车前子多糖抗脂质过氧化作用的研究

目的 研究车前子多糖对硫酸亚铁-维生素C(Fe2+-VitC)致大鼠肝微粒体脂质过氧化的影响.方法 通过大鼠肝微粒体的提取,制备Fe2+-VitC系统诱导的脂质过氧化损伤模型,检测车前子多糖对丙二醛(MDA) 的抑制作用以及对超氧化物歧化酶(SOD)活性的影响,观察车前子多糖的抗脂质过氧化作用.结果 车前子多糖显著抑制肝微粒体脂质过氧化,表明车前子多糖具有抑制Fe2+-VitC增强肝微粒体脂质过氧化的效应.结论 车前子多糖可能通过与Fe2+络合,降低反应体系中Fe2+游离浓度,而抑制微粒体脂质过氧化.     

阿霉素致大鼠肝细胞凋亡及亚硒酸钠的保护作用

目的　探讨阿霉素对肝细胞的损伤机制及亚硒酸钠对肝细胞的保护作用。方法　通过复制大鼠阿霉素性心肌损伤的动物模型,以亚硒酸钠作为保护因素,应用原位末端标记法（ Ｔ Ｕ Ｎ Ｅ Ｌ）和免疫组化技术检测大鼠肝细胞凋亡和肝细胞转化生长因子 β１ 表达,并观察了大鼠血清中脂质过氧化含量。结果　阿霉素组大鼠肝组织可见细胞凋亡和肝细胞中转化生长因子 β１ 的异常表达;阿霉素组大鼠血清中脂质过氧化物明显升高;亚硒酸钠对阿霉素的损伤有明显的保护作用。结论　阿霉素诱导肝细胞凋亡可能是其肝脏损伤机制之一,并且细胞凋亡与转化生长因子 β１的高表达和血清中脂质过氧化水平升高有密切关系。     

SOD对氟致大鼠肝微粒体脂质过氧化作用的影响

应用大鼠肝微粒体模型，研究SOD对氟所致脂质过氧化作用的影响。结果表明，加氟可使微粒体系统MDA含量显著增加，说明脂质过氧化作用增强；同时加入SOD可拮抗氟致微粒体系统的脂质过氧化作用。     

抗氧化剂丹参对四氯化碳所致肝损害的保护作用

本文观察抗氧化剂丹参对四氯化碳所致大鼠急性肝损害的保护作用。结果显示，丹参能防止肝损害时血清转氨酶升高，减轻肝细胞病变，抑制肝脏过氧化脂质（LPO）产生，降低血LPO水平，并能提高细胞SOD活性，提示抗脂质过氧化作用是丹参护肝的重要机理。     

巴戟天醇提物对实验性心肌缺血及缺氧再给氧损伤的影响

目的 研究巴戟天醇提物对实验性心肌缺血及缺氧再给氧损伤的影响.方法 取杂种犬30只,随机分为模型组、阳性药对照组(刺五加注射液,10.0 mg/kg)、巴戟天醇提物(2.5、5.0、10.0 mg/kg)组每组6只.结扎犬左冠状动脉前降支,制备急性心肌梗死模型,观察巴戟天醇提物对磷酸肌酸激酶(CK)、乳酸脱氢酶(LDH)、天门冬氨酸氨基转移酶(AST)、游离脂肪酸(FFA)、过氧化脂质(LPO)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物(GSH-Px)的影响.新生大鼠随机分为正常组,损伤组,阳性药对照组(刺五加注射液),巴戟天醇提物1000、500、250 μg/ml组,每组8只.观察巴戟天醇提物对缺氧缺糖新生大鼠心肌细胞LDH的影响.结果 巴戟天醇提物降低血清中CK、LDH、AST的活性,降低血清中FFA、LPO含量,提高SOD、GSH-Px活性,减少新生大鼠心肌细胞LDH的释放.结论 巴戟天醇提物对实验性心肌缺血引起的脂质过氧化损伤具有保护作用.     

