Myrica nagi Attenuates Cumene Hydroperoxide‐Induced Cutaneous Oxidative Stress and Toxicity in Swiss Albino Mice

In recent years, considerable efforts have been made to identify new chemopreventive agents which could be useful for man. Myrica nagi, a subtropical shrub, has been shown to possess significant activity against hepatotoxicity and other pharmacological and physiological disorders. We have shown a chemopreventive effect of Myrica nagi on cumene hydroperoxide‐induced cutaneous oxidative stress and toxicity in mice. Cumene hydroperoxide treatment at a dose level of 30 mg/animal/0.2 ml acetone enhances susceptibility of cutaneous microsomal membrane for iron‐ascorbate‐induced lipid peroxidation and induction of xanthine oxidase activity which are accompanied by decrease in the activities of cutaneous antioxidant enzymes such as catalase, glutathione peroxidase, glutathione reductase, glucose‐6‐phosphate dehydrogenase and depletion in the level of cutaneous glutathione. Parallel to these changes a sharp decrease in the activities of phase II metabolizing enzymes such as glutathione S‐transferase and quinone reductase has been observed. Application of Myrica nagi at doses of 2.0 mg and 4.0 mg/kg body weight in acetone prior to that of cumene hydroperoxide (30 mg/animal/0.2 ml acetone) treatment resulted in significant inhibition of cumene hydroperoxide‐induced cutaneous oxidative stress and toxicity in a dose‐dependent manner. Enhanced susceptibility of cutaneous microsomal membrane for lipid peroxidation induced by iron ascorbate and xanthine oxidase activities were significantly reduced (P<0.05). In addition the depleted level of glutathione, the inhibited activities of antioxidants, and phase II metabolizing enzymes were recovered to a significant level (P<0.05). The protective effect of Myrica nagi was dose‐dependent. In summary our data suggest that Myrica nagi is an effective chemopreventive agent in skin and capable of ameliorating cumene hydroperoxide‐induced cutaneous oxidative stress and toxicity.     

Puerarin Attenuates Carbon Tetrachloride‐Induced Liver Oxidative Stress and Hyperlipidaemia in Mouse by JNK/c‐Jun/CYP7A1 Pathway

Puerarin (PU), a natural flavonoid, has been reported to have many benefits and medicinal properties. The aim of this study was to investigate the effects of puerarin on hepatic oxidative stress and hyperlipidaemia in mice exposed to carbon tetrachloride (CCl₄). Male ICR mice were injected with CCl₄ with or without puerarin co‐administration (200 and 400 mg/kg intragastrically once‐daily) for 8 weeks. Our data showed that puerarin significantly prevented CCl₄‐induced hepatotoxicity, indicated by both diagnostic indicators of the liver damage (serum aminotransferase levels) and histopathological analysis. Puerarin decreased the thiobarbituric acid reactive substances (TBARS) and the protein carbonyl content (PCO) in the liver of CCl₄‐treated mice. Puerarin also restored the levels of reduced glutathione (GSH) and total antioxidant capacity (TAC) in the liver. Furthermore, the increase in serum cholesterol, triglycerides and low‐density lipoproteins (LDL) induced by CCl₄ was effectively suppressed by puerarin. The high‐density lipoprotein (HDL) level in the CCl₄ treatment mice was also increased by puerarin. Western blot analysis showed that puerarin remarkably inhibited hyperlipidaemia by regulating the expression of phosphorylated Jun N‐terminal kinases (JNK), phosphorylated c‐Jun protein and cholesterol 7a‐hydroxylase (CYP7A1) in the liver of CCl₄‐treated mice. Altogether, these results suggest that puerarin could protect the CCl₄‐induced liver injury and hyperlipidaemia by reducing reactive oxygen species S production, renewing the total antioxidant capacity and influencing expression of hepatic lipid biosynthesis and metabolism genes.     

