Ketogenesis evaluation in perfused liver of diabetic rats submitted to short‐term insulin‐induced hypoglycemia

Ketogenesis, inferred by the production of acetoacetate plus ß‐hydroxybutyrate, in isolated perfused livers from 24‐h fasted diabetic rats submitted to short‐term insulin‐induced hypoglycemia (IIH) was investigated. For this purpose, alloxan‐diabetic rats that received intraperitoneal regular insulin (IIH group) or saline (COG group) injection were compared. An additional group of diabetic rats which received oral glucose (gavage) (100 mg kg^?1) 15 min after insulin administration (IIH + glucose group) was included. The studies were performed 30 min after insulin (1.0 U kg^?1) or saline injection. The ketogenesis before octanoate infusion was diminished (p < 0.05) in livers from rats which received insulin (COG vs. IIH group) or insulin plus glucose (COG vs. IIH + glucose group). However, the liver ketogenic capacity during the infusion of octanoate (0.3 mM) was maintained (COG vs. IIH group and COG vs. IIH + glucose group). In addition, the blood concentration of ketone bodies was not influenced by the administration of insulin or insulin plus glucose. Taken together, the results showed that inspite the fact that insulin and glucose inhibits ketogenesis, livers from diabetic rats submitted to short‐term IIH which received insulin or insulin plus glucose showed maintained capacity to produce acetoacetate and ß‐hydroxybutyrate from octanoate. Copyright © 2009 John Wiley & Sons, Ltd.     

大黄醇提液抗家兔实验性高脂血症及脂肪肝的实验研究

目的:检验大黄醇提液抗家兔实验性高脂血症及脂肪肝的影响。方法:将30只雄性健康白兔随机分为5组(n=6):对照组给予基础饲料;模型组给予高脂饲料;三个大黄组给予高脂饲料同时分别灌胃不同药量的大黄醇提液。实验过程中进行一般性指标观测,检测不同阶段五组家兔血脂水平,检测脂肪肝病变程度。结果:大黄醇提液具有降低血清甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C),升高高密度脂蛋白胆固醇(HDL-C),降低肝细胞脂肪变性的作用。并且大黄醇提液的以上作用存在一定的量效关系。结论:大黄醇提液可降低动脉粥样硬化兔模型的血脂水平、降低脂肪肝的发生发展。     

不同剂量玛咖对力竭运动致大鼠运动性低血糖的保护作用

目的：探讨不同剂量玛咖对力竭运动致大鼠运动性低血糖的保护作用。方法：采用递增负荷力竭游泳训练的方法建立运动性低血糖动物模型。55只42 d龄雄性Wistar大鼠随机分为5组：①静止对照组（C组）,②运动对照组（M组）,③~⑤运动+低、中、高剂量玛咖组（LM I、LM Ⅱ,LM Ⅲ组）,每组10只（剔除不符合实验要求的大鼠5只）。每天灌胃（ig）1次,LM各组灌胃玛咖的剂量为0.2,0.4,1.2 g/kg体重,灌胃体积为5 ml/kg体重,C、M组灌胃等体积生理盐水。运动大鼠采用递增负荷力竭游泳训练42 d,42 d力竭游泳训练后,测定体重、力竭游泳时间,取血、肝脏及深层股四头肌检测相关生化指标。结果：与C组比较,M组体重、血糖水平、肌糖原与肝糖原含量、肝细胞磷酸烯醇式丙酮酸羧激酶（phosphoenol pyruvate carboxy kinase,PEPCK）表达、肝细胞阳性染色累计吸光度均值等均明显降低（P<0.05或P<0.01）;力竭游泳时间无明显差异;血乳酸含量明显升高（P<0.01）。与M组比较,LM各组体重、血糖水平、肌糖原与肝糖原含量、肝细胞PEPCK表达、肝细胞阳性染色累计吸光度均值等均明显升高（P<0.05或P<0.01）,力竭游泳时间明显延长（P<0.01）,血乳酸含量明显降低（P<0.01）。与LM I组比较,LMⅢ组体重无明显差异,LM Ⅲ组血糖水平、肌糖原与肝糖原含量、肝细胞PEPCK表达、肝细胞阳性染色累计吸光度均值等均明显升高（P<0.05）,力竭游泳时间明显延长,血乳酸含量明显降低（P<0.05）。结论：高剂量玛咖可有效抑制和延缓长时间、大负荷运动导致的运动性低血糖和运动性疲劳的发生与发展,其机制可能与优化肌糖原和肝糖原的储备量及上调糖异生限速酶PEPCK的表达,提高PEPCK活性,促进糖异生有关。     