肝硬变肝脏热缺血损伤耐受性的实验研究

对肝硬变肝脏缺血再灌注损伤的耐受性进行了实验研究。发现肝硬变大鼠较正常大鼠肝脏超氧化物歧化酶(SOD)明显降低、过氧化脂质丙二醛(MDA)明显升高。在缺血再灌注损伤后肝硬变大鼠肝脏SOD下降幅度较正常鼠为小,MDA水平较后者明显升高。血清ALT、LDH及肝脏组织学变化均显示肝硬变大鼠的肝细胞损伤较重。上述结果表明肝硬变肝脏对缺血再灌注损伤的耐受性较差,抗氧化能力降低可能是其主要原因之一。     

肝脂消煎剂对脂肪肝大鼠肝微粒体膜流动性及心肌黄酶、丙二醛的作用

目的探讨肝脂消煎剂治疗脂肪肝药效学机制.方法采用高脂饮食加白酒灌胃建立大鼠脂肪肝模型,以东宝肝泰作对照,观察肝脂消煎剂对脂肪肝大鼠肝微粒体膜流动性及心肌黄酶(DTD)、丙二醛(MDA)的影响.结果模型对照组MDA与肝微粒体膜荧光偏振度较正常对照组明显增大,且两者成正相关(r=0.974 6),表示肝脏因脂质过氧化引起膜流动性降低;肝脂消煎剂能降低MDA含量及荧光偏振度,拮抗膜流动性的下降,提高肝脏DTD活性,均明显优于东宝肝泰.结论肝脂消煎剂可抑制肝微粒体脂质过氧化,拮抗其膜流动性降低,具有良好的防治脂肪肝作用.     

氟对原代培养大鼠肝细胞的氧化损伤作用研究

目的探讨氟对原代培养大鼠肝细胞的氧化损伤作用。方法采用半原位酶消化法分离大鼠肝细胞，氟化物染毒24h后用噻唑蓝(MTT)比色法检测细胞存活率，检测培养液中谷丙转氨酶(ALT)、谷草转氨酶(AST)的活性及脂质过氧化产物丙二醛(MDA)的含量。结果氟对大鼠肝细胞具有明显的毒性作用，表现为细胞存活率下降，ALT、AST的活性升高，MDA含量增加。结论脂质过氧化引起的氧化损伤作用是氟致原代培养大鼠肝细胞毒性的主要原因。     

肝脂消煎剂对脂肪肝大鼠肝微粒体膜流动性及心肌黄酶、丙二醛的作用

目的 :探讨肝脂消煎剂治疗脂肪肝药效学机制。方法 :采用高脂饮食加白酒灌胃建立大鼠脂肪肝模型 ,以东宝肝泰作对照 ,观察肝脂消煎剂对脂肪肝大鼠肝微粒体膜流动性及心肌黄酶 (DTD)、丙二醛 (MDA)的影响。结果 :模型对照组 MDA与肝微粒体膜荧光偏振度较正常对照组明显增大 ,且两者成正相关 (r =0 .974 6 ) ,表示肝脏因脂质过氧化引起膜流动性降低 ;肝脂消煎剂能降低 MDA含量及荧光偏振度 ,拮抗膜流动性的下降 ,提高肝脏DTD活性 ,均明显优于东宝肝泰。结论 :肝脂消煎剂可抑制肝微粒体脂质过氧化 ,拮抗其膜流动性降低 ,具有良好的防治脂肪肝作用。     

绞股蓝总皂甙对原代培养大鼠肝细胞四氯化碳损伤的影响

采用四氯化碳(CCl_4)制成原代培养大鼠肝细胞损伤模型,观察了绞股蓝总皂甙(GPS)对肝细胞损伤的保护作用。结果表明,预先用 GPS 处理肝细胞 lhr,可明显减轻 CCl_4引起的肝细胞 DNA 合成速率降低,减少肝细胞 ALT 逸出,抑制培养上清液中 MDA 含量的升高和 SOD/MDA 比值的缩小,并与 GPS 浓度呈依赖关系。提示 GPS 能减轻 CCl_4对离体培养的大鼠肝细胞损伤,保护肝细胞 DNA 合成,其作用机理与抗脂质过氧化有关。     

Hypoglycemic effect of Costus pictus D. Don on alloxan induced type 2 diabetes mellitus in albino rats

ObjectiveTo demonstrate the effect of aqueous extract of Costus pictus (C. pictus) leaves on blood glucose, lipid profile and liver antioxidant enzymes and lipid peroxidation in alloxan induced diabetic rats.MethodsAqueous extract of C. pictus (AECP) leaves was administered orally for 30 days and its effect on blood glucose, lipid profile, hepatic marker enzymes such as serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), serum urea, creatinine, protein and albumin content and liver antioxidant enzymes such as catalase, peroxidase, superoxide dismutase and lipid peroxidation in alloxan induced diabetic rats were examined.ResultsOral administration of aqueous extract of C. pictus leaves to diabetic rats for 30 days significantly reduced the levels of blood glucose, lipid profile, lipid peroxidation, liver marker enzymes, urea, creatinine and increased the levels of antioxidant enzymes.ConclusionsThe aqueous extract of C. pictus leaves controls the blood glucose level, improves lipid metabolism and prevents diabetic complications associated with lipid peroxidation and also maintains the antioxidant enzymes in experimental diabetic rats. Therefore, it can be recommeded for the prevention of diabetes mellitus.     

