益生菌联合白藜芦醇对小鼠慢性酒精性肝损伤的改善作用及机制研究

利用C57BL/6J小鼠构建慢性酒精性肝损伤模型,探究益生菌联合白藜芦醇对慢性酒精性肝损伤的保护作用及可能机制。小鼠被随机分为空白对照组（Con组)和酒精模型组(Mod组）,三组益生菌分别联合白藜芦醇（Resveratrol,Res）干预组（Lactobacillus paracasei J5+Res（J5+Res）、Lactobacillus casei YRL577+Res（YRL577+Res）、Bifidobacterium animalis F1-7+Res（F1-7+Res））和阳性药物硫普罗宁组（LP组）。实验结束后,通过分析小鼠肝脏脂质含量、酒精代谢酶活性、氧化应激水平等指标,对益生菌联合白藜芦醇的作用效果进行评价。为了进一步探究联合作用机制,对肝脏中氧化应激相关基因CYP2E1、核因子 E2 相关因子 2（Nuclear factor erythroid-2-related factor 2, Nrf2）、血红素加氧酶1（Heme oxygenase-1,HO-1）的mRNA表达进行分析。结果表明,相较于Mod组,益生菌联合白藜芦醇能够显著降低小鼠肝脏中甘油三脂、总胆固醇含量、血清谷草转氨酶和谷丙转氨酶活力（P<0.05）,提高肝脏乙醇脱氢酶、乙醛脱氢酶活性并抑制肝脏CYP2E1活性及其mRNA表达,显著提高肝脏还原型谷胱甘肽含量和超氧化物歧化酶、过氧化氢酶活性（P<0.05）,并能有效激活Nrf2/HO-1通路,其中,Nrf2 mRNA表达量在J5+Res、YRL577+Res、F1-7+Res三组益生菌联合干预组中分别被上调了2.6、3.7和2.7倍,HO-1 mRNA表达量被上调了2.0、6.2和4.0倍。因此,益生菌联合白藜芦醇可能通过激活Nrf2/HO-1途径预防慢性酒精性肝损伤。     

Prevention of ethanol-induced hepatotoxicity by fermented Curcuma longa L. in C57BL/6 mice

The protective effect of fermented Curcuma longa L. (FC) was investigated in male C57BL/6 mice under ethanol-induced oxidative stress. Ethanol markedly elevated levels of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in mice. However, mice receiving FC prior to ethanol treatment did not display hepatotoxicity as evidenced by the significant reductions of AST and ALT activities. When compared to the ethanol-alone treated group, FC group exhibited a significant decrease in cytochrome P-450 2E1 (CYP2E1) activity, an enzyme associated with oxidative stress. Indicators of the hepatic antioxidant defense system, such as levels of superoxide dismutase, catalase, glutathione reductase and glutathione were also increased in FC-pretreated mice. The amelioration of malondialdehyde was indicative of the protective effect of FC against liver damage mediated by ethanol. These results suggest that FC could be a candidate used for the prevention against alcoholic liver diseases by the alleviation of oxidative stress via suppressing CYP2E1.     

Vitamin E protects developing rat hippocampus and cerebellum against ethanol-induced oxidative stress and apoptosis

It has been suggested that developmental alcohol-induced brain damage is mediated through increases in oxidative stress. Current research suggests that antioxidant therapy may afford some level of protection against the toxicity of alcohol and alcoholic beverage in cellular and genomic levels. Seven day pregnant wistar rats were randomly divided into three groups: control, ethanol and vitamin E treated alcoholic groups. Apoptosis, lipid peroxidation and protein oxidation amounts, as well as, catalase and superoxide dismutase (SOD) activities were compared in male offspring hippocampus and cerebellum in the end of lactation. Offspring from ethanol-exposed animals showed significant increase in apoptosis, protein carbonyl and lipid hydroperoxide (LPO) in hippocampus and cerebellum than controls. Vitamin E treatment significantly decreased apoptosis in ethanol group and restored the increased protein carbonyl and LPO contents and catalase activity to the level of controls. Our findings strongly support oxidative nature of alcohol-induced cellular stress in developing hippocampus and cerebellum, prove that oxidative stress induced cell apoptosis plays a crucial role in pathogenic consequences, and imply that a strong protective effect could be achieved using vitamin E as an antioxidant.     