Heritability and genetic loci of fatty liver in familial combined hyperlipidemia

VLDL overproduction, a process that is driven by an excess amount of hepatic fat, is a well-documented feature of familial combined hyperlipidemia (FCHL). The aims of this study were to investigate whether fatty liver, measured with ultrasound and as plasma alanine aminotransferase (ALT) levels, develops against a genetic background in FCHL and to identify chromosomal loci that are linked to these traits. In total, 157 FCHL family members and 20 spouses participated in this study. Radiological evidence of fatty liver was more prevalent not only in FCHL probands (40%) but also in their relatives (35%) compared with spouses (15%) (P < 0.05). Heritability calculations revealed that 20-36% of the variability in ALT levels could be attributed to genetic factors. Nonparametric quantitative trait locus (QTL) analysis revealed three significant (P < 0.001) loci with either the ultrasound or the ALT trait in the male sample: 1q42.3, 7p12-21, and 22p13-q11; none was found in the female sample or the entire group. Of these QTLs, the 7p region was consistent over time, because reanalysis with ALT levels that were determined during a visit 5 years earlier yielded similar results. This study shows that fatty liver is a heritable aspect of FCHL. Replication of particularly the 7p region is awaited.     

Chromium induced clinical improvement in symptomatic hypoglycemia

The present study included 20 patients indicating clinical symptoms of hypoglycemia, of which 19 showed a minimal glucose level in the tolerance curve above 2.2 mmol/L (limit for glucose induced hypoglycemia). This clinical state is defined here as “symptomatic hypoglycemia”. All individuals were studied for effects of a daily intake for three mo of a yeast chromium supplement (125 μg Cr/d). The patients were followed by means of their oral glucose tolerance curve (1 g glucose/kg body wt) and by an interrogation scheme prior to during and after chromium supplementation. During three mo of chromium supplementation, a decrease was found in the negative part of the glucose tolerance curve, i.e., the part of the curve being below the fasting level in eight patients (40%). However, one mo after treatment, 10 patients out of 13 (77%) showed decreased areas of the negative part of the glucose tolerance curve compared to the values during treatment, and 11 out of 15 (73%) showed decreases in the negative part of the curve when posttreatment data were compared to ante-treatment data. The subjective clinical effects were followed by means of a questionnaire. Subjectively, the effects of organo-chromium were especially pronounced on chilliness. Thus seven (47%) indicated improvement and two (15%) indicated that the chilliness disappeared. However, trembling, emotional instability, and disorientation symptoms improved as well.     

A method for producing regional hypoglycemia in blood perfused tissue

Numerous studies have focused on the metabolic contributions of glucose and other substrates in isolated tissue preparations by examining the effects of eliminating glucose from the physiologic perfusate or bath solution. To date, however, an effective method of glucose removal from the blood supply to selected tissue in the whole animal model has not been available. We have developed a method for blood glucose removal by continuous flow dialysis. This method was used to generate isolated coronary hypoglycemia for an investigation of myocardial metabolic substrate selection during hypoperfusion in open-chest, anesthetized dogs. Arterial blood was passed through the dialysis system against an isotonic and physiologic dialysate solution prior to controlled coronary perfusion. During normal perfusion pressure (100 mmHg), with a coronary blood flow of 32 ± 4 ml/min, arterial blood glucose was reduced from 3.26 ± 0.31 to 0.54 ± 0.14 mM. When blood flow was reduced to 12 ± 3 ml/min with lower perfusion pressure (40 mmHg), dialysis reduced arterial glucose from 3.53 ± 0.36 to 0.15 ± 0.03 mM. We conclude that this is an effective method for producing regional hypoglycemia.     

Cellular mechanisms of brain hypoglycemia

Data on intracellular processes induced by a low glucose level in nerve tissue are presented. The involvement of glutamate and adenosine receptors, mitochondria, reactive oxygen species (ROS), and calcium ions in the development of hypoglycemia-induced damage of neurons is considered. Hypoglycemia-induced calcium overload of neuronal mitochondria is suggested to be responsible for the increased ROS production by mitochondria.     