叔丁基痉基茴香醚对小鼠醋氨酚中毒性肝损伤的操作作用

目的：采用小鼠醋氨酚中毒性肝损伤模型探讨２（３）－叔丁基－４－羟基茴香醚（ＢＨＡ）对肝脏的保护作用。方法：通过腹腔注射醋氨酚制备小鼠肝损伤模型,测定小鼠血清丙氨酸转氨酶（ＡＬＴ）活笥和肝匀浆液中的丙二醛（ＭＤＡ）含量、超氧化的岐化酶（ＳＯＤ）活性及谷胱甘肽（ＧＳＨ）含量。结果：０．２％及０．５％的ＢＨＡ都能显著对抗醋氨酚所致小鼠肝损伤的血清ＡＬＴ活性升高,肝组织ＭＤＡ含量升高、ＳＯＤ活性降低及还原     

Hypoglycemic activity of Hemidesmus indicus R. Br. on streptozotocin-induced diabetic rats

OBJECTIVE:

To evaluate the antidiabetic activity of an aqueous extract of the roots of Hemidesmus indicus on blood glucose, serum electrolytes, serum marker enzymes, liver microsomal P-450 enzymes, and lipid peroxidation in the liver and kidney of streptozotocin-induced diabetic rats.

MATERIALS AND METHODS:

Effect of H. indicus extract on blood glucose was studied with fed, fasted and glucose-loaded diabetic and nondiabetic rat models. The effect of the extract on serum electrolytes, serum levels of key glucose metabolizing enzymes, hepatic microsomal protein and hepatic cytochrome P-450-dependent mono-oxygenase enzyme systems and lipid peroxidation in the liver and kidney of diabetic rats. One way analysis of variance and Duncan''s multiple range test was used for statistical analysis.

RESULTS:

Oral administration of H. indicus aqueous extract to fed, fasted and glucose-loaded diabetic rats decreased blood glucose level significantly at 5 h and restored serum electrolytes, glycolytic enzymes and hepatic cytochrome P-450-dependent enzyme systems by preventing the formation of liver and kidney lipid peroxides at the end of 12 weeks of the study period.

CONCLUSION:

From the studies, it can be concluded that the aqueous extract of the roots of H. indicus at a dosage of 500 mg/kg/day exhibits significant antidiabetic activity. It restores the concentrations of electrolytes, glucose metabolizing enzymes, hepatic microsomal protein and hepatic cytochrome P-450-dependent mono-oxygenase enzyme systems to near normal level and also corrects the related metabolic alterations in experimentally induced diabetic rats. H. indicus administration also decreased liver and kidney lipid peroxidation products. On the basis of our findings, H. indicus could be used as an antidiabetic and antioxidant agent for the prevention and treatment of diabetes mellitus.     

Hepatoprotective effect of the aqueous extract of the roots of Decalepis hamiltonii against ethanol-induced oxidative stress in rats.

The hepatoprotective activity of the aqueous extract of the roots of Decalepis hamiltonii was investigated against ethanol-induced oxidative stress and liver damage. Pretreatment of rats with aqueous extract of the roots of D. hamiltonii, single (50, 100 and 200mg/kg b.w.) and multiple doses (50 and 100mg/kg b.w. for 7 days) significantly prevented the ethanol (5g/kg b.w.) induced increases in the activities of the serum enzymes, aspartate and alanine transaminases, alkaline phosphatase and lactate dehydrogenase in a dose dependent manner. Parallel to these changes, the root extract inhibited the ethanol-induced oxidative stress in the liver by suppressing lipid peroxidation and protein carbonylation and maintaining the levels of antioxidant enzymes and glutathione. The biochemical changes were consistent with histopathological observations suggesting marked hepatoprotective effect of the root extract. The protective effect of the root extract against hepatotoxicity of alcohol was more pronounced by the multiple dose pretreatment. Hepatoprotective activity of the aqueous extract of the roots of D. hamiltonii could be attributed to the antioxidant effect of the constituents and enhanced antioxidant defenses.     