Quercetin attenuates ethanol-derived microsomal oxidative stress: Implication of haem oxygenase-1 induction

As the main source of reactive oxygen species (ROS), hepatic microsomes are susceptible to ROS attack, especially upon CYP2E1 activation by ethanol. The objective of this study was to evaluate the hepatoprotective effect of quercetin, by inducing haem oxygenase-1 (HO-1), on ethanol-induced microsomal oxidative stress. Chronic alcohol administration to adult rats (4.0 g/kg for 90 days) resulted in microsomal redox disturbance and liver dysfunction, accompanying CYP2E1 upregulation and HO-1 downregulation of both protein expression and enzymatic activity. Quercetin (100 mg/kg) induced HO-1, which was not completely suppressed by ethanol. Moreover, quercetin pretreatment to ethanol-fed rats lowered CYP2E1 induction, partially normalised ethanol-overwhelmed microsomal antioxidative system, decreased ROS level and lipid peroxidation, and alleviated the leakage of transaminases. Given the beneficial effect of HO-1, its induction by quercetin may contribute to the protective role against CYP2E1-mediated oxidative stress on hepatic microsomes.     

菊苣醇提物对对乙酰氨基酚诱导小鼠肝损伤的保护作用

目的研究菊苣醇提物对对乙酰氨基酚(acetaminophen,APAP)诱导的小鼠肝损伤的保护作用。方法将56只昆明小鼠随机分为7组:分别是阴性对照组,APAP模型组,水飞蓟宾阳性对照组,菊苣醇提物单独给药组(200 mg/kg体重),菊苣醇提物低、中和高剂量(50、100和200 mg/kg体重)与APAP联用组。各剂量组小鼠灌胃给予对应药物连续7 d后,一次性腹腔注射APAP(300 mg/kg体重)构建肝损伤模型,24 h后采集肝组织样品和血清。分别测定肝组织和血清的多种氧化指标以及细胞色素P450 2E1酶(CYP2E1)的蛋白表达水平。结果菊苣醇提物能够显著降低血清中谷丙转氨酶(alanine aminotransferase,ALT)和谷草转氨酶(aspartate aminotransferase,AST)水平。降低肝组织中过氧化氢(hydrogen peroxide,H2O2)和谷胱甘肽(glutathione,GSH)的含量以及提高抗氧化酶系中过氧化氢酶(catalase,CAT)和总超氧化物歧化酶(total superoxide dismutase,T-SOD)活性;同时,体外抗氧化实验亦表明其具有良好的清除自由基的能力。另外,菊苣醇提物还能够显著抑制CYP2E1的蛋白表达。结论菊苣醇提物有助于维持小鼠体内酶防御系统功能,提高机体清除自由基的能力,并通过减少CYP2E1的蛋白表达对APAP所致小鼠肝损伤具有明显保护作用。     

Antialcoholic liver activity of whey fermented by Lactobacillus casei isolated from koumiss

Whey fermented liquid (WFL) was studied for its hepatoprotective effects by using chronic alcohol-induced mice. Whey fermented liquid, prepared by inoculating whey with 4% (vol/vol) Lactobacillus casei and then incubating at 41°C for 8 h, was used to orally treat alcohol-induced mice at 3 dosages for 5 wk. Ethanol consumption significantly reduced the activity of superoxide dismutase and glutathione peroxidase, while lowering glutathione content and increasing levels of aspartate aminotransferase, alanine aminotransferase, total triglyceride, malondialdehyde, and cytochrome P450 2E1. Treatment with WFL significantly attenuated the increased levels of alanine aminotransferase, aspartate aminotransferase, triglyceride, and cytochrome P450 2E1, while decreasing superoxide dismutase, glutathione peroxidase, malondialdehyde, and glutathione levels. Pathological changes in the livers of mice who had ingested alcohol were improved by the administration of WFL. These results suggest that WFL may exert a protective effect against alcoholic liver disease by increasing antioxidant activity, which supports the use of WFL as an antialcoholic liver disease treatment.     