Hypolipemia,hypoglycemia, and inactivation of glycogen phosphorylase in Locusta migratoria

Feeding starved adult migratory locusts, Locusta migratoria, caused decreases of hemolymph lipid concentrations and of the percentage of active fat body glycogen phosphorylase which suggested that a molecule(s) from the neurosecretory system or the midgut may have been released to regulate metabolism. Fat body phosphorylase was also inactivated after insects were transferred from 0 to 25 ° C. In adults with elevated hemolymph lipid levels after the injection of small doses of corpus cardiacum extract (CC), feeding did not induce a decrease in hemolymph lipid concentrations. It appears that the processes initiated by feeding could not override the effects of the continued presence of adipokinetic hormone(s) (AKHs) in the hemolymph or their long-term effects. Aqueous, methanolic, or ethanolic extracts of brains or storage lobes (SL) of fed locust CC did not lead to decreases of hemolymph lipid concentrations. Bovine insulin was equally inactive when tested at doses which were previously reported to reduce lipid levels. Fractions of ethanolic brain extracts from 3-day-starved males collected after high-performance size-exclusion chromatography, however, produced hypoglycemic effects in fed males. Two biologically active fractions were found, one with high (≥ 10 kDa) and one with low molecular weight (approximately 1 kDa). © 1995 Wiley-Liss, Inc.     

Somatostatin concentration and binding in the rat hypothalamus and striatum during severe insulin-induced hypoglycemia

Hypoglycemia was induced by administration of insulin (40 I.U./kg) to 24 h fasted rats. Somatostatinlike immunoreactivity (SLI) and¹²⁵I-Tyr¹¹-somatostatin binding were measured in the striatum and hypothalamus at the onset of hypoglycemic coma (5–10 min). No significant changes in SLI concentration were detected in either site although the total number of specific somatostatin receptors in the striatum membranes, but not in the hypothalamus, decreased in insulin-injected rats when compared with the control group.     

糖尿病低血糖昏迷急诊救治的临床效果

目的探讨糖尿病低血糖昏迷患者采用急诊系统干预方案实施救治的临床效果。方法对我院收治的糖尿病低血糖昏迷患者120例,按随机分组方案分为对照组和观察组,每组60例。对照组采用常规急诊干预方案进行救治,观察组采用急诊系统干预方案进行救治,比较两组糖尿病低血糖昏迷患者的急诊救治效果、救治后苏醒时间和治疗总时间、急诊救治期间不良事件发生情况。结果观察组糖尿病低血糖昏迷的急诊救治总有效率达91.7%,高于对照组的71.7%,组间比较差异有显著统计学意义(P0.05);救治后苏醒时间和治疗总时间比较,观察组均短于对照组,差异均具统计学意义(P0.05);观察组急诊救治期间发生不良事件1例,对照组发生不良事件8例,差异亦有统计学意义(P0.05)。结论糖尿病低血糖昏迷患者采用急诊系统干预方案实施救治,能促使患者短时间内苏醒,维持血糖稳定,改善患者预后。     

