骆驼乳清蛋白对热应激所致大鼠肝氧化损伤的保护作用

本试验旨在研究骆驼乳清蛋白（CWP）对热应激（HS）大鼠肝损伤、氧化应激及肝功能的保护作用。选取6周龄SD大鼠36只,适应性饲养2周后随机分为6组：正常对照组饲喂基础日粮;CWP对照组添加400 mg·kg^-1的CWP;HS组除饲喂基础日粮外,每天进行2 h HS处理,连续8 d;3个CWP干预组分别于每次HS前灌服100、200和400 mg·kg^-1的CWP。试验结束后,取大鼠肝组织,HE染色观察肝组织病理学变化,同时检测肝功能生物标志物、氧化应激标志物水平及抗氧化酶活性。结果表明：CWP降低了HS大鼠血清谷草转氨酶（AST）和谷丙转氨酶（ALT）活性,400 mg·kg^-1的CWP干预效果最好（P<0.01）;400 mg·kg^-1CWP干预组有效降低了HS诱导的大鼠肝组织病理学改变; CWP降低了大鼠肝活性氧（ROS）及丙二醛（MDA）水平,增加了超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）活性及谷胱甘肽（GSH）水平,400 mg·kg^-1的CWP干预效果最好（P<0.01）。结果提示,CWP干预能够以剂量依赖性方式降低大鼠肝氧化应激,增加抗氧化系统防御能力,从而缓解HS所致大鼠肝损伤。     

Protective Effects of Platycodon grandiflorum Aqueous Extract on Thioacetamide-induced Fulminant Hepatic Failure in Mice

The aim of the present study was to evaluate the protective activity of aqueous extract from Platycodon grandiflorum (BC703) on thioacetamide (TA)-induced hepatotoxicity in mice. We found that BC703 significantly decreased mortality and the change in serum transaminase following TA administration. The group treated with BC703 at doses of 1, 5, and 10 mg/kg produced significant hepatoprotective effects against TA-induced liver damage by decreasing the activities of serum enzymes, nitric oxide and lipid peroxidation in dose-dependent manners. Histopathological studies further substantiated the protective effect of BC703. These results show the hepatoprotective activity of aqueous extract from Platycodon grandiflorum on thioacetamide-induced fulminant hepatic failure.     

Hepatic endogenous defense potential of propolis after mercury intoxication

Exposure to mercuric chloride (HgCl₂; 5 mg kg^?1 body weight; i.p.) induced oxidative stress in mice and substantially increased lipid peroxidation (LPO) and oxidized glutathione (GSSG) levels, decreased the level of reduced glutathione (GSH) and various antioxidant enzymes in liver and also increased the activities of liver marker enzymes in serum. Therapy with propolis extract, a resinous wax‐like beehive product (200 mg kg^?1 orally, after mercury administration), for 3 days inhibited LPO and the formation of GSSG and increased the level of GSH in the liver. Release of serum transaminases, alkaline phosphatase, lactate dehydrogenase and γ‐glutamyl transpeptidase were significantly restored after propolis treatment. The activities of antioxidant enzymes, that is, superoxide dismutase, catalase, glutathione‐S‐transferase and glucose‐6‐phosphate dehydrogenase, were also concomitantly restored towards normal levels after propolis administration. These observations clearly demonstrate that propolis treatment augments antioxidant defense against mercury‐induced toxicity and provide evidence that propolis has therapeutic potential as a hepatoprotective agent.     