Melatonin Protects Against Mercury(II)‐Induced Oxidative Tissue Damage in Rats

Abstract: Mercury exerts a variety of toxic effects in the body. Lipid peroxidation, DNA damage and depletion of reduced glutathione by Hg(II) suggest an oxidative stress‐like mechanism for Hg(II) toxicity. Melatonin, the main secretory product of the pineal gland, was recently found to be a potent free radical scavenger and antioxidant. N‐Acetylcysteine, a precursor of reduced glutathione and an antioxidant, is used in the therapy of acute heavy metal poisoning. In this study the protective effects of melatonin in comparison to that of N‐acetylcysteine against Hg‐induced oxidative damage in the kidney, liver, lung and brain tissues were investigated. Wistar albino rats of either sex (200–250 g) were divided into six groups, each consisting of 8 animals. Rats were intraperitoneally injected with 1) 0.9% NaCl, control (C) group; 2) a single dose of 5 mg/kg mercuric chloride (HgCl₂), Hg group; 3) melatonin in a dose of 10 mg/kg, 1 hr after HgCl₂ injection, Hg‐melatonin group; 4) melatonin in a dose of 10 mg/kg one day before and 1 hr after HgCl₂ injection, melatonin‐Hg‐melatonin group; 5) N‐acetylcysteine in a dose of 150 mg/kg, 1 hr after HgCl₂ injection, Hg‐N‐acetylcysteine group, and 6) N‐acetylcysteine in a dose of 150 mg/kg one day before and 1 hr after HgCl₂ injection, N‐acetylcysteine‐Hg‐N‐acetylcysteine group. Animals were killed by decapitation 24 hr after the injection of HgCl₂. Tissue samples were taken for determination of malondialdehyde, an end‐product of lipid peroxidation; glutathione (GSH), a key antioxidant, and myeloperoxidase activity, an index of neutrophil infiltration. The results revealed that HgCl₂ induced oxidative tissue damage, as evidenced by increases in malondialdehyde levels. Myeloperoxidase activity was also increased, and GSH levels were decreased in the liver, kidney and the lungs. All of these effects were reversed by melatonin or N‐acetylcysteine treatment. Since melatonin or N‐acetylcysteine administration reversed these responses, it seems likely that melatonin or N‐acetylcysteine can protect all these tissues against HgCl₂‐induced oxidative damage.     

维生素C对顺铂所致大鼠肾损伤的保护作用

目的研究维生素C（Vit C）对顺铂所致肾损伤的保护作用,并探讨其可能的机制。方法将40只成年雌性SD大鼠按体重分成5组,分别为正常对照组（A组,生理盐水）、Vit C对照组（B组,500mg／kg）、顺铂化疗模型组（C组,6mg／kg）、顺铂（6mg／kg）＋Vit C（50mg／kg或500mg／kg）干预组（D1组及D2组）。腹腔注射Vit C进行前、中、后期全程保护,并于顺铂给药5d后采血处死动物,测定血清尿素氮（BUN）、肌酐（Cr）、肾皮质匀浆丙二醛（MDA）含量及谷胱甘肽过氧化物酶（GSH—Px）、超氧化物歧化酶（SOD）活力的变化。结果与C组相比,D1组及D2组的血清Cr及BUN、肾皮质匀浆MDA含量明显下降（P〈0．01或P〈0．05）,GSH—Px和SOD活力略有增加。结论Vit C可以减轻顺铂所致肾损伤,作用机制可能与其抗氧化作用和清除自由基活性密切相关。     

褪黑激素对精神分裂症小鼠行为及氧化应激的影响

目的探讨褪黑激素对精神分裂症小鼠行为及氧化应激的影响。方法制备小鼠精神分裂症模型,第15天开始,利培酮组小鼠灌胃给予利培酮(0.025 mg/kg),褪黑素组小鼠灌胃给予褪黑素(5 mg/kg),对照组和模型组小鼠灌胃给予等量生理盐水,连续14 d后测定相关指标。结果与对照组比较,其他3组小鼠社会交往时间和穿越平台次数减少,跨格总数和逃避潜伏期增加,脑组织中丙二醛(MDA)和一氧化氮(NO)含量显著升高,谷胱甘肽(GSH)含量显著降低(P<0.05);与模型组比较,利培酮组和褪黑素组小鼠社会交往时间和穿越平台次数增加,跨格总数和逃避潜伏期降低,脑组织中MDA和NO含量显著降低,GSH含量显著增加(P<0.05);利培酮组和褪黑素组小鼠各指标的差异不显著(P>0.05)。结论褪黑激素能减轻精神分裂症模型小鼠的行为异常症状,可阻断大脑氧化应激反应。     