莪术醇对非酒精性脂肪性肝大鼠肝功能和肝纤维化的影响及机制*

目的:探讨莪术醇(CC)对非酒精性脂肪性肝(NAFLD)大鼠模型肝功能和肝纤维化的影响及机制。方法:采用高脂饮食构建非酒精脂肪肝炎(NASH)伴肝纤维化的大鼠模型,将60只SD大鼠随机分为:空白对照组、模型组(NASH)、NASH+复方鳖甲软肝片(CBT)组(阳性对照组)、NASH+CC组(25、50、100 mg/kg),每组10只。测量大鼠肝脏占体重的百分比,测量大鼠高密度脂蛋白(HDL)、甘油三酯(TG)、谷丙转氨酶(ALT)、谷草转氨酶(AST)水平,HE染色观察肝纤维化情况,免疫组化检测鼠肝组织α-平滑肌肌动蛋白(α-SMA)表达及肝组织核因子κB p65(NF-κB p65)的阳性染色情况,蛋白印迹(Western blot)检测α-SMA、基质金属蛋白酶-1(MMP-1)、基质金属蛋白酶抑制剂-1(TIMP-1)蛋白表达及Toll样受体-4(TLR4)、转化生长因子激活激酶-1(TAK1)、NF-κB p65、血管细胞粘附分子-1(VCAM-1)蛋白的表达情况,酶联免疫吸附法(ELISA)检测肝组织中白介素(IL-6、IL-10、IL-1β)、肿瘤坏死因子-α(TNF-α)的表达。结果:与空白对照组相比,模型组大鼠HDL、 IL-10含量、MMP-1蛋白表达量显著降低(P＜0.05),TG、ALT、AST、肝组织P65阳性率,α-SMA、TIMP-1、TLR4、TAK1、NF-κB p65、VCAM-1表达、IL-6、TNF-α及IL-1β含量显著升高(P＜0.05)。与模型组相比,CBT和CC处理后大鼠HDL、 IL-10含量、MMP-1蛋白表达量显著升高(P＜0.05),TG、ALT、AST、肝组织P65阳性率,α-SMA、TIMP-1、TLR4、TAK1、NF-κB p65、VCAM-1表达、IL-6、TNF-α及IL-1β含量显著降低(P＜0.05),其中模型+CC组以高浓度组改善最显著(P＜0.05),但各剂量改善幅度均低于模型+CBT组(P＜0.05)。结论:莪术醇通过调节TLR4、TAK1、NF-κB p65信号通路,减轻炎症反应,改善肝功能,从而缓解非酒精性脂肪肝肝肝纤维化,且在一定范围内呈浓度依赖性。     

Expression of neuronal plasticity markers in hypoglycemia induced brain injury

The expression of neuroplasticity markers was analyzed in four brain regions, namely cerebral hemispheres (CH), cerebellum (CB), brain stem (BS) and diencephalon (DC) from insulin-induced hypoglycemic young adult rats. Significant decrease in neural cell adhesion molecule (NCAM) isoforms and growth-associated protein-43 (GAP-43) was observed following hypoglycemic injury from majority of brain regions studied. The glial fibrillary acidic protein (GFAP) level increased significantly in cerebral hemispheres and diencephalon regions, whereas, synaptophysin level increased in cerebellum, brain stem and diencephalon regions. The selective downregulation of the neuronal plasticity marker proteins (GAP-43 and NCAM), and enhanced expression of GFAP and synaptophysin suggests that in acute hypoglycemia, mechanisms other than energy failure may also contribute to neuronal cell damage in the brain.     

Effects of zinc deficiency on the fatty acid composition and metabolism in rats fed a fat-free diet

The effects of dietary zinc deficiency (ZD) on the composition and metabolism of the fatty acyl chains of phospholipids in rat liver were investigated with a fat-free diet. The levels of (n−9) fatty acids such as 18∶1 and 20∶3(n−9) in liver phospholipids (PL) were significantly lower in ZD-rats (19.4% and 5.4%, respectively) than in PF-rats (25.2 and 8.3%). On the other hand, the level of (n−6) acids such as 18∶2 and 20∶4 were higher in ZD-rats (3.3 and 19.1%, respectively) than in PF-rats (2.1 and 14.9%). In order to study the metabolism of fatty acids in vivo,¹⁴C-18∶0 or¹⁴C-18∶2 was intravenously injected, and then the conversion to the respective metabolite was examined. After the injection of¹⁴C-18∶0, the radioactivity was found in 18∶0 (49.3% of the total), 18∶1 (33.2%), and 20∶3 (n−9) (9.1%) in liver PL in PF-rats at 24h. In ZD-rats, the radioactivity was dramatically lower in 18∶1 (23.5%) and 20∶ (n−9) (3.6%), suggesting that the conversion of 18∶0 to 18∶1 and 20∶3 (n−9) was strongly inhibited in ZD-rats. When¹⁴C-18∶2 was injected, the radioactivity was mainly found in 18∶2, 20∶3(n−6), and 20∶4. The radioactivity in 20∶4 in ZD-rats was slightly higher than that in control rats. These results indicate that zinc deficiency affects the fatty acid metabolism in liver, in particular, it causes a reduction in δ9 desaturase activity, when rats are fed a fat-free diet.     