Hepatoprotection using sweet orange peel and its bioactive compound,hesperidin, for CCl4-induced liver injury in vivo

The hepatoprotective effect of water extracts of sweet orange (Citrus sinensis) peel (WESP) and its biological compound, hesperidin (HD), on oxidative stress in vivo, were investigated. HD was the major compounds among the ten compounds identified using HPLC-DAD and HPLC-MS/MS analysis. Oral administration of WESP to rats at 10 and 100 mg/kg bw for 28 consecutive days before a single dose of CCl₄ (2 ml/kg bw) demonstrates a significant protective effect by lowering the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and by improving the histological architecture of the rat liver. WESP attenuated oxidative stress by increasing the content of hepatic glutathione (GSH), and by a dramatic increase in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). WESP induced a significant CYP2E1 activity, which suggests that WESP may be a substrate of CYP2E1. WESP at a dose of 1.0 mg/kg bw and HD at 0.1 mg/kg bw did not sustain the protective effect against oxidative stress, in vivo. This study demonstrated that citrus peel protects rat liver from CCl₄-induced injury by attenuating hepatic oxidative stress, which suggests that WESP can be used as a therapeutic antihepatotoxic agent for the treatment of hepatic injury.     

Yerba-mate (Ilex paraguariensis) extract prevents ethanol-induced liver injury in rats

Ethanol metabolism-associated oxidative stress contributes to the pathogenesis of alcoholic liver disease. We examined the effect of a Mate tea extract on ethanol-induced liver injury in vitro and in vivo models. Isolated hepatocytes were incubated with ethanol. An extract of Yerba-Mate tea (EMT) was added to the cultures simultaneously with ethanol. EMT treatment suppressed the ethanol-induced increase in cell death by inhibiting cytochrome p450 2E1 (CYP2E1) activity, which is related to the production of reactive oxygen species. Furthermore, we examined the effects of EMT on serum transaminase activity, and the progression of liver fibrosis in rats treated with ethanol and CCl₄. Rats were fed a diet that included 0.005% or 0.02% EMT or no EMT. For a period of 3 weeks, the animals were provided drinking water containing 5% ethanol and were also treated with carbon tetrachloride (CCl₄) (0.1 ml/kg of body weight). EMT treatment suppressed plasma ALT and AST activities in the ethanol- and CCl₄-treated rats. EMT treatment also decreased CYP2E1 expression and increased ADH expression in the ethanol- and CCl₄-treated rats. EMT treatment fully protected the rats against ethanol- and CCl₄-induced liver injury. These results suggest that EMT may serve as a candidate for preventing ethanol-induced liver injury.     

Effects of Graptopetalum paraguayense consumption on serum lipid profiles and antioxidative status in hypercholesteremic subjects

BACKGROUND: Oxidative stress is known to be an important component of cellular damage regarding hypercholesterolemia and its complications. In vitro study had demonstrated that extracts of Graptopetalum paraguayense E. Walther exhibited strong antioxidative activities. This study was aimed at investigating the effect of G. paraguayense consumption on antioxidative status and serum lipid profiles in hypercholesterolemic subjects. RESULTS: Eighteen hypercholesterolemic subjects were instructed to consume 100 g G. paraguayense as a serving of vegetable daily for 8 consecutive weeks. After consumption, there were no changes in waist measurement, body mass index, body fat component, blood pressure, hepatic function (serum alanine aminotransferase activity), renal function (serum creatinine, uric acid) or fasting plasma glucose levels. Daily G. paraguayense consumption significantly increased ascorbic acid and α‐tocopherol levels and decreased malondialdehyde level in plasma. Furthermore, daily G. paraguayense consumption significantly increased glutathione levels, glutathione peroxidase and catalase activities in erythrocyte. However, there were no significant changes in serum total cholesterol, triglyceride, low‐density lipoprotein cholesterol or high‐density lipoprotein cholesterol after G. paraguayense consumption. CONCLUSION: The present study demonstrated that consumption of G. paraguayense may increase in vivo antioxidant activities and have some protective effects in decreasing oxidative stress in hypercholesterolemic subjects. Copyright © 2011 Society of Chemical Industry     