血根碱对脂多糖致H9c2细胞氧化损伤的改善作用

目的 观察血根碱（sanguinarine,SAN）对脂多糖（lipopolysaccharide,LPS）诱导的H9c2细胞氧化应激的影响,并对其与HO-1/NOX2途径之间的关系进行探讨。方法 不同因素干预H9c2细胞后,采用细胞活性试剂盒检测不同浓度SAN和/或LPS对H9c2细胞生存的影响;酶标仪及荧光显微镜检测SAN对LPS诱导细胞产生活性氧（reactive oxygen species,ROS）的影响; Real time RT-PCR检测SAN对LPS诱导的NOX2、P47PHOX、HO-1、SOD1、SOD2基因表达的影响; MDA检测试剂盒检测MDA的变化。结果 单用SAN对H9c2细胞活性无影响,LPS可显著降低细胞活性,而SAN与LPS共同干预则可呈浓度依赖性地提高细胞活性,降低ROS产生。LPS处理12 h上调H9c2细胞NOX2、p47phox mRNA表达、下调HO-1 mRNA表达; SAN预处理后,细胞内NOX2、p47phox mRNA下调、HO-1 mRNA上调,而SAN与锌原卟啉IX预处理则可逆转这种现象。SAN上调SOD1及SOD2 mRNA表达,降低MDA产生。结论 SAN可通过活化HO-1/NOX2途径,抑制ROS的产生,从而使H9c2细胞免受LPS介导的损伤,提高细胞活力。     

Clonidine Attenuates Naloxone‐Induced Opioid‐Withdrawal Syndrome in Cholestatic Mice*

Abstract: Cholestasis is associated with elevated plasma level of endogenous opioid peptides. Naloxone‐precipitated withdrawal syndrome has been described in a mouse model of acute cholestasis. Thus we aimed at determining whether central noradrenergic hyperactivity is involved in manifestation of naloxone‐precipitated withdrawal syndrome in mice with obstructive cholestasis. Acute cholestasis was induced by bile duct resection in mice and physical dependence was observed by precipitating a withdrawal syndrome with naloxone (2 mg/kg, intraperitoneally) 5 days after induction of cholestasis. Administration of clonidine (0.1 mg/kg, intraperitoneally), an α₂‐adrenoceptor agonist, 15 min. before naloxone injection significantly alleviates withdrawal severity in cholestatic mice. However, pretreatment of animals with yohimbine (3 mg/kg, intraperitoneally), an α₂‐adrenoceptor antagonist, 15 min. before clonidine blocked this ameliorative effect of clonidine. The results of this study support the evidence for involvement of the α₂‐adrenoceptors in the withdrawal syndrome of cholestasis in a mouse model.     

Procyanidins Produce Significant Attenuation of Doxorubicin‐Induced Cardiotoxicity via Suppression of Oxidative Stress

Abstract: Doxorubicin is widely prescribed in the chemotherapy of haematological malignancies and solid tumours. The major side effect of doxorubicin is oxidative injury‐related cardiotoxicity, which has dramatically hindered its usage. Procyanidins from grape seeds are potent free radical scavengers that have been shown to protect against anthracycline‐induced cardiotoxicity. In the present study, we tested whether procyanidins would prevent the doxorubicin‐induced cardiotoxicity in rats. Rats were intraperitoneally treated with doxorubicin at a cumulative dose of 15 mg/kg with and without pre‐administration of procyanidins. Our data showed that doxorubicin led to cardiac function deterioration, myocardial injury and increased oxidative stress in cardiac tissues. The cardiac function deterioration by doxorubicin included increased QT‐interval and ST‐interval in electrocardiograph (ECG) and decreased left ventricular developed pressure. Doxorubicin‐induced myocardial injury was shown by the increased creatine kinase, alanine aminotransferase and aspartate aminotransferase in serum as well as in myocardial lesions. Pretreatment with procyanidin (150 mg/kg daily) effectively hindered the adverse effects of doxorubicin, such as myocardial injury and impaired heart function. Procyanidin pretreatment attenuated cytoplasmic vacuolization, increased left ventricular developed pressure and improved the ECG. The cardioprotective effect of procyanidin corresponded to the decrease of lipid peroxidation and the increase of cardiac antioxidant potency in doxorubicin‐treated rats that were also given procyanidin. An in vitro cytotoxic study showed that procyanidins did not attenuate the antineoplastic activity of doxorubicin to A549 adenocarcinoma cells. All the above lines of evidence suggest that procyanidins protect cardiomyocytes from doxorubicin‐induced cardiotoxicity via suppression of oxidative stress.     

