银杏黄酮对非酒精性脂肪肝模型小鼠的作用及NF-κB在其机制中的相关性分析

本文观察银杏黄酮对非酒精性脂肪性肝(NAFLD)模型小鼠的作用,并分析NF-κB与小鼠肝脏脂肪变性及血清丙氨酸氨基转移酶(ALT)的相关性。170只昆明小鼠随机分为正常对照组、模型组、银杏黄酮高[300mg/(kg·d)]、中[150 mg/(kg·d)]、低[75 mg/(kg·d)]剂量组。采用高脂饲料构建非酒精性脂肪肝小鼠动物模型,分别于给药后4周、8周和12周末处死,观察肝脏病理变化,计算肝指数,检测血清总胆固醇(TC)、ALT、TNF-α以及肝组织NF-κB的表达。各剂量银杏黄酮组小鼠肝指数,血清TC、ALT和TNF-α水平,肝组织NF-κBp65的表达量比模型组显著降低,肝脏脂肪变性明显减轻(P0.05或P0.01);肝组织NF-κBp65相对表达量与肝脏脂肪变性程度及血清ALT含量呈正相关(r0、P0.01或P0.05)。实验结果表明:银杏黄酮可降低NAFLD小鼠血脂、减轻肝脏脂肪变性、改善肝功能指标及肝脏大体形态,且有一定的剂量和时间依赖性;NF-κB上游炎症通路可能是其作用的主要机制。     

蕨菜黄酮对染矽尘小鼠氧化应激及肺纤维化的影响

为探讨蕨菜黄酮对染矽尘小鼠的抗氧化应激及肺纤维的影响,采用超声雾化石英粉尘混悬液,使小鼠染尘,蕨菜黄酮(Pteridium aqulinum flavonoids,PAF)连续灌胃染尘小鼠3周,取血测血清中超氧化物歧化酶(superoxide dismutase,S0D)、丙二醛(malonaldehyde,MDA),并测肺组织中SOD、MDA、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、羟脯氨酸(hydroxyproline,Hyp),计算肺质量系数,取右肺下叶做病理组织观察;结果显示蕨菜黄酮组血及肺组织MDA值显著下降、SOD活力显著升高,肺组织GSH-Px活力显著升高,肺Hyp含量及肺指数显著下降,肺纤维化进程延缓,表明蕨菜黄酮对染矽尘小鼠具有较好的抗氧化应激效应,延缓了肺纤维化进程。     

复方中草药提取物对小鼠机体抗氧化能力的影响北大核心CSCD

研究以乌梅、马齿苋等为主要成分的复方中草药提取物对小鼠机体抗氧化能力的影响。以昆明种雌性小鼠作为实验动物,试验设3个剂量组(100、200、400 mg/kg·bw)和1个溶剂对照组。灌胃28 d后,检测小鼠血清以及心、肝、脾、肾组织中的超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性及丙二醛(MDA)的含量。复方中草药提取物在100、200、400 mg/kg·bw三个剂量水平上均可导致小鼠血清、心、肝、脾、肾组织中SOD和GSH-Px活性显著增强,降低小鼠上述组织中MDA含量,并呈现剂量反应关系。本研究中的复方中草药提取物可提高昆明种雌性小鼠机体的抗氧化能力,具有潜在的研究价值。     

复方中草药提取物对小鼠机体抗氧化能力的影响

研究以乌梅、马齿苋等为主要成分的复方中草药提取物对小鼠机体抗氧化能力的影响。以昆明种雌性小鼠作为实验动物,试验设3个剂量组(100、200、400 mg/kg·bw)和1个溶剂对照组。灌胃28 d后,检测小鼠血清以及心、肝、脾、肾组织中的超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性及丙二醛(MDA)的含量。复方中草药提取物在100、200、400 mg/kg·bw三个剂量水平上均可导致小鼠血清、心、肝、脾、肾组织中SOD和GSH-Px活性显著增强,降低小鼠上述组织中MDA含量,并呈现剂量反应关系。本研究中的复方中草药提取物可提高昆明种雌性小鼠机体的抗氧化能力,具有潜在的研究价值。     