Enhanced insulin-hypoglycemic activity in rats consuming a specific glycoprotein extracted from maitake mushroom

Lipid accumulation in non-adipose tissues leads to cell dysfunction and apoptosis, a phenomenon known as lipotoxicity. Recent evidence suggests that lipotoxicity in hepatocytes involves endoplasmic reticulum (ER) stress and c-Jun NH₂-terminal kinase-mediated apoptosis. The present study examined (1) the dose–response and time course characteristics of fatty acid-mediated ER stress and apoptosis in H4IIE liver cells; (2) whether saturated fatty acid-induced apoptosis involved the ER-associated caspase-12; and (3) whether trans-10, cis-12-conjugated linoleic acid, an inhibitor of stearoyl-CoA desaturase, influenced fatty acid-mediated ER stress and apoptosis. Saturated fatty acids induced ER stress in a dose-dependent manner with a time course that was delayed relative to chemical-induction of ER stress. Saturated fatty acids increased caspase-9 and caspase-3 activity, however increased caspase-12 activity was not observed. Inhibition of stearoyl-CoA desaturase, using conjugated linoleic acid (trans-10, cis-12), augmented saturated fatty acid-induced ER stress and apoptosis. These data suggest that saturated fatty acids induce ER stress and apoptosis at physiologic concentrations and with a relatively rapid time course. It would appear that saturated fatty acid-mediated apoptosis occurs independently of caspase-12 activation. Since conjugated linoleic acid inhibited stearoyl-CoA desaturase activity, it is hypothesized that saturation, per se, plays a role in lipotoxicity in liver cells.     

双歧杆菌三联活菌肠溶胶囊对高脂饮食所致大鼠非酒精性脂肪肝的疗效及机制探讨

目的 观察微生态制剂贝飞达(双歧杆菌三联活菌肠溶胶囊)治疗高脂饮食所致大鼠非酒精性脂肪肝的疗效并探讨其可能的作用机制.方法 雄性SD大鼠32只,适应性饲养1周后,随机分为3组,正常组:12只给予普通饲料喂养;模型组:12只,贝飞达治疗组:8只,均给予高脂饲料喂养;于喂养12周末正常组及模型组各处死4只,经肝组织HE染色确定造模成功后,贝飞达治疗组给予贝飞达[0.113 g/(kg·d)]灌胃,于16周末全部处死.检测大鼠血清AST、ALT、TC、TG、LDL、HDL、血清内毒素水平,观察其肝组织学变化.结果 模型组于高脂饲料喂养12周末出现脂肪肝,与正常组比较,模型组大鼠血清AST、ALT、TG、TC、LDL、HDL及血清内毒素水平均明显升高(P＜0.01).贝飞达治疗组大鼠各项指标较模型组均有显著改善,肝脏脂肪变性程度减轻.结论 微生态制剂贝飞达可能通过改善肠道菌群紊乱,减轻内毒素血症,从而调节肝脏脂质代谢紊乱,对非酒精性单纯性脂肪肝起到治疗作用.     

Induction of aldehyde dehydrogenase by polycyclic aromatic hydrocarbons in rats

Short-term intragastric administration of selected polycyclic aromatic hydrocarbons (100 mg/kg daily for 4 days) to male Wistar rats resulted in marked changes in liver cytosolic aldehyde dehydrogenase activity. Non-carcinogenic anthracene, phenanthrene and chrysene produced a 2.5–3-fold increase in the activity assayed with propionaldehyde as substrate and NAD as coenzyme. Weakly carcinogenic 1,2-benzanthracene enhanced aldehyde dehydrogenase activity 9-fold and the potent carcinogens 3,4-benzpyrene and 3-methylcholanthrene 30-fold. With benzaldehyde as substrate and NADP as coenzyme the differences between the groups were even more pronounced. Somewhat similar but less manifest effects on aldehyde dehydrogenase activity were detected also in the liver microsomes and in the postmitochondrial fractions of the small intestinal mucosa. On the basis of their ability to induce aldehyde dehydrogenase activity the compounds could be divided into three groups. This classification was found to correlate well with the carcinogenic potency of the compounds. It appeared that the exposure to polycyclic aromatic hydrocarbons, especially the carcinogenic ones, was followed by synthesis of a new aldehyde dehydrogenase form. This new form was differentiated from the normally existing cytosolic aldehyde dehydrogenase by its ability to oxidize benzaldehyde in the presence of NADP.     

