multiple doses of carbon tetrachloride

The in vivo-in vitro DNA repair and DNA replication assay in mouse hepatocytes has promise as a short-term test for detecting potential mouse liver carcinogens. In addition, this assay may provide information on the mode of action of known hepatic carcinogens. The induction of DNA repair is clearly a response to hepatic DNA damage. However, it is unclear whether induction of replicative DNA synthesis (S phase) represents regenerative hyperplasia in response to hepatotoxicity or is a result of direct mitogenic stimulation of the hepatocytes by the test compound. The objective of the present study was to examine the relationship between hepatotoxicity, which was assessed by measuring serum concentrations of glutamic-oxalacetic transaminase (SGOT), glutamic-pyruvic transaminase (SGPT), alkaline phosphatase (AP), and gammaglutamyl transferase (GGT), and induction of S phase following either single or multiple doses of the model mouse hepatocarcinogen carbon tetrachloride (CCl4). Under the experimental conditions in this study, CCl4 elevated SGPT and SGOT but did not affect serum concentrations of AP or GGT. CCl4 did not induce DNA repair. An increase in the percentage of hepatocytes in S phase followed the appearance of elevated SGOT and SGPT in all single-dose studies. The results from the multiple-dose studies showed a similar relationship except that with 20 mg/kg X d the concentrations of SGOT and SGPT decayed to control values after 14 d of dosing whereas the percentage of hepatocytes in S phase remained markedly elevated (greater than 10 X control). The daily dose of CCl4 that gave a no-observed-effect level for induction of S phase was lower with multiple administrations than it was following a single exposure. A single administration of CCl4 at 25 mg/kg did not increase S phase, SGOT, or SGPT, but if 20 mg/kg X d was given for 7 d the number of hepatocytes in S phase and the concentrations of SGOT and SGPT increased more than 10-fold. These data support the hypothesis that induction of replicative DNA synthesis in the mouse liver following CCl4 administration is related to hepatotoxicity. In single-dose studies elevation in S phase was always associated with elevation of SGOT and SGPT. However, in the multidose studies, SGOT and SGPT declined after 14 d of administering 20 mg/kg X d while S phase remained elevated.(ABSTRACT TRUNCATED AT 400 WORDS)     

三氧化二砷、黄磷、四氯化碳的急性肝脏毒作用的研究

大鼠每日分别经口染毒三氧化二砷（45mg/kg)、黄磷（3mg/kg)、四氯化碳（990mg/kg)，连续4日后，均出现肝脏病理改变，黄磷及四氯化碳组大鼠的血清GPT和GOT活性明显升高，但三氧化二砷组则无显著变化，三个染毒组大鼠的血清和肝微粒体过氧化脂质含量、血清IgM和补体C3含量均较对照组显著升高。     

Hepatoprotective and immunomodulatory properties of Tinospora cordifolia in CCl4 intoxicated mature albino rats

Effect of Tinospora cordifolia extract on modulation of hepatoprotective and immunostimulatory functions in carbon tetrachloride (CCl4) intoxicated mature rats is reported here. Administration of CCl4 (0.7 ml/kg body weight for 7 days) produces damage in the liver as evident by estimation of enzymes such as serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transminase (SGPT) and alkaline phosphatase (ALP) as well as serum bilirubin level. CCl4 administration also causes immunosuppressive effects as indicated by phagocytic capacity, chemotactic migration and cell adhesiveness of rat peritoneal macrophages. However, treatment with T. cordifolia extract (100 mg/kg body weight for 15 days) in CCl4 intoxicated rats was found to protect the liver, as indicated by enzyme level in serum. A significant reduction in serum levels of SGOT, SGPT, ALP, bilirubin were observed following T. cordifolia treatment during CCl4 intoxication. Treatment with T. cordifolia extract also deleted the immunosuppressive effect of CCl4, since a significant increment in the functional capacities of rat peritoneal macrophages (PM phi) was observed following T. cordifolia treatment. The results of our experiment suggest that treatment by T. cordifolia extract may be the critical remedy for the adverse effect of CCl4 in liver function as well as immune functions.     