小刺猴头发酵浸膏多糖对肉鸡抗氧化功能的影响

以小刺猴头发酵浸膏多糖为试验材料,研究其对肉鸡肝脏及血清中T-SOD和CAT的活力以及MDA含量的影响。空白组饲喂基础日粮,试验组在基础日粮中添加不同水平(1 000,3 000,5 000 mg/kg)的小刺猴头发酵浸膏多糖,试验期为28 d,检测肉鸡血清及肝脏中T-SOD和CAT的活力及MDA的含量。结果显示:当添加量为1 000,3 000 mg/kg时,肉鸡血清及肝脏中的T-SOD和CAT的活力与空白组相比差异显著(P<0.05),添加量为1 000,3 000,5 000 mg/kg时,肉鸡血清及肝脏中MDA的含量与空白组相比极显著降低(P<0.01)。小刺猴头发酵浸膏多糖可以增强肉鸡血清及肝脏中的SOD和CAT的活力,而对MDA有抑制或清除作用。     

黔产毛蒟水提物对急性肝损伤小鼠的保护作用

探讨黔产毛蒟水提物(PTE)对四氯化碳(CCl_4)诱导小鼠急性肝损伤的保护作用及其作用机制。本研究中将50只昆明种小鼠随机分为5组,各组10只,分别为空白组、模型组(0.01 g/kg的0.15%CCl_4菜油溶液造模)、PTE组(低剂量组0.5 g/kg和高剂量组1.0 g/kg)和阳性对照组(联苯双酯0.15 g/kg)。检测各组小鼠谷丙转氨酶(ALT)、谷草转氨酶(AST)、肿瘤坏死因子(TNF-α)含量;测定肝组织匀浆中脂质过氧化产物丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性;计算肝脏的湿重指数;HE染色法观察肝脏组织的病理学变化。与空白对照组相比,模型组血清ALT、血清AST、肝脏指数、肝组织MDA含量以及血清TNF-α明显增高(均P0.01),肝组织SOD活性明显降低(P0.01),肝组织病理损伤明显。与模型组相比,PTE高剂量组和阳性对照组血清ALT显著降低(P0.01),PTE低、高剂量组和阳性对照组血清AST、肝脏指数、肝组织MDA含量以及血清TNF-α含量均明显降低(P0.05或P0.01),肝组织SOD活性明显升高(P0.01),并减轻了肝组织病理损害。PTE可减轻CCl_4诱导的急性肝损伤,其机制可能与抗氧化、抑制TNF-α的产生有关。     

二甲双胍对D-半乳糖诱导雄性中年小鼠衰老的干预作用*

目的:探讨二甲双胍(Met)对D-半乳糖(D-gal)诱导雄性中年小鼠衰老的干预作用。方法:50只ICR 9月龄雄性小鼠,在SPF级实验环境饲养,自由摄食与饮水。随机分5组:对照组,模型组,二甲双胍低、中、高剂量(Met 50 mg/kg,Met 100 mg/kg,Met 200 mg/kg)组,每组10只。Met组和模型组小鼠每日颈背部皮下注射D-gal 100 mg/ kg,同时分别给予Met(50、100、200 mg/kg)或等体积NS灌胃。对照组注射和灌胃等体积NS。连续8周给药。检测小鼠一般状态,体重,空腹血糖,血清和肝脏超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量水平;水迷宫实验检测学习记忆能力;HE染色观察小鼠海马组织结构。结果:每日Met 200 mg/kg干预,能减少模型小鼠的体重。Met干预对模型鼠正常空腹血糖无影响。每日Met 50、100、200 mg/kg剂量干预,与模型组相比,均能显著提升模型小鼠血清和肝组织的SOD活性(P＜0.05)、降低血清MDA含量(P＜0.05),改善学习记忆能力测试的大部分指标(P＜0.05),HE染色显示海马齿状回核固缩、深染的神经元明显减少。Met干预在大部分指标上呈剂量-效应依赖关系。结论:每日Met 50～200 mg/kg长期处理,以Met 200 mg/kg为显著,能延缓D-gal 诱导的雄性中年衰老模型小鼠的衰老进程,机制可能与降低小鼠体重与增强机体抗氧化水平有关。     