基于Nrf2/CYP2E1通路探讨刺梨多糖对酒精性肝损伤小鼠的保护机制

目的:探讨刺梨多糖（Rosa roxburghii polysaccharide,RP）对食用酒精诱导的酒精中毒小鼠肝脏的影响及保护机制。方法:采用热水浸提法制得纯度为64％的RP。将60只健康KM雄性小鼠分为空白组、模型组、阳性组、RP低、中、高剂量组,连续给药15d,于末次给药4h后,除空白组外,其余各组一次性灌胃16 mL/kg 50％的食用酒精建立酒精性肝损伤（alcoholic liver disease,ALD）小鼠模型;解剖后记录脏器质量,测定血清中谷草转氨酶（aspartate aminotransferase,AST）、谷丙转氨酶（alanine aminotransferase,ALT）、总胆固醇（total cholesterol,TC）、甘油三酯（triglyceride,TG）含量、测定肝脏氧化应激指标含量,核因子-红细胞2相关因子2（nuclear factor erythroid2-related factor 2,Nrf2）信号通路相关蛋白表达量及细胞色素P450 2E1（cytochrome P450 2E1,CYP2E1）蛋白表达量、并进行肝脏病理和肝细胞凋亡观察。结果:与模型组相比,RP各剂量组均能降低肝脏指数、血清中转氨酶AST、ALT,血脂指标TC、TG含量、肝脏丙二醛（Malonaldehyde,MDA）含量,提高谷胱甘肽（glutathione,GSH）、超氧化物歧化酶（superoxide dismutase,SOD）含量,上调Nrf2、血红素氧合酶1(heme oxygenase-1,HO-1)、超氧化物歧化酶1（superoxide dismutase-1,SOD-1）蛋白表达量,下调CYP2E1蛋白表达量,并改善肝脏病变和肝细胞凋亡情况。结论:RP对酒精性肝损伤小鼠起到良好的护肝效果,这可能与调控Nrf2信号通路起到抗氧化作用及调节脂质代谢有关。     

芦荟皮提取物对急性酒精性肝损伤的保护作用与机制

目的:研究芦荟皮提取物（Aloe bark extract,ABE）对急性酒精性肝损伤的保护效应与机制。方法:首先采用DPPH、ABTS和羟基自由基清除法对ABE的抗氧化活性进行检测;再利用不同浓度（5,10 μg/mL）的ABE分别处理酒精诱导HepG2细胞24 h,检测各组细胞天冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）活力和丙二醛（MDA）含量,采用RT-PCR检测其对Nrf2、SOD、ADH、IL-6和IL-1β基因表达的影响;以50%乙醇灌胃雄性C57BL/6J小鼠,造成急性酒精性肝损伤,建立体内动物模型,给予低、中、高剂量组（50、100、200 mg/kg）ABE干预,连续灌胃3 d,检测各组小鼠血清中AST、ALT活力含量,检测肝脏中MDA含量,通过H&E染色观察肝脏病理变化,利用RT-PCR检测肝组织中Nrf2、HO-1、SOD、CAT、ADH和ALDH基因的表达。结果:ABE具有显著的体外抗氧化活性,芦荟皮提取物的DPPH、ABTS和羟基自由基清除能力的IC₅₀值分别为2.03、0.131和0.74 mg/mL。在细胞模型和动物模型中,ABE高、中、低剂量组中细胞和小鼠血清中ALT和AST活性水平显著下降（P<0.05）,同时细胞和肝组织中MDA水平也显著降低（P<0.05）。H&E染色结果表明ABE能改善酒精引起的肝脏氧化应激和脂肪变性。分子机制的研究显示其主要通过直接调控酒精代谢相关酶、抗氧化酶和炎症反应起到保肝作用。结论:芦荟皮提取物能够显著缓解酒精引起的肝损伤,是一种潜在的治疗急性酒精性肝损伤的活性原料。     