Role of active oxygen species and lipid peroxidation in liver injury induced by ischemia-reperfusion

The role of superoxide and lipid peroxidation in liver injury induced by ischemia-reperfusion was investigated in rats. Ischemic condition of the liver was created by applying small clamps to the right branch of portal vein and the right hepatic artery for 15 min. Clamping of hepatic artery and portal vein could decrease the hepatic blood flow to about 30% of that measured before the clamping. Levels of serum GPT and thiobarbituric acid (TBA) reactive substances in the liver tissue were significantly increased 30 min after the reperfusion following 15 min of ischemia. The increase in serum GPT and TBA reactants in the liver tissue was significantly inhibited by the treatment with superoxide dismutase combined with catalase. The treatment with allopurinol significantly inhibited the elevation of serum GPT levels and showed a tendency to inhibit the increase in TBA reactants in liver tissue. These results suggest that active oxygen species and lipid peroxidation may play an important role in the pathogenesis of ischemia-reperfusion injury in the liver, and hypoxanthine-xanthine oxidase system may be one of the main sources of active oxygen species.     

Role of active oxygen, lipid peroxidation, and antioxidants in the pathogenesis of gastric mucosal injury induced by indomethacin in rats.

The roles of active oxygen, lipid peroxidation, and the antioxidative defence mechanism in gastric mucosal injury induced by treatment with indomethacin in rats were investigated. The total area of gastric erosions and concentration of lipid peroxides in the gastric mucosa increased with time after administration of indomethacin (20 mg/kg, orally). The alpha-tocopherol:total cholesterol ratio in serum was significantly decreased and the activity of glutathione peroxidase, an important enzyme to scavenger of lipid peroxides, was inhibited by the administration of indomethacin. Treatments with superoxide dismutase and catalase inhibited the increases in gastric mucosal erosions and lipid peroxides in the gastric mucosa, and the reduction of serum alpha-tocopherol. Treatment with these scavengers did not improve the decreased glutathione peroxidase activity. These findings suggest that active oxygen species and lipid peroxidation play an important part in the pathogenesis of gastric mucosal injury induced by indomethacin, and that the decreased glutathione peroxidase activity aggravated the injury due to accelerated accumulation of hydrogen peroxide and lipid peroxides in the gastric mucosal cell.     

Hepatoprotective effect of pentoxifylline against D-galactosamine-induced hepatotoxicity in rats

The present study was conducted to investigate effect of pentoxifylline (PTX) on acute liver injury caused by galactosamine (D-Gal) in rats and the underlying mechanism involved in this setting. Moreover, we attempted to compare its effect to the well-established hepatoprotective agent, silymarin (SYM). The rats were randomly assigned 5 groups, control, PTX-treated (100 mg/kg, 3 weeks), SYM-treated (100 mg/kg, 3 weeks) and their combination. Hepatic injury was induced by intraperitoneal single dose injection of D-Gal (800 mg/kg). Hepatic functions parameters, including serum albumin and alkaline phosphatase (ALP) levels were determined. Antioxidants enzyme activities such as superoxide dismutase (SOD), catalase (CAT) as well as lipid peroxides and hepatic total nitrites were measured. Besides, histopathological examination was also performed using portions of liver tissues. Results showed that the liver injury induced by D-Gal was improved in the three pretreated groups to variable extents. Pretreatment with PTX prevented D-Gal-induced reduction of antioxidante enzyme activities, SOD and CAT, and attenuated the elevated malonaldahyde (MDA) level in hepatic tissue as marker of lipid peroxidation. In addition, pretreatment with PTX resulted in an increase in hepatic triglycerides, normalization of nitric oxide level, and lowering serum ALP activity as well as inhibited the decreased serum albumin level caused by D-Gal. These biochemical changes were reflected on attenuation the structural alterations of the liver integrity. Collectively, our data suggest that PTX exhibits a potential hepatoprotective effect against D-Gal-induced hepatotoxicity and this effect might be attributed to its antioxidant properties.     