金银花黄酮对小鼠免疫调节作用的研究

目的:探讨金银花黄酮对小鼠血清免疫酶活性与淋巴器官的抗氧化作用。方法:将50只昆明小鼠随机分为5组(n=10):正常组、模型组、低剂量组、中剂量组、高剂量组。模型组和正常组小鼠生理盐水灌胃,低、中、高剂量组分别给予金银花黄酮100 mg/kg、200 mg/kg、400 mg/kg体重灌胃。连续灌胃7周后,除正常组注射生理盐水,其他各组小鼠均采用25 mg/kg体重的地塞米松连续3 d皮下注射,造成免疫抑制后继续灌胃1周,处死全部小鼠,取血和胸腺、脾脏,称重胸腺和脾脏,计算小鼠脏器指数,测定血浆中酸性磷酸酶(ACP)、碱性磷酸酶(AKP)、溶菌酶(LSZ)活力,以及胸腺和脾脏匀浆中单胺氧化酶(MAO)、总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、丙二醛(MDA)。结果:金银花黄酮能显著提高免疫抑制小鼠的脏器指数,增加免疫抑制小鼠血清ACP、AKP和LSZ活力,提高免疫抑制小鼠的脾脏、胸腺组织T-AOC和SOD活性,而明显降低MAO和MDA含量。结论:金银花黄酮能显著调节小鼠血清免疫酶活性,提高淋巴器官的抗氧化功能,表明具其有良好的免疫调节功能。     

维生素E对青鱼幼鱼生长、免疫及抗氨氮胁迫能力的影响

以初始体质量(7.270.40) g的青鱼为研究对象, 采用维生素E(VE)有效含量分别为14.36(对照组)、25.14、37.66、62.97、113.92和210.45 mg/kg 6种等氮等能的实验饲料, 饲养青鱼幼鱼8周后, 根据生长情况选取对照组、62.97和210.45 mg/kg VE组进行24h氨氮胁迫(20 mg/L), 研究VE对青鱼幼鱼生长、免疫及抗氨氮胁迫能力的影响。结果表明: 以特定生长率为指标, 折线模型分析表明青鱼有效维生素E需要量为45.00 mg/kg。肌肉、肝脏和血清VE含量与饲料中VE含量呈明显正相关, 当饲料VE含量超过113.92 mg/kg时, 肌肉和肝脏VE含量均达到饱和。VE对鳃丝Na+/K+-ATP酶活性(NKA)和血清皮质醇(COR)无显著影响, 但随着饲料VE含量的升高, 过氧化氢酶(CAT)和总超氧化物歧化酶活性(T-SOD)呈上升趋势, 丙二醛含量(MDA)呈下降趋势。氨氮胁迫对各处理组肌肉VE含量和血清CAT活性无影响, 但肝脏VE含量均显著降低(P0.05), 且62.97和210.4 5 mg/kg VE组血清VE水平有所升高。在胁迫后, 对照组血清T-SOD、鳃丝NKA活性显著降低, 皮质醇含量显著增加(P0.05)。与对照组相比, 62.97和210.45 mg/kg VE组T-SOD、NKA活性和皮质醇含量在胁迫前后无显著变化。各处理组MDA含量在胁迫后虽均显著升高, 但210.45 mg/kg VE组在胁迫后MDA含量仍显著低于对照组(P0.05)。以上结果说明, 青鱼幼鱼获得最大生长的有效维生素E需求量为45.00 mg/kg, 且较高VE能有效提高青鱼机体免疫力, 缓解氨氮胁迫对青鱼机体的负面影响。       

金线风总黄酮对四氯化碳致急性肝损伤小鼠的保护作用及机制研究

研究金线风总黄酮(TFC)对四氯化碳(CCl4)致急性肝损伤小鼠的保护作用,并从氧化应激、炎症反应和TLR-4/NF-κB信号通路探讨其作用机制。60只小鼠随机分为正常组、模型组、水飞蓟素组(150 mg/kg)、TFC低、中、高剂量组(100、200、400 mg/kg)、连续灌胃给药10 d。末次给药2 h后,除正常组外,各组腹腔注射0.1%的CCl4花生油溶液(10 m L/kg),建立小鼠急性肝损伤模型,16 h后,收集血清和肝组织。血清指标检测表明,与模型组比较,TFC能够显著降低肝脏指数、ALT和AST活性(P0.05),并减少ALP、TBIL和γ-GT含量(P0.05),且降低MDA含量(P0.05),同时增强T-SOD和GSH-Px活性(P0.05)。ELISA法检测肝组织指标结果表明,与模型组比较,TFC能够显著下调TNF-α、IL-1β和IL-6含量(P0.05)。Western blot检测结果显示,与模型组比较,TFC能够明显降低肝组织中TLR-4和NF-κB蛋白表达(P0.05)。HE染色分析肝组织病理学变化结果表明,TFC能够有效改善肝组织损伤程度。综上所述,TFC对CCl4诱导的急性肝损伤小鼠具有保护作用,其保肝作用机理可能与抑制氧化应激、炎症反应以及TLR-4/NF-κB信号通路有关。     