胎盘因子对小鼠四氯化碳肝损伤的保护作用

用超滤方法从健康产妇胎盘中提取胎盘因子（PF），观察PF对四氯化碳（CCl4）引起的小鼠急性肝损伤的影响。结果发现ip或poPF15ml／（kg·d），连续7d，能明显抑制血清谷丙转氨酶的升高和肝脏脂质过氧化物的产生，减轻肝脏病理变化，增加肝脏还原型谷眈甘肽的含量。提示PF对小鼠CCl4肝损伤有保护作用，其作用机制可能与抑制脂质过氧化作用、提高肝细胞的抗氧化能力有关。     

Interaction of carbon tetrachloride with beta-naphthoflavone-mediated cytochrome P450 induction in winter flounder (Pseudopleuronectes americanus)

The interaction between beta-naphthoflavone induction (BNF: 100 mg/kg) and carbon tetrachloride (CCl4; 1 ml/kg) hepatotoxicity was examined in the flounder. Treatment groups composed of control, BNF, CCl4, and BNF/CCl4 were compared in terms of cytochrome P450 isozyme content (LM4b; LM2), catalytic activity, isozyme distribution. SGOT-SGPT levels, and pathology. CCl4 administration resulted in significant reductions in both the constitutive P450 (LM2) and the BNF-inducible isozyme (LM4b) as well as elevations in SGPT and SGOT levels. The decline in LM4b isozyme content was reflected by stoichiometric decreases in ethoxyresorufin-O-deethylase activities. BNF/CCl4 coadministration was protective in part against CCl4 hepatotoxicity. Immunohistochemistry indicated that LM4b was diffusely distributed throughout the liver. These interactions have demonstrated a multiple P450 isozyme involvement, the protective nature of BNF against CCl4 hepatotoxicity in the flounder, the ability to maintain an inductive response in face of CCl4 coadministration, and the diffuse distributional pattern of LM4b in the flounder liver.     

仙人掌多糖对小鼠急性肝损伤的保护作用

目的研究仙人掌多糖(OPS)对CCl4肝损伤小鼠的保护作用。方法采用OPS溶液预先灌胃30 d,末次灌胃后2 h,腹腔注射0.10%CCl4(20 mL/kg)的花生油溶液,造成小鼠急性肝损伤,测定血清ALT活性和AST活性及肝脏GSH含量、GR活性、GST活性和GSH-Px活性,取肝组织做病理学检测。结果预先灌胃OPS溶液,可显著地抑制CCl4引起的小鼠血清ALT和AST活性升高,改善肝中毒小鼠GSH含量及GST活性和GSH-Px活性水平,并减轻肝组织的病理变化。结论OPS对CCl4致小鼠肝损伤具有保护作用,这可能与增强谷胱甘肽系统抗氧化能力有关。     

Hepatoprotective effect of Himoliv, a polyherbal formulation in rats

The effect of Himoliv (HV) was evaluated in carbon tetrachloride or paracetamol induced hepatotoxicity in rats. Liver necrosis was produced by administering single dose of either carbon tetrachloride (CCl4, 1 ml/kg, 50% v/v with olive oil, s.c.) or paracetamol (PC, 1 g/kg, p.o.). The liver damage was evidenced by elevated levels of serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) and serum alkaline phosphatase (ALP) and hepatic thiobarbituric acid reacting substances (TBARS) and superoxide dismutase (SOD). HV pretreatment (0.5 and 1.0 ml/kg, p.o.) significantly (P < 0.001) reduced CCl4 or PC-induced elevations of the levels of SGOT, SGPT, ALP and TBARS, while the reduced concentration of SOD due to CCl4 or PC was reversed. Silymarin (25 mg/ kg, p.o.), a known hepatoprotective drug showed similar results.