维生素C保护糖尿病大鼠主动脉的作用机制

目的：观察维生素C对糖尿病大鼠血脂和主动脉纤维连接蛋白（FN）表达的影响。方法：利用链脲佐菌素腹腔注射法诱导建立1型糖尿病大鼠模型，将用实验SD大鼠随机分正常对照组、造模组（包括糖尿病组和维生素C治疗组）。治疗16周，观察治疗期间及治疗后大鼠的一般状况、血糖（BG）、三酰甘油（TG）、胆固醇（TC）、低密度脂蛋白（LDL）、高密度脂蛋白（HDL）、糖化血红蛋白（HbA1c）和糖化低密度脂蛋白（G-LDL）。大鼠麻醉处死，分离主动脉，HE染色及免疫组织化学检测主动脉内膜FN表达。结果：造模组大鼠均出现血脂异常及主动脉病理形态改变。维生素C对血糖无影响，但能降低糖尿病大鼠的三酰甘油、胆固醇、LDL、HbA1c、G—LDL，升高HDL，且能降低主动脉纤维连接蛋白表达。结论：维生素C无降糖作用，但可通过调节血脂，抑制主动脉纤维连接蛋白表达对糖尿病大鼠主动脉起到保护作用。     

3‐Keto‐1,5‐bisphosphonates Alleviate Serum‐Oxidative Stress in the High‐fat Diet Induced Obesity in Rats

Obesity has become a leading global health problem owing to its strong association with a high incidence of oxidative stress. Many epidemiologic studies showed that an antioxidant supplementation decreases the state of oxidative stress. In the present work, a HFD ‐induced rat obesity and oxidative stress were used to investigate the link between fat deposition and serum‐oxidative stress markers. We also studied the effect of a chronic administration of 3‐keto‐1,5‐bisphosphonates 1 (a & b) (40 μg/kg/8 weeks/i.p.). Exposure of rats to HFD during 16 weeks induced fat deposition, weight gain and metabolic disruption characterized by an increase in cholesterol, triglyceride and glycemia levels, and a decrease in ionizable calcium and free iron concentrations. HFD also induced serum‐oxidative stress status vocalized by an increase in ROS ( H ₂ O ₂ ), MDA and PC levels, with a decrease in antioxidant enzyme activity ( CAT , GP x , SOD ). Importantly, 3‐keto‐1,5‐bisphosphonates corrected all the deleterious effects of HFD treatment in vivo, but it failed to inhibit lipases in vitro and in vivo. These studies suggest that 3‐keto‐1,5‐bisphosphonates 1 could be considered as safe antioxidant agents that should also find other potential biological applications.     

In Vitro Anti-oxidant Effect of Vitamin E on Oxidative Stress Induced due to Pesticides in Rat Erythrocytes

An attempt was made to study the antioxidant property of vitamin E in endosulfan and chlorpyrifos toxicity. Erythrocytes were collected from healthy rats and exposed to 1 ppm endosulfan and chlorpyrifos pesticides individually and also along with vitamin E treatment. Results showed that endosulfan was more toxic in comparison of chlorpyrifos. Activities of superoxide dismutase and catalase were significantly decreased, while lipid peroxidation and glutathione-S-transfarase were increased in comparison to the control values. The results of the present study suggest that vitamin E acts as an effective antioxidant for endosulfan and chlorpyrifos pesticide toxicity, in reducing oxidative stress burden.     

褪黑素对实验性糖尿病肾脏氧化应激的影响

［摘要］目的观察褪黑素对糖尿病大鼠肾脏氧化应激和过氧亚硝基阴离子（ONOO–）特异性标志物硝基酪氨酸（NT）表达的影响。方法实验动物分为糖尿病肾病组（DN组）、糖尿病褪黑素处理组（DM组）、正常对照组（NC组），8周后比较各组体重、血糖、血胆固醇、三酰甘油及肾脏丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH Px）含量，免疫组化观察各组大鼠肾组织中NT的表达。结果和DN组比较，DM组大鼠血胆固醇、三酰甘油及肾脏MDA水平显著降低（P＜0.05），抗氧化酶SOD、GSH Px活性升高（P＜0.05），NT表达明显降低。结论褪黑素可显著提高糖尿病大鼠肾脏的抗氧化能力和降低氧化应激，对糖尿病大鼠肾脏具有保护作用。     

The Polyphenol Chlorogenic Acid Attenuates UVB-mediated Oxidative Stress in Human HaCaT Keratinocytes