Antioxidant activities of lotus leaves (Nelumbo nucifera) and barley leaves (Hordeum vulgare) extracts

This study evaluated the antioxidant activities of lotus leaf extracts by methanol (L/M) and ethanol (L/E), and barley leaf extracts, also by methanol (B/M), and ethanol (B/E). The 2,2-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity of L/M was higher than that of the other extracts at 250 ppm, with the exception of butylhydroxytoluene (BHT). The reducing powers of the treatments at 250 ppm were in the following order: BHT (2.91)>L/M (2.90)>L/E (2.26)>B/E (2.09)>B/M (2.01). In addition, L/M showed the highest concentration of total phenols, total flavonoids, and strongest superoxide dismutase (SOD)-like activity among the treatments. Thus, lotus and barley leaves extracted by methanol and ethanol that have antioxidant activities may be alternatives to synthetic antioxidants in the food industry.     

夏枯草水提物对吡唑-脂多糖诱导肝损伤的 保护作用

目的研究夏枯草水提物对吡唑-脂多糖诱导的小鼠肝脏损伤的保护作用。方法将42只小鼠随机分为6组:正常对照组、模型组、夏枯草水提物低、中、高剂量组以及阳性对照组。灌胃给予小鼠夏枯草水提物,同时采用腹腔注射吡唑-脂多糖造成小鼠肝损伤模型,检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)和肝组织过氧化氢(H2O2)、丙二醛(MDA)、过氧化氢酶(CAT)、总超氧化物歧化酶(T-SOD)和谷胱甘肽(GSH)的活性/含量以及细胞色素酶CYP2E1和CYP2A5的蛋白表达水平。结果吡唑-脂多糖能够引起提高CYP2E1和CYP2A5的蛋白表达以及肝脏氧化应激并造成肝损伤;夏枯草水提物能够显著降低CYP2E1和CYP2A5的蛋白表达,降低氧化产物H2O2和MDA的含量,以及提高抗氧化系统中CAT、T-SOD活性和GSH含量。结论研究表明夏枯草可能通过抑制CYP2E1和CYP2A5的蛋白表达降低吡唑-脂多糖诱导肝组织内的氧化应激,从而对吡唑-脂多糖引起的肝损伤起保护作用。     

酒精对人原代培养肝细胞的氧化损伤与CYP 2E1关系的研究

目的 研究急性酒精暴露下对人原代培养肝细胞中CYP 2E1依赖的毒性作用和氧化损伤。方法 分离培养人原代肝细胞，以25-100mmol/L乙醇作用于人原代肝细胞9h及100mmol／L乙醇作用于人原代肝细胞0～24h后，检测人原代肝细胞中CYP 2E1的含量，并研100mmol/L乙醇作用于人原代肝细胞0～24h后，天冬氨酸转胺酶(aspartate transaminase，AST)的释放量及肝细胞中谷胱甘肽(Glutathione，GSH)、丙二醛(Malonclialdehyde，MDA)的含量。结果 急性酒精暴露导致人原代肝细胞中CYP 2E1的释放增加，并呈明显的剂量效应和时间效应关系；在100mmol/L乙醇作用下，AST和MDA明显升高，在0～24h内呈明显的时间效应关系，而GSH含量在6h后明显降低。结论 100mmol／L乙醇急性暴露可导致人原代培养肝细胞明显的氧化损伤，这种损伤与CYP 2E1活性的变化直接相关。     