Immunization against intestinal bacterial endotoxin prevents alcoholic fatty liver in rats

Accumulating evidences indicate that an endotoxin originating from intestinal gram-negative bacteria may be involved in alcohol-induced liver injury including fatty liver. Therefore, whether immunization against intestinal bacterial endotoxin blocked fatty liver induced by chronic alcohol and diet including much-unsaturated fatty acid was investigated in rats. The titer of antibody against the endotoxin increased significantly after 13 weeks of continuous immunization. Daily alcohol treatment was initiated at 12 weeks and continued for 4 weeks. Plasma glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT) and triglyceride (TG) levels increased significantly in non-immunized rats receiving alcohol, but not in immunized rats. Continuous alcohol treatment gradually decreased the survival rate to 60% from 13 days after beginning administration in non-immunized, but not immunized, rats. A histochemical study revealed that continuous treatment with alcohol and unsaturated fatty acids caused fatty liver in non-immunized, but not immunized, rats. This study strongly supports the hypothesis that alcohol-induced fatty liver is due to a circulating endotoxin, and suggests that immunization for endotoxin prevent the alcoholic fatty liver.     

Effect of mercury chloride on oxidative stress and nuclear factor erythroid 2‐related factor 2 signalling molecule in liver and kidney of laying hens

This study investigated the effects of mercury chloride (HgCl₂) on the deposition of mercury (Hg), histopathology and oxidative stress in liver and kidney of laying hens. The gene expressions of antioxidant enzymes and nuclear factor erythroid 2‐related factor 2 (Nrf2)‐Kelch‐like ECH‐associated protein 1 (Keap1) were further studied to uncover the molecular mechanism. A total of 960 40‐week‐old Hyline brown laying hens were randomly allocated to five treatments with eight pens per treatment and 24 hens per pen. The hens were fed with five experimental diets containing graded levels of Hg at 0.270, 1.250, 3.315, 9.405 and 27.230 mg/kg respectively. Results revealed that both deposition of Hg and score of injury in liver and kidney were significantly increased as dietary Hg dosage up to 27.230 mg/kg diet. Deposition of Hg was positively related to score of injury in liver and kidney of laying hens. Besides, the activities of superoxidative dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GSH‐Px), and glutathione (GSH) content all significantly decreased (p < 0.05), while malondialdehyde (MDA) content significantly increased (p < 0.05) after Hg exposure in liver and kidney of laying hens. In addition, positive relationships occurred between antioxidant enzyme activities and antioxidant enzyme gene expressions except between SOD activity and manganese superoxide dismutase (MnSOD) gene expression in liver. Meanwhile, Nrf2 gene expression was positively related to antioxidant gene expressions and negatively connected with Keap1 gene expression. Negative relationships occurred between Nrf2 and Keap1 protein levels in liver and kidney. In conclusion, Hg could dose‐dependently damage liver and kidney and induced hepatic and renal oxidative stress by means of suppressing Nrf2‐Keap1 signalling molecule in laying hens.     

桦木酸对小鼠免疫器官抗氧化能力的影响

本试验旨在研究桦木酸(BA)对小鼠免疫器官抗氧化能力的影响.选取健康的昆明系小鼠28只,随机分为4组(每组7只),每天每只分别按每千克体重0、0.25、0.50、1.00 mg的剂量给予BA,BA混悬于0.2 mL1％可溶性淀粉溶液中.以灌胃方式给予,每天灌胃1次,连续灌胃14 d后,检测各组小鼠脾脏和胸腺中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GHS-Px)活性,丙二醛(MDA)含量以及总抗氧化能力(T-AOC).结果表明:BA可使小鼠脾脏和胸腺中SOD、GSH-Px活性以及T-AOC升高,MDA含量降低.其中,每千克体重灌胃0.50 mg BA能显著或极显著提高脾脏和胸腺中GSH-Px活性和T-AOC(P＜0.05或P＜0.01),显著或极显著降低胸腺和脾脏中MDA含量(P＜0.05或P＜0.01);每千克体重灌胃1.00 mg BA能显著或极显著提高脾脏和胸腺中SOD活性、T-AOC以及脾脏中GSH-Px活性(P＜0.05或P＜0.01),极显著降低胸腺和脾脏中MDA含量(P＜0.01).由此得出,BA能有效地增强小鼠免疫器官的抗氧化能力.     

