益母草碱抑制人脑血管外膜成纤维细胞增殖并促进细胞凋亡的机制研究

目的 探讨益母草碱对人脑血管外膜成纤维细胞(HBVAFs)增殖和凋亡的影响,并研究其作用机制.方法 采用不同浓度的益母草碱干预体外培养的HBVAFs,