Aqueous Extract of Gynura Bicolor Attenuated Hepatic Steatosis,Glycative, Oxidative,and Inflammatory Injury Induced by Chronic Ethanol Consumption in Mice

Gynura bicolor leaf aqueous extract (GAE) is rich in phytochemicals including phenolic acids, flavonoids, carotenoids, and anthocyanins. Effects of GAE upon hepatic injury in mice with chronic ethanol intake were examined. Lieber–DeCarli liquid diet with ethanol was used to induce hepatic lipid accumulation, oxidative, glycative, and inflammatory injury. GAE at 0.25% or 0.5% was added in feeds, and supplied to mice consumed Lieber–DeCarli liquid diet with ethanol for 6 wk. Blood and liver were collected for analyses. Results showed that ethanol increased plasma and hepatic triglyceride and cholesterol content, and affected plasma levels of insulin, adiponectin, leptin, and ghrelin. GAE at both doses decreased lipid accumulation, and at high dose improved hormones abnormality. Histological data revealed that GAE supplement mitigated hepatic lipid deposit. Ethanol increased plasma N^ε‐(carboxyethymethyl)‐lysine and pentosidine levels. GAE at high doses lowered those glycative factors. Ethanol depleted glutathione content, increased CYP2E1 activity and reactive oxygen species production, and reduced the activity of glutathione peroxide, glutathione reductase and catalase in liver. GAE supplement at both doses reversed these alterations and attenuated hepatic oxidative stress. GAE supplement also at both doses decreased hepatic inflammatory cytokines release in ethanol treated mice. These findings support that leaves of G. bicolor is a functional food with liver protective activities against ethanol.     

Hepatoprotective effect of Handaeri-gomchi (Ligularia fischeri var. spiciformis Nakai) extract against chronic alcohol-induced liver damage in rats

Handaeri-gomchi (Ligularia fischeri var. spiciformis Nakai) (LF) is well known as a medicinal plant in Korea, especially to treat a variety of human disease including hepatic function failure. In this study, we examined the activity of LF extract against the liver injuries and oxidative stress by chronic alcohol in Spargue-Dawley rats. Severe liver damage caused by alcohol intake with increasing activity of hepatic markers was decreased in the group of rats fed LF extract. The results were confirmed through hematoxylin and eosin staining. Antioxidative capacity was decreased by alcohol but it was recovered by LF extract. Elevated indicators of oxidative stress by chronic alcohol were diminished in the group of LF extract. Furthermore, LF extracts increased antioxidative capacity and the activity of antioxidant enzymes. In conclusion, LF extract has a protective effect against chronic alcohol hepatotoxicity, suggesting it could be developed as a functional food or medicine for protection of liver disease.     

Protective effects of protein hydrolysate from marine microalgae Navicula incerta on ethanol-induced toxicity in HepG2/CYP2E1 cells

Ethanol is independently known to cause tissue damage through various mechanisms. This study was designed to evaluate the protective effect of marine microalgae, Navicula incerta protein enzymatic hydrolysates (NEHs) against ethanol-induced hepatotoxicity in HepG2 cells transfected with human CYP2E1. Induction of CYP2E1 by ethanol is one of the central pathways by which ethanol generates a state of oxidative stress in hepatocytes. When the alcohol-induced cells were treated with NEHs at various concentrations, there was a dose-dependent decrease of gamma-glutamyl transpeptidase (GGT) activity in the culture media and loss of cell viability. Among the NEHs constituents the hydrolysates which were obtained by papain (P-NEH), pronase-E (PR-NEH) and α-chymotrypsin (A-NEH) activity attenuated the ethanol cytotoxicity effectively, respectively. The activity appeared to be a GGT inhibitor. Therefore, the cytoprotective effects at alcohol-induced HepG2/CYP2E1 cells could be attributed to the inhibition of GGT activity by NEHs. This study suggests that NEHs have enough potential to be considered as highly active compounds against ethanol toxicity which leads NEHs to be significant nutraceuticals.     