地顶孢霉培养物对大鼠生长性能、血清与肝脏抗氧化及免疫指标的影响

本试验旨在研究地顶孢霉培养物对大鼠生长性能、血清与肝脏抗氧化以及免疫指标的影响。选用体重相近的SD大鼠40只,随机分成5组,每组8个重复,每个重复1只大鼠。5组分别是对照组和4个不同地顶孢霉培养物剂量组(10、50、250和1 250 mg/kg BW组),连续灌胃21 d。结果表明:地顶孢霉培养物极显著提高大鼠的平均日增重(P0.01);提高了大鼠肝脏指数、胸腺指数;提高了大鼠血清中总蛋白(TP)、白蛋白(ALB)、球蛋白(GLB)和葡萄糖(GLU)含量,降低了谷丙转氨酶(ALT)、谷草转氨酶(AST)活力和低密度脂蛋白(LDL)含量;提高了血清和肝脏中谷胱甘肽过氧化物酶(GSH-Px)活力和总抗氧化能力(T-AOC),降低丙二醛(MDA)含量,同时提高了肝脏中的总超氧化物歧化酶(T-SOD)含量;提高了血清免疫球蛋白A、免疫球蛋白G和免疫球蛋白M含量,同时提高血清和肝脏中白介素-4(IL-4)含量,降低白介素-1β(IL-1β)和白介素-17(IL-17)含量。综合各项指标,地顶孢霉培养物能够提高SD大鼠平均日增重,改善血清生化指标,提高大鼠机体抗氧化能力和免疫能力,其中以250 mg/kg BW的添加量为最佳。     

甘草提取物对酒精性肝损伤的防治作用研究

以酒精性肝损伤小鼠为动物模型,探讨甘草提取物对酒精性肝损伤的防治作用.将64只昆明系小白鼠随机分为8组,即正常对照组、治疗组（低、中、高剂量）、预防组（低、中、高剂量）、模型组.模型组以56度白酒16 mL/kg灌胃,预防组和治疗组在酒精灌胃的基础上分别采用低（4.8 g/kg）、中（9.6 g/kg）、高（16 g/kg）不同剂量甘草提取物灌胃,连续14 d,取血液和肝脏样品,测定肝组织谷草转氨酶（GOT）、谷丙转氨酶（GPT）及血清乙醇脱氢酶（ADH）含量,同时采用H.E染色对肝组织进行组织学观察.血样测定结果表明,与模型组比较,低剂量预防组和治疗组GOT降低均不明显,中、高剂量预防组和治疗组GOT降低显著（P＜0.05,P＜0.01）;低剂量治疗组（P＜0.05）和其他给药组（P＜0.01）均能显著降低GPT含量;中、高剂量治疗组（P＜0.05）和低、中剂量预防组（P＜0.05）与高剂量预防组（P＜0.01）均能显著提升ADH含量;组织学观察表明,与模型组比较,中、高剂量治疗组及预防组能有效缓解和恢复肝损伤组织结构.提示甘草提取物对酒精引起的肝损伤具有一定的保护和治疗作用.     

Forsythia suspensa extract attenuates lipopolysaccharide‐induced inflammatory liver injury in rats via promoting antioxidant defense mechanisms

Reactive oxygen species (ROS) have been shown to have a role in inflammation. We investigated whether Forsythia suspensa extract (FSE) could exert its antioxidant potential against lipopolysaccharide (LPS)‐induced inflammatory liver injury in rats. Rats were orally fed FSE once daily for 7 consecutive days prior to LPS (Escherichia coli, serotype O55:B5) injection. LPS treatment caused liver dysfunction as evidenced by massive histopathological changes and increased serum alanine aminotransferase and aspartate aminotransferase activities which were ameliorated by FSE pretreatment. FSE attenuated LPS‐induced depletion of cytosolic nuclear factor‐erythroid 2‐related factor 2 (Nrf2) and suppression of Nrf2 nuclear translocation in liver, and the generation of ROS and malondialdehyde in serum and liver. FSE increased the Nrf2‐mediated induction of heme oxygenase‐1 in liver, as well as superoxide dismutase and glutathione peroxidase activities in serum and liver. Importantly, FSE attenuated LPS‐induced nuclear factor‐кB (NF‐кB) nuclear translocation in liver, and subsequently decreased tumor necrosis factor‐α, interleukin (IL)‐1β and IL‐6 levels in serum and liver, which were associated with FSE‐induced activation of Nrf2 in liver. These results indicate that the protective mechanisms of FSE may be involved in the attenuation of oxidative stress and the inhibition of the NF‐кB‐mediated inflammatory response by modulating the Nrf2‐mediated antioxidant response against LPS‐induced inflammatory liver injury.     