Sex-related differences in cadmium-induced lipid peroxidation in the rat

Male and female rats were dosed once a day for 2 days injection with 1.5 mg of Cd/kg as CdCl₂. 24 hr after administration of cadmium, lipid peroxidation determined by estimation of malondialdehyde (MDA) was greatly increased in male rat liver, but was not in female rats. Cadmium in a larger dose of 4.5 mg/kg, subcutaneous single injection, significantly increased content of MDA in female rat liver. These results suggest that sex-related differences exist in the ability of cadmium to induce MDA formation in rat liver, although administration of cadmium causes the enhancement of MDA formation in both male and female rats. The reason why sex-related differences exist in lipid peroxidation of rat liver is discussed.     

Pirfenidone attenuates nonalcoholic fatty liver disease through activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway

Nonalcoholic fatty liver disease (NAFLD) originates from the hepatopathy of fatty liver. Pirfenidone is a novel broad-spectrum anti-fibrosis agent used for treating various kinds of tissue fibrosis. The present study will evaluate the effects of Pirfenidone on liver injury in high-fat diet (HFD)-fed mice to evaluate the value of Pirfenidone in treating NAFLD. The pathology of NAFLD was simulated by feeding mice with an HFD in the present study, followed by treating the HFD mice with 150 and 300 mg/kg/day Pirfenidone once a day. The pathological state of HFD mice was identified by the elevated liver weight, promoted serum triglyceride (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels, declined serum high-density lipoprotein cholesterol (HDL-C) levels, increased alanine aminotransferase and aspartate aminotransferase activity, and histopathological changes to the liver tissues, all of which were dramatically ameliorated by 150 and 300 mg/kg Pirfenidone administration. Furthermore, the excessive production of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and IL-6, as well as upregulated phosphorylated nuclear factor kappa-B (p- NF-κB p65), were observed in HFD-fed mice, but significantly reversed by Pirfenidone. Finally, activated oxidative stress, identified by promoted malondialdehyde (MDA) levels and declined catalase (CAT) activity, was observed in HFD-fed mice, accompanied by the downregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and sterol-regulatory element-binding proteins-1c (SREBP-1c). After the treatment with Pirfenidone, oxidative stress was greatly mitigated. Our results imply that Pirfenidone ameliorated the progression of NAFLD by mediating inflammation and oxidative stress.     

Late protective effect of pharmacological preconditioning with total flavones of rhododendra against myocardial ischemia-reperfusion injury

The aim of the present study was to investigate the protective effect of total flavones of rhododendra (TFR) pharmacological preconditioning against myocardial ischemia-reperfusion (I/R) injury and its probable mechanisms in rats. Rat myocardial I/R injury was induced by ligating and untying the left anterior descending coronary artery. Male Sprague-Dawley rats were anesthetized and the chests were opened. All animals were subjected to 30 min of occlusion and 1 h of reperfusion. Twenty-four hours before the 30-minute occlusion, rats received 3 cycles of 5 min intravenous perfusion of TFR (10, 20, 40 mg/kg) or morphine hydrochloride (0.3 mg/kg) or normal saline interspersed with drug-free periods. Changes in the ST segment of ECG, the content of cardiac troponin I (cTnI), malondialdehyde (MDA), and nitric oxide (NO), and the activity of superoxide dismutase (SOD), lactate dehydrogenase (LDH), creatine phosphokinase (CK), and nitric oxide synthase (NOS) in serum were measured. Infarct size (IS), as a percentage of the area at risk (AAR), was determined by TTC staining. The expression of inducible nitric oxide synthase (iNOS) mRNA in rat myocardium was detected by RT-PCR and the expression of iNOS protein was detected by Western blot. Pretreatment with TFR (10, 20, 40 mg/kg) markedly inhibited I/R-induced ST segment elevation of ECG. TFR (20, 40 mg/kg) pretreatment decreased I/R-induced IS/AAR, markedly inhibited the increase of MDA content and the activity of CK and LDH, and also significantly inhibited the decline of NO content and the activity of NOS and SOD in serum. TFR (40 mg/kg) preconditioning significantly inhibited the increase of serum cTnI induced by I/R injury and increased the expression of iNOS both at mRNA and protein levels in rat myocardium. Our findings indicate that TFR preconditioning has a protective effect against myocardial I/R injury in rats. The cardioprotection involves the stimulation of NO release and the inhibition of lipid peroxidation.     