Influence of zinc sulfate intake on acute ethanol-induced liver injury in rats

AIM: To investigate the role of metallothionein and proliferating cell nuclear antigen (PCNA) on the morphological and biochemical effects of zinc sulfate in ethanol-induced liver injury. METHODS: Wistar albino rats were divided into four groups. GroupⅠ; intact rats, groupⅡ; control rats given only zinc, groupⅢ; animals given absolute ethanol, group IV; rats given zinc and absolute ethanol. Ethanol-induced injury was produced by the 1 mL of absolute ethanol, administrated by gavage technique to each rat. Animals received 100 mg/kg per day zinc sulfate for 3 d 2 h prior to the administration of absolute ethanol. RESULTS: Increases in metallothionein immunoreactivity in control rats given only zinc and rats given zinc and ethanol were observed. PCNA immunohistochemistry showed that the number of PCNA-positive hepatocytes was increased significantly in the livers of rats administered ethanol + zinc sulfate. Acute ethanol exposure caused degenerative morphological changes in the liver. Blood glutathione levels decreased, serum alkaline phosphatase and aspartate transaminase activities increased in the ethanol group when compared to the control group. Liver glutathione levels were reduced, but lipid peroxidation increased in the livers of the group administered ethanol as compared to the other groups. Administration of zinc sulfate in the ethanol group caused a significant decrease in degenerative changes, lipid peroxidation, and alkaline phosphatase and aspartate transaminase activities, but an increase in liver glutathione. CONCLUSION: Zinc sulfate has a protective effect on ethanol-induced liver injury. In addition, cell proliferation may be related to the increase in metallothionein immunoreactivity in the livers of rats administered ethanol + zinc sulfate.     

Pathogenesis of diquat-induced liver necrosis in selenium-deficient rats: Assessment of the roles of lipid peroxidation and selenoprotein P

A dose of diquat below the amount injurious to selenium-replete animals causes lipid peroxidation and massive liver necrosis in selenium-deficient rats. The current study was undertaken to characterize the lipid peroxidation with respect to the liver injury and to correlate the presence of several selenoproteins with the protective effect of selenium. Lipid peroxidation was assessed by measurement of F₂ isoprostanes. Diquat caused an increase in liver and plasma F₂ isoprostanes. A gradient of these compounds was detected across the liver in some animals, indicating that this organ was a source of some of the plasma F₂ isoprostanes. A time-course experiment showed that liver F₂ isoprostane concentration increased before plasma alanine transaminase (ALT) levels rose. Selenium-deficient rats were injected with selenium doses from 2 to 50 μg/kg and studied 12 hours later. A dose of 10 μg/kg or more prevented diquat-induced lipid peroxidation and liver injury. This dose increased plasma selenoprotein P substantially, and a dose-response was present. Liver cellular and plasma glutathione peroxidase activities remained below 2% of their values in control rats for all selenium doses. In selenium-deficient rats given diquat, hepatic lipid peroxidation precedes hepatic necrosis and could therefore be an important mechanism of the necrosis. Selenoprotein P levels were increased by selenium injections, which protected against diquat injury, but glutathione peroxidase activity was not increased. This is consistent with selenoprotein P being the mediator of the selenium effect.     

Protective effect of some vitamins against the toxic action of ethanol on liver regeneration induced by partial hepatectomy in rats

AIM： To investigate the effects of vitamins （A, C and E） on liver injury induced by ethanol administration during liver regeneration in rats. METHODS： Male Wistar rats subjected to 70% partial hepatectomy were divided into five groups （groups 1-5）. During the experiment, animals of Group 1 drank only water. The other four groups （2-5） drank 30 mL of ethanol/L of water. Group 3 additionally received vitamin A, those of group 4 vitamin C and those of group 5 received vitamin E. Subsequently serum alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, albumin and bilirubin were measured colorimetrically. Lipid peroxidation （thiobarbituric-acid reactive substances, TBARS） both in plasma and liver was measured, as well as liver mass gain assessment and total DNA. RESULTS： Compared with sham group, serum AST and ALT increased significantly under ethanol treatment （43% and 93%, respectively, with P 〈 0.05）. Vitamin C and vitamin E treatment attenuated the ethanol-induced increases in ALT and AST activity. Ethanol treatment also decreased serum albumin concentration compared to sham group （3.1 ± 0.4 g/dL vs 4.5 ± 0.2 g/dL; P 〈 0.05）. During liver regeneration vitamins C and E significantly ameliorated liver injury for ethanol administration in hepatic lipid peroxidation （4.92 nmol/mg and 4.25 nmol/mg vs 14.78 nmol/mg, respectively, with P 〈 0.05）. In association with hepatic injury, ethanol administration caused a significant increase in both hepatic and plasma lipid peroxidation. Vitamins （C and E） treatment attenuated hepatic and plasma lipid peroxidation. CONCLUSION： Vitamins C and E protect against liver injury and dysfunction, attenuate lipid peroxidation, and thus appear to be significantly more effective than vitamin A against ethanol-mediated toxic effects during liver regeneration.