Orally administered phenylbutazone causes oxidative stress in the equine gastric mucosa

Phenylbutazone (PBZ) is widely used in equine medicine, and its side effects on the gastrointestinal tract are well known. The inhibition of prostaglandins and the oxidative stress induced by nonsteroidal anti‐inflammatory drugs (NSAIDs) are described as mechanisms of gastric mucosal injury in humans. In horses, only the secondary effect of changes in cyclooxygenases is related to gastric mucosal injury. The objective of this study was to evaluate the effect of PBZ on certain antioxidative/oxidative parameters of the gastric mucosa. The concentrations of antioxidants and oxidants (superoxide dismutase, SOD; catalase, CAT; nitric oxide, NO; total glutathione, GSH; myeloperoxidase, MPO; and malondialdehyde, MDA), PGE₂ levels, and the ulcerative lesions score were assessed. The results demonstrated decreased levels of antioxidant variables, increased levels of oxidant variables, and alterations in the prostaglandin E₂ (PGE₂), myeloperoxidase (MPO), and glutathione (GSH) levels. In conclusion, PBZ induces oxidative stress in the gastric glandular mucosa of horses by changing the antioxidant–oxidant balance of this surface, which might be regarded as another mechanism of injury in the horse stomach.     

芽孢杆菌发酵五味子提取液对肉鸡肝损伤的影响

为探索中药与益生菌联用治疗肉鸡肝损伤的新方法,从而改善畜禽＂亚健康＂,本研究以CCl4注射肉鸡,建立肝损伤模型,并利用芽孢杆菌发酵五味子提取液,将发酵提取液混饮肝损伤肉鸡,检测外周血谷草转氨酶（Aspar-tate transaminase,AST）、谷丙转氨酶（Alanine aminotransferase,ALT）、过氧化物岐化酶（Superoxide dismutase,SOD）、丙二醛（Malondialdehyde,MDA）、谷胱甘肽还原酶（Glutathione reductase,GR）含量,并进行组织病理学观察。结果显示,芽孢杆菌在五味子提取液与培养基1∶1（V/V）混合液中生长良好,五味子有效成分在发酵前后含量无明显变化,发酵提取液按0.5%、1%混饮7d后,与肝损伤阳性对照组相比,2个用药组AST（P〈0.05）、ALT（P〈0.05）、SOD（P〈0.05）、GR（P〈0.01）含量显著升高,MDA（P〈0.05）含量显著降低,肝脏病变较轻。结果表明,芽孢杆菌发酵五味子提取液对提高机体抗氧化能力具有一定的作用,能够治疗肉鸡肝损伤。     

Tea polyphenols increase the antioxidant status of laying hens fed diets with different levels of ageing corn