We investigated the protective effects of chlorogenic acid (CGA), a polyphenol compound, on oxidative damage induced by UVB exposure on human HaCaT cells. In a cell-free system, CGA scavenged 1,1-diphenyl-2-picrylhydrazyl radicals, superoxide anions, hydroxyl radicals, and intracellular reactive oxygen species (ROS) generated by hydrogen peroxide and ultraviolet B (UVB). Furthermore, CGA absorbed electromagnetic radiation in the UVB range (280–320 nm). UVB exposure resulted in damage to cellular DNA, as demonstrated in a comet assay; pre-treatment of cells with CGA prior to UVB irradiation prevented DNA damage and increased cell viability. Furthermore, CGA pre-treatment prevented or ameliorated apoptosis-related changes in UVB-exposed cells, including the formation of apoptotic bodies, disruption of mitochondrial membrane potential, and alterations in the levels of the apoptosis-related proteins Bcl-2, Bax, and caspase-3. Our findings suggest that CGA protects cells from oxidative stress induced by UVB radiation.     

Epigallocatechin‐3‐Gallate Attenuates Oxidative Stress and Inflammation in Obstructive Nephropathy via NF‐κB and Nrf2/HO‐1 Signalling Pathway Regulation

Oxidative stress and inflammation contribute importantly to the pathogenesis of chronic kidney disease (CKD). Epigallocatechin‐3‐gallate (EGCG), which is the most abundant and most active catechin polyphenol extracted from green tea, has been proved to have many bioactivities. In this study, the renoprotective effect of EGCG was evaluated in a widely used kidney disease model, the unilateral ureteral obstruction (UUO) mice model. After 14 days of EGCG administration, mean arterial blood pressure, body‐weight and obstructed kidney weight were measured. Levels of blood urea nitrogen (BUN) and creatinine (CR) and activities of glutamic–pyruvic transaminase (GPT) and lactate dehydrogenase (LDH) in serum were estimated as indicators of renal function. Periodic acid–Schiff (PAS) staining was performed to observe the pathological changes of the obstructed kidney. Antioxidant enzymes and pro‐inflammatory cytokine production were estimated to reflect the oxidative stress and inflammatory state in the obstructed kidney. Finally, the main proteins in the NF‐κB and Nrf2 signalling pathway and DNA binding activity of NF‐κB and Nrf2 were measured to investigate the effect of EGCG on these two pathways. The results demonstrated that EGCG could restore UUO‐induced kidney weight loss and renal dysfunction. In addition, UUO‐induced oxidative stress and inflammatory responses in the obstructed kidney were also prevented by EGCG. Furthermore, EGCG could induce both NF‐κB and Nrf2 nuclear translocation in the UUO kidney and promote heme oxygenase‐1 (HO‐1) production. These results indicated that the renoprotective effect of EGCG might be through its NF‐κB and Nrf2 signalling pathway regulations.     

Alcohol‐related mortality in Ukraine

Introduction and Aims. To substantiate public health policies aimed at diminishing alcohol‐related harm, the level of alcohol‐related deaths needs to be documented on a national level. The aim of this study was to explore the opportunities provided by the 1985–1988 anti‐alcohol campaign related data for estimation of alcohol‐related mortality in Ukraine. Design and Methods. Ecological study design based on the aggregate‐level data analysis regarding the natural experiment in Ukraine. All‐cause and cause‐specific observed mortality levels in 1986‐88 compared to the extrapolated 1980–84 trends. The number and proportion of ‘prevented’ deaths were calculated for those causes, for which were observed: (1) reduction of mortality levels during the campaign and (2) increase after 1988. Alcohol‐attributable fractions of mortality per one litre of per capita consumption were calculated for each death cause based on prevented deaths and consumption decrease estimates. The total number of alcohol‐related deaths for a specific year was also calculated. Results. Ukraine experienced a large mortality reduction during the campaign. The estimates of prevented deaths revealed that at least 76% of the mortality reduction was attributable to alcohol. Alcohol‐related mortality due to injuries is much higher for men, while coronary heart disease (CHD) alcohol‐attributable fractions were about 0.5 in middle age both for men and women. Discussion and Conclusions. While in Western countries alcohol is considered as a protective factor for CHD, in Ukraine alcohol‐related cardiovascular mortality is rather high. In 2004 in Ukraine total number of alcohol‐related deaths was about 119,000 or 251 per 100,000 of population.[Krasovsky K. Alcohol‐related mortality in Ukraine. Drug Alcohol Rev 2009;28:396–405]     

Curcumin Attenuates Diet‐Induced Hepatic Steatosis by Activating AMP‐Activated Protein Kinase