Dietary freshwater clam (Corbicula fluminea) extract suppresses accumulation of hepatic lipids and increases in serum cholesterol and aminotransferase activities induced by dietary chloretone in rats

We investigated the ameliorative effect of freshwater clam extract (FCE) on fatty liver, hypercholesterolemia, and liver injury in rats exposed to chloretone. Furthermore, we examined the effects of major FCE components (fat and protein fractions) to determine the active components in FCE. Chloretone increased serum aminotransferase activities and led to hepatic lipid accumulation. Serum aminotransferase activities and hepatic lipid content were lower in rats fed total FCE or fat/protein fractions of FCE. Expression of fatty acid synthase and fatty acid desaturase genes was upregulated by chloretone. Total FCE and fat/protein fractions of FCE suppressed the increase in gene expression involved in fatty acid synthesis. Serum cholesterol levels increased twofold upon chloretone exposure. Total FCE or fat/protein fractions of FCE showed hypocholesterolemic effects in rats with hypercholesterolemia induced by chloretone. These suggest that FCE contains at least two active components against fatty liver, hypercholesterolemia, and liver injury in rats exposed to chloretone.     

Oxidative stress in the pathogenesis of nonalcoholic fatty liver disease,in rats fed with a choline-deficient diet

Background/Aim : The pathogenesis of Nonalcoholic Fatty Liver Disease remains largely unknown, but oxidative stress seems to be involved. The aim of this study was to evaluate the role of oxidative stress in experimental hepatic steatosis induced by a choline-deficient diet. Methods : Fatty liver disease was induced in Wistar rats by a choline-deficient diet. The animals were randomized into three groups: I (G1) and II (G2), n=6 each - fed with a choline-deficient diet for four and twelve weeks respectively; Group III (control-G3; n=6) - fed with a standard diet for twelve weeks. Samples of plasma and liver were submitted to biochemical, histological and oxidative stress analysis. Variables measured included serum levels of aminotransferases (AST, ALT), cholesterol and triglycerides. Oxidative stress was measured by lucigenin-enhanced luminescence and the concentration of hydroperoxides (CE-OOH-cholesteryl ester) in the liver tissue. Results: We observed moderate macro- and microvesicular fatty change in periportal zones G1 and G2 as compared to controls (G3). In G2, fatty change was more severe. The inflammatory infiltrate was scanty and no fibrosis was seen in any group. There was a significant increase of AST and triglycerides in G1 and G2 as compared to control group G3. The lucigenin-amplified luminescence (cpm/mg/min × 10³) was significantly increased in G1 (1393±790) and G2 (7191±500) as compared to controls (513±170), p <0.05. The concentrations of CE-OOH were higher in G1 (5.7±0.9 nmol/mg protein) as compared to control (2.6±0.7 nmol/mg protein), p <0.05. Conclusion: 1) Oxidative stress was found to be increased in experimental liver steatosis; 2) The production of reactive oxygen species was accentuated when liver steatosis was more severe; 3) The alterations produced by oxidative stress could be an important step in the pathogenesis of nonalcoholic fatty liver disease.     

富硒大豆多肽对高脂致大鼠脂肪肝和抗氧化功能的影响

目的：探讨富硒大豆多肽改善高脂所致脂肪肝大鼠肝抗氧化功能的影响及机制。方法：将40只Wistar大鼠分成4组（n=10）,分别饲喂标准饲料＋水（NC）、标准饲料＋富硒大豆多肽液（SeN）、高脂饲料＋水（HC）、高脂饲料＋富硒大豆多肽液（SeH）,10周后处死,用苏丹Ⅲ染色肝脏组织切片观察脂肪变性程度,免疫组织化学方法测定肝组织葡萄糖调节蛋白78（GRP78）表达情况,并分析其肝功能、血脂及血清和肝匀浆中谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量的变化情况。结果：HC组在血清TC、TG水平、肝脏脂肪化程度、GRP78表达情况都明显高于NC、SeN、SeH组（P〈0.01）。SeH组血清和肝组织中MDA含量较HC组降低（P〈0.01）,GSH-Px、SOD活性升高。NC和SeN两组各项指标之间无明显差异。结论：富硒大豆多肽能有效提高脂肪肝大鼠肝内抗氧化酶活性,抑制脂质过氧化反应,降低肝组织内GRP78表达。