茶多酚对NASH 大鼠肝脏组织VEGF 及氧化应激的影响

目的:茶多酚对NASH大鼠肝脏组织VEGF及氧化应激的影响。方法:雄性SD大鼠30只,随机分为3组,正常对照组、模型组、茶多酚治疗组。正常组普通饲料喂养,模型组喂高脂饮食,茶多酚治疗组在高脂饮食12周后茶多酚(150mg(/kg.d)灌胃治疗,16周末处死各组大鼠,留取肝脏组织,观察各组大鼠肝组织病理改变,测定其肝脏丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性以及血管内皮生长因子(VEGF)、Ⅰ、Ⅲ型胶原的表达。结果:模型组大鼠肝组织中SOD活性降低而MDA含量以及VEGF、Ⅰ、Ⅲ型胶原表达均明显高于正常组。茶多酚治疗可减轻肝纤维化程度,显著升高肝组织中SOD活性、降低MDA含量以及VEGF、Ⅰ、Ⅲ型胶原表达水平。结论:茶多酚可通过抑制肝纤维化组织VEGF表达,降低肝组织氧化应激水平而发挥抗肝纤维化作用。     

Silymarin modulates Cisplatin-induced oxidative stress and hepatotoxicity in rats

Cisplatin (CDDP) is a widely used anticancer drug, but at high dose, it can produce undesirable side effects such as hepatotoxicity. Because silymrin has been used to treat liver disorders, the protective effect of silymarin on CDDP-induced hepatotoxicity was evaluated in rats. Hepatotoxicity was determined by changes in serum alanine aminotransferase [ALT] and aspartate aminotransferase [AST], nitric oxide [NO] levels, albumin and calcium levels, and superoxide dismutase [SOD], glutathione peroxidase [GSHPx] activities, glutathione content, malondialdehyde [MDA] and nitric oxide [NO] levels in liver tissue of rats. Male albino rats were divided into four groups, 10 rats in each. In the control group, rats were injected i.p. with 0.2 ml of propylene glycol in saline 75/25 (v/v) for 5 consecutive days [Silymarin was dissolved in 0.2 ml of propylene glycol in saline 75/25 v/v]. The second group were injected with CDDP (7.5 mg /kg, I.P.), whereas animals in the third group were i.p. injected with silymarin at a dose of 100 mg/kg/day for 5 consecutive days. The Fourth group received a daily i.p. injection of silymarin (100 mg/kg/day for 5 days) 1 hr before a single i.p. injection of CDDP (7.5 mg/kg). CDDP hepatotoxicity was manifested biochemically by an increase in serum ALT and AST, elevation of MDA and NO in liver tissues as well as a decrease in GSH and the activities of antioxidant enzymes, including SOD, GSHPx in liver tissues. In addition, marked decrease in serum NO, albumin and calcium levels were observed. Serum ALT, AST, liver NO level, MDA was found to decreased in the combination group in comparison with the CDDP group. The activities of SOD, GSHPx, GSH and serum NO were lower in CDDP group than both the control and CDDP pretreated with silymarin groups. The results obtained suggested that silymarin significantly attenuated the hepatotoxicity as an indirect target of CDDP in an animal model of CDDP-induced nephrotoxicity.     

槲皮素体外抗氧化及对小鼠血脂代谢作用的研究

本研究旨在探讨槲皮素体外抗氧化能力以及对高脂日粮小鼠血脂代谢的影响.体外分别测定了槲皮素对DPPH·,·OH和ABTS+·自由基的清除作用.动物实验:将昆明种雄性小鼠32只,随机分为4组,分别饲喂正常、高脂、高脂+0.05g/kg槲皮素、高脂+0.1g/kg槲皮素日粮.9周后测定小鼠肝脏活性氧(Reactive oxygen species,ROS)水平、丙二醛(Malondialdehyde,MDA)含量、抗氧化酶活力及血脂水平.结果表明:槲皮素对DPPH·,·OH和ABTS+·具有较强的清除作用,在一定范围内呈现出明显的剂量增加-效应增强的关系.0.05g/kg槲皮素能显著降低肝脏自由基水平及MDA含量(P＜0.05),增强抗氧化能力(P＜0.05),改善血脂水平(P＜0.05),而0.1g/kg槲皮素效果不显著.结论:0.05g/kg槲皮素可有效提高机体抗氧化能力,缓解高脂膳食造成的氧化应激,改善血脂代谢.     