Curcumin is a well‐known component of traditional turmeric (Curcuma longa), which has been reported to prevent obesity and diabetes. However, the effect of curcumin on hepatic lipid metabolism remains unclear. The aim of this study was to examine the effects of curcumin on hepatic steatosis in high‐fat/cholesterol diet (HFD)‐induced obese mice. Male C57BL/6J mice were fed a normal diet (ND), HFD or HFD with 0.15% curcumin (HFD+C) for 11 weeks. We found that curcumin significantly lowered the body‐weight and adipose tissue weight of mice in the HFD+C group compared with the findings for the HFD group (p < 0.05). The levels of total cholesterol, fasting glucose and insulin in serum were decreased, and HFD‐induced impairment of insulin sensitivity was improved by curcumin supplementation (p < 0.05). Curcumin protected against the development of hepatic steatosis by reducing hepatic fat accumulation. Moreover, curcumin activated AMP‐activated protein kinase (AMPK) and elevated the gene expression of peroxisome proliferator‐activated receptor alpha. By contrast, curcumin suppressed the HFD‐mediated increases in sterol regulatory element‐binding protein‐1, acetyl‐CoA carboxylase 1, fatty acid synthase and cluster of differentiation 36 expression. Taken together, these findings indicate that curcumin attenuates HFD‐induced hepatic steatosis by regulating hepatic lipid metabolism via AMPK activation, suggesting its use as a therapeutic for hepatic steatosis.     

Role of Oxidative Stress in Reproductive Toxicity Induced by Co‐administration of Chloramphenicol and Multivitamin–Haematinics Complex in Rats

Abstract: Concurrent administration of chloramphenicol (CAP) with multivitamin–haematinics complex (MHC) is a common practice to cushioning anticipated anaemic effect of CAP in most developing countries. This study investigated the mechanism involved in CAP‐induced reproductive toxicity as well as the effects of its co‐administration with MHC in male rats. CAP and MHC were administered orally at therapeutic doses of 28 mg/kg body‐weight and 0.08 ml/kg body‐weight, respectively, every 6 hr for 10 days. After exposure, while there was body‐weight loss in CAP, MHC and CAP plus MHC‐treated animals, there were no treatment‐related changes in the absolute and relative weights of the testes in all treated groups. Alone, MHC treatment markedly decreased catalase (CAT), glutathione S‐transferase (GST), and 5′ nucleotidase (5′ NTD) activities whereas it resulted in significant increase in superoxide dismutase (SOD) activity. Activities of SOD, CAT and GST as well as H₂O₂ levels were not significantly affected in CAP and CAP plus MHC‐treated rats whereas GSH level and 5′ NTD activity were markedly decreased in CAP plus MHC‐treated rats. Significant increase in testicular alkaline phosphatase activity, lipid peroxidation and sperm abnormalities were accompanied by reduction in epididymal sperm number, sperm motility and live–dead ratio in all treatment groups whereas aminotransferase activities were unaffected. Treatment‐related degeneration of the testes was evident in all treated animals. In summary, while MHC‐induced testicular toxicity via oxidative stress, CAP did not and their combination is implicated in reproductive dysfunction within the time course of our investigation.     

灵芝多糖对糖尿病大鼠胸主动脉氧化应激的影响

目的：研究灵芝多糖对链脲佐菌素（STZ）诱导的糖尿病大鼠胸主动脉内皮损伤的保护作用及对糖尿病大鼠胸主动脉氧化应激的影响。方法：SD 大鼠经过4周高脂饮食后腹腔注射链脲佐菌素（30 mg·kg-1）造模,随机分为正常对照组、模型组、灵芝多糖（GLPs）高、低剂量组。经过12周给药治疗后,测定血清中过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-PX）、总胆固醇（TC）和甘油三酯（TG）的水平;然后胸主动脉切片 HE 染色,观察胸主动脉超微结构及病理改变。结果：GLPs-H 组血糖浓度较模型组相比均明显下降（P<0.01）,血清 CAT 和 GSH-PX 水平较模型组相比均明显上升（P<0.01）;血清 TC、TG 含量较模型组相比均明显下降（P<0.01）。 HE 染色,与模型组相比,GLPs-H 组光镜下主动脉内膜增厚、内皮损伤、中膜增厚的情况有所改善。结论：灵芝多糖可减轻糖尿病大鼠体内氧化应激水平,具有减轻脂质过氧化作用,对糖尿病胸主动脉并发症的发生发展有一定的预防作用。