This study was conducted to evaluate the effects of ageing corn levels (stored for 4 years) with or without the supplementation of tea polyphenols (TPP) on the performance, egg quality and antioxidant status of laying hens. A total of 288 Lohmann commercial laying hens (63-week-old) were used under a 2 × 4 factorial arrangement with 4 levels of dietary ageing corn (0%, 25%, 50%, or 100%) and 2 levels of TPP (0 and 600 mg/kg) for 8 wk. Dietary ageing corn linearly decreased (P < 0.05) the egg production, serum total antioxidant capacity (T-AOC), liver glutathione peroxidase (GSH-Px) of laying hens, yolk index, yolk colour, 1,1-diphenyl-2-picrylhydrazyl (DPPH) value and the reducing power value of egg yolk, but it linearly increased (P < 0.05) the feed conversion rate, ovary malondialdehyde (MDA) content of laying hens, and the protein carbonyl content of egg yolk. Tea polyphenol supplementation increased (P < 0.05) the serum T-AOC, serum superoxide dismutase (SOD), liver SOD, liver GSH-Px, ovary SOD, GSH-Px, the expression of antioxidant-related genes of laying hens, albumen height, Haugh unit, DPPH value and the majority free amino acids of egg yolk, but it decreased (P < 0.05) the serum MDA content of laying hens, MDA and protein carbonyl of egg yolk. In conclusion, the ageing corn significantly reduced the performance, egg quality, antioxidant status and egg antioxidant capacity of laying hens, while TPP supplementation partially counteracted the adverse effects, especially antioxidant status and egg antioxidant capacity of laying hens.     

Protective Effect of Saccharum alhagi Against N-acetyl-para-aminophenol induced Liver Injury in Mice

N-acetyl-para-aminophenol (APAP) overdose use induced liver damage.This study was aimed to evaluate the hepatoprotective effect of Saccharum alhagi against APAP-induced liver injury in mice. The aqueous extract of Saccharum alhagi was prepared, ant its ingredients were measured by phenol-sulfuric acid method and aluminium salt chromogenic method. The mice were randomly divided into seven groups,including normal control group,APAP model group,Saccharum alhagi (150, 300 and 600 mg/kg·BW)+APAP groups,positive control group and Saccharum alhagi control group. Administration once per day for 3 consecutive days,with 300 mg/(kg·BW) of APAP after 1 h from the last administration of Saccharum alhagi. 300 mg/(kg·BW) APAP were used to induce liver injury, and after 24 h from APAP challenge,the experimental animals were sacrificed to collect blood and liver tissue samples. The level of serum transaminase (ALT and AST) and the liver pathological changes were observed. The results indicated that the levels of serum AST and ALT were extremely significant lower in the Saccharum alhagi treated groups than the APAP treated group (P<0.01), and the pathological changes were significantly improved. This study showed that Saccharum alhagi could be an effective therapeutic source in APAP-induced liver injuries in mice.     

刺糖对对乙酰氨基酚诱导的肝损伤的保护作用

对乙酰氨基酚（N-acetyl-para-aminophenol,APAP）过量使用能够引起肝脏损伤,本研究旨在探讨刺糖对APAP所致小鼠急性肝损伤的保护作用及潜在的作用机理。采用水提法提取刺糖的有效成分,通过苯酚硫酸法和铝盐显色法进行刺糖提取物成分鉴定;49只雌性小鼠随机分为7组,正常对照组、模型组、刺糖不同浓度的提取物（600、300和150 mg/kg体重）+APAP组、水飞蓟宾阳性对照组及刺糖对照组（600 mg/kg体重）,灌胃3 d,末次给药1 h后,腹腔注射APAP 300 mg/kg体重,24 h后处死小鼠并采集血样和肝脏组织样品。检测血清谷丙转氨酶（ALT）和谷草转氨酶（AST）的活性;用HE染色制作病理标本,观察肝脏病理学变化。结果显示,刺糖提取物能够极显著降低小鼠血清中AST、ALT的含量（P<0.01）,APAP所引起的病理变化明显改善。本研究结果表明,刺糖对APAP所致的小鼠急性肝损伤有一定的保护作用。     

Sidr honey abrogates the oxidative stress and downregulates the hyaluronic acid concentration and gene expression of TGF‐β1 and COL1a1 in rat model of thioacetamide‐induced hepatic fibrosis