Garlic and vitamin E provides antioxidant defence in tissues of female rats treated with nicotine

Nicotine is known to induce oxidative stress in rat tissues and the antioxidant properties of garlic have been reported. This study was designed to determine if the peroxidative damage caused by nicotine administration can be effectively prevented with garlic juice, and vitamin E, a known antioxidant.Four groups of six rats each were divided into: Group I: (control) received 0.2ml of 0.9% normal saline, group II (received nicotine 0.6mg/kg b.w subcutaneously), group III (received nicotine 0.6mg/kg b.w + garlic juice 100mg/kg b.w orally), and group IV (received nicotine 0.6mg/kg b.w + Vitamin E 100mg/kg b.w orally). All animals were treated for 21 days. The pituitary gland, ovary, uterus, heart, liver and kidney of the animals were harvested, weighed and homogenized. Malondialdehyde (MDA), superoxide dismutase (SOD) and reduced glutathione (GSH) were then measured.Concentration of MDA was significantly increased in tissues of nicotine treated rats when compared with the control. In group III and IV, MDA levels were significantly reduced when compared with nicotine group. The activities of SOD and GSH significantly decreased in group II (nicotine only) rat tissues, while it was significantly increased in group III and IV rat tissues. The study showed that garlic juice extract (100mg/kg b.w) and vitamin E (100mg/kg b.w) administration prevented oxidative damage in rat tissues treated with nicotine. The study also showed that vitamin E has a more potent antioxidant activity than garlic juice in preventing nicotine induced oxidative damage in rat. Keywords: Nicotine, Vitamin E, Garlic, antioxidant.     

The potential protective role of folic acid against acetaminophen-induced hepatotoxicity and nephrotoxicity in rats

Folic acid (FA), is a group B vitamin, has high reactive oxygen radicals quenching ability, resulting in protection against oxidative damage in aerobic cell. Acetaminophen (N-acetyl-p-aminophenol, APAP) is a nonsteroidal anti-inflammatory drug, and can promote oxidative damage in liver and kidney tissues. The aim of this study was to investigate whether folic acid has protective effects on oxidative liver and kidney injury caused by experimental APAP toxication. Forty female Sprague dawley rats were divided into 5 groups; control, APAP, FA, APAP+FA, and APAP+N-acetylcysteine (NAC) groups. APAP toxication was induced by oral gavage (3 g/kg bodyweight). FA (20 mg/kg bodyweight) and NAC (150 mg/kg bodyweight) were given by oral gavage to the specified groups. Oxidant and antioxidant parameter were determined in liver and kidney tissues. In addition, the liver and kidney tissues were histological evaluated. When compared with APAP group, superoxide dismutase (SOD) and catalase activities and glutathione levels were statistically higher, malondialdehyde (MDA) level and myeloperoxidase activity (except liver tissue) were statistically lower in both APAP+FA and APAP+NAC. Liver and kidney MDA level and kidney SOD activity were significantly lower in APAP+NAC group compared with APAP+FA group. Co-administration of NAC with APAP was found to provide protection, but hepatic cords were defective in some places and some glomerular tubules also had dilatation. Necrotic areas was reduced in the liver and the glomerular structure was in good condition in the APAP+FA group. As a result, FA might have a protective effect against APAP-induced hepato-nephrotoxicity and oxidative stress in rat.     

山楂总黄酮联合茶多酚对高脂膳食大鼠血脂及氧化应激的影响

为了探讨山楂总黄酮联合茶多酚对高脂膳食大鼠血脂及氧化应激的影响。将山楂总黄酮联合茶多酚灌胃高脂膳食大鼠5周,取血测血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C);并测血清及肝组织丙二醛(MDA)、超氧化物歧化酶(S0D)、谷胱甘肽过氧化物酶(GSH-Px);计算肝指数及进行肝病理组织学观察。结果发现,与模型组相比,山楂总黄酮联合茶多酚组大鼠血清TC、TG、LDL-C水平显著下降,血清HDL-C水平显著升高,血清及肝组织MDA显著降低,S0D、GSH-Px活力明显升高,肝指数明显降低,肝细胞脂肪化程度明显减轻。表明山楂总黄酮联合茶多酚增强了高脂饮食大鼠的抗氧化水平,调节了脂质紊乱。