核桃低聚肽对亚健康大鼠氧化应激和炎症反应的影响

目的:研究核桃低聚肽(walnut oligopeptides,WOPs)对亚健康大鼠的保护作用及其机制。方法:50只健康雄性SD大鼠随机分成5组:正常对照组、模型对照组和3个核桃低聚肽干预组(剂量分别为220、440、880 mg/kg·bw)。模型对照组和3个核桃低聚肽剂量组大鼠连续睡眠剥夺5 d后,进行负重力竭游泳实验,记录力竭游泳时间,并测定大鼠血清生化指标、氧化应激和脂质过氧化指标及细胞因子水平。结果:与模型对照组相比,核桃低聚肽组大鼠力竭游泳时间明显延长,血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)水平显著降低,超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)活性显著升高(P<0.05或P<0.01)。结论:桃低聚肽可以防治亚健康状态对机体的伤害,其机制可能与提高机体抗氧化水平,降低炎症因子水平相关。     

忧遁草乙醇提取物对秀丽隐杆线虫的抗衰老作用及机制

目的：以秀丽隐杆线虫为模式生物,探究忧遁草乙醇提取物（Clinacanthus nutans ethanol extract,CNEE）对线虫的抗衰老作用及作用机制。方法：通过寿命、产卵、运动等实验检测忧遁草乙醇提取物对线虫抗衰老的作用;通过急性氧化应激、抗氧化酶活力测定、活性氧（ROS）测定、实时荧光定量PCR等实验初步探究忧遁草乙醇提取物的抗氧化能力及延缓衰老的作用机制。结果：忧遁草乙醇提取物在100μg/mL时能延长N2野生型线虫寿命（P<0.001）,对其运动能力也有促进作用（P<0.001）,同时对产卵能力没有毒性影响（P>0.05）;该提取物还可以提高线虫在急性氧化应激条件下的寿命（P<0.05）及过氧化氢酶的活力（P<0.01）,并有效降低体内ROS的堆积情况（P<0.05）,上调daf-16(P<0.01)及下游ctl-1(P<0.001)基因的表达水平。但在daf-16突变株线虫中,没有观察到正常条件或急性氧化应激条件下延寿的作用,也没有提高过氧化氢酶的活力、降低ROS水平、提高daf-16和ctl-1表达水平的情况（P...     

紫穗槐蜂蜜对小鼠急性酒精性胃溃疡的预防作用

为研究紫穗槐蜂蜜对小鼠急性酒精性胃溃疡的预防作用，本实验采用紫穗槐蜂蜜对小鼠连续灌胃10 d，随后通过灌胃体积分数65%的乙醇溶液诱导小鼠急性酒精性胃溃疡损伤。通过观察小鼠胃组织病理结构、测定溃疡指数，分析紫穗槐蜂蜜对小鼠胃组织的保护作用；通过测定氧化应激和炎症因子相关生化指标，评价紫穗槐蜂蜜对急性酒精性胃溃疡小鼠胃组织抗氧化和抗炎能力的影响。结果显示：紫穗槐蜂蜜可以有效保护胃黏膜的完整性，显著缓解乙醇摄入引起的超氧化物歧化酶活性和还原型谷胱甘肽含量的降低，显著抑制丙二醛的过量生成（P＜0.05）；与模型组相比，紫穗槐蜂蜜处理组小鼠胃组织中一氧化氮和前列腺素E2含量显著升高（P＜0.05），肿瘤坏死因子α含量显著降低（P＜0.05）。免疫组织化学及实时荧光核酸定量检测分析结果表明，紫穗槐蜂蜜能够显著抑制胃溃疡相关炎症因子蛋白和基因的表达（P＜0.05）。结论：紫穗槐蜂蜜能够通过保护机体胃黏膜、调节氧化应激和炎症因子表达等途径预防酒精性胃溃疡。