Liver fibrosis is a major health concern, which might progress to cirrhosis. To date, treatment trials rely mainly on the removal of the causative factor. The current study investigated the potential ameliorative role of sidr honey on thioacetamide (TAA)‐induced liver fibrosis in rats. Forty‐eight Wistar albino rats were equally allocated into four groups: control; sidr honey (5g/kg body weight (BW), orally); TAA (200 mg/kg BW, IP three times weekly/15 weeks); and sidr honey plus TAA at the same dose and administration rout. Rats co‐treated with sidr honey plus TAA revealed significant reduction in hepatic malondialdehyde, hyaluronic acid (HA), alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma glutamyl transferase, direct bilirubin, and hepatic mRNA expression of transforming growth factor (TGF)‐β1 and collagen type I alpha 1 chain (COL1a1) compared to TAA‐exposed rats. In addition, the hepatoprotective potential of sidr honey was indicated via improvement of histopathologic picture of hepatocytes and upregulation of total antioxidant capacity, reduced glutathione, catalase, glutathione peroxidase, superoxide dismutase, total protein, and albumin compared to TAA‐treated rats. In conclusion, daily administration of sidr honey (5 g/kg BW) is a promising natural antioxidant and fibrosuppressive agent that could ameliorate liver fibrosis via downregulation of fibrosis genes including TGF‐β1 and COL1a1 and HA and via enhancement of antioxidant system.     

The neuroprotective effect of submicron and blended Lycium barbarum for experiment retinal ischemia and reperfusion injury in rats

The purpose of this study was to investigate the neuroprotective potential of submicron (milled) and blended Lycium barbarum (LB) in glaucomatous retinal neuropathy using a rat model of high intraocular pressure (HIOP) induced retinal ischemia. The rats were treated with 500, 250, 100 mg/kg LB (submicron or blended form) orally once daily for 56 days respectively after 1 week of retinal ischemia induction. We conducted electroretinography (ERG), histopathological analysis in retina and antioxidative level assays, such as total glutathione (GSH (glutathione) + reduced glutathione) + GSSH (glutathione disulfide), catalase activity, SOD (superoxide dismutase) activity, and lipid peroxidant malondialdehyde (MDA) in the retina and plasma of test rats. The results indicated that the amplitudes of a and b wave of ERG were preserved in rats treated with submicron and blended LB groups, the best protective effect on ERG b wave amplitudes was observed at the dosage of 250 mg/kg of both forms of LB. Retinal thickness was best preserved, particularly significant in the retinal inner nuclear layer in submicron 250 mg/kg LB group. The levels of antioxidant GSSH+GSH, SOD and catalase activity in the retina were higher in blended 500 mg/kg and submicron 250 mg/kg groups than other groups, while the MDA level was lower in submicron LB groups than that in blended LB and non-LB IR group. In the plasma, there was no significant difference in the levels of GSSH+GSH and catalase activity between treated groups, but higher levels of SOD and lower levels of MDA were observed in 250 mg/kg submicron and 500 mg/kg submicron LB groups than the blended LB and non-LB IR groups. Generally better antioxidative effects were observed in the submicron LB than blended LB among treated groups, especially the 250 mg/kg submicron LB, providing good retinal neuroprotection by preserving retinal structure and function with improved antioxidative capacity. The submicron LB may have clinical implication as an adjuvant therapy of oxidative stress and retinal damage caused by HIOP induced retinal ischemia and reperfusion injury.     

Betaine Alleviates Heat Stress-Induced Hepatic and Mitochondrial Oxidative Damage in Broilers

The aim of this study was to evaluate the effects of dietary betaine (BET) on growth performance, redox state, and related gene expression in broilers under heat stress (HS). A total of 144 21-day-old male broiler chickens with similar body weights were assigned randomly to three treatments with six replicates (eight chickens per replicate cage). Broilers in the control (CON) group were kept at thermoneutral (TN, 22±1°C) conditions and fed a basal diet until they were 42 days of age. Broilers in the other two groups (defined as HS and HS + BET) were exposed to HS (34±1°C, 8 h/day) and fed the basal diet without or with 1000 mg/kg BET, respectively. Rectal and cockscomb temperature of broilers was increased (P<0.05) in HS and HS + BET groups compared with the CON group, whereas there was no difference between HS and HS + BET groups. Dietary BET supplementation restored (P<0.05) average daily gain (ADG) and average daily feed intake (ADFI) of broilers and reversed (P<0.05) the increase in serum alanine transaminase (ALT) activity and malondialdehyde (MDA) content in the liver tissue of broilers under HS. The HS + BET group had higher (P<0.05) activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) in the liver tissue and mitochondria than the HS group, and the same pattern was observed for glutathione (GSH) and GSH/glutathione disulphide (GSSG) in the liver tissue. The decreased mRNA levels of GPX1 and uncoupling protein (UCP) in the liver induced by HS were restored by BET supplementation. In conclusion, dietary BET supplementation can alleviate HS-induced hepatic and mitochondrial oxidative damage of broilers by regulating mRNA expressions of GPX1 and UCP.     

高温应激致麒麟鸡(卷羽鸡)肝损伤试验动物模型的建立

本试验旨在建立急性应激致禽类肝损伤的试验动物模型.对麒麟鸡(卷羽鸡)进行持续高温应激后,检测血清中的肝损伤酶谷丙转氨酶(ALT)、天冬氨酸转氨酶(AST)、胆碱脂酶(CHE)和乳酸脱氢酶(LDH)活性的改变,观察肝脏病理组织学变化.结果显示,高温应激前期,麒麟鸡血清肝损伤酶AST和ALT活性极显著升高(P <0.01),高温应激后期,AST活性显著低于正常水平(P <0.05),而ALT活性极显著低于正常水平(P <0.01);持续高温应激期间,CHE的活性一直低于正常水平,高温应激后期,CHE活性极显著低于正常水平(P <0.01);在高温应激下LDH活性呈先下降后上升再下降的变化趋势,高温应激后期,LDH活性极显著高于正常水平(P <0.01).高温应激引起麒麟鸡肝细胞出现水泡变性、肝细胞核浓缩现象.结果表明,采用急性热应激可诱导麒麟鸡肝损伤试验模型,试验模型具备肝脏水泡变性和核浓缩病理特征.     

A comparison of parameters used to assess liver damage in sheep treated with carbon tetrachloride.

Changes in serum enzyme levels, liver histology and liver function tests have been correlated to determine the usefulness of these tests in assessing liver status. The effects of carbon tetrachloride administration on these parameters has been determined in a group of 20 sheep. Normal levels, elevated levels after injury and the effect of elapsed time after injury are reported for serum glutamic dehydrogenase, sorbitol dehydrogenase, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, lactate dehydrogenase, fructose-1-phosphate adlolase, alkaline phosphatase, cholesterol and proteins. Variation in the time of elevation of enzyme activities may be useful in determining the elapsed time between acute injury and serum sampling. In comparison to sheep fed an adequate diet, a diet with a restricted protein intake was associated with increased severity of histological lesions and decreased liver function.     

Moderate protective effect of 6-MFA, a microbial metabolite obtained from Aspergillus ochraceus on immunological liver injury in mice

Hepatoprotective effect of 6-MFA, obtained from fungus Aspergillus ochraceus ATCC 28706, was evaluated by employing three different immunological liver injury mice models. The first liver injury model was induced by injecting anti-basic liver protein (BLP) antibody into mice previously immunised with rabbit IgG (RGG). The other models were simulated by injecting antiliver specific protein (LSP) antibody or by injecting bacterial lipopolysaccharide (LPS) into mice pretreated with Corynebacterium parvum (C. parvum). 6-MFA treatment inhibited the increased transaminases (GOT and GPT) activities and showed a tendency to inhibit the histopathological changes of the liver in all the models studied. Furthermore, 6-MFA treatment inhibited deoxycholic acid induced transaminase release from cultured rat hepatocytes in vitro, but failed to affect the formation of hemolytic plaque forming cells in immunised mice spleens and hemolytic activity of guinea pig complement in immunohemolytic reaction. Our findings, therefore, suggested that the moderate hepatoprotective effect of 6-MFA could be related to it's protective effect on hepatocyte plasma membrane rather than the direct inhibitory effects on the antibody formation and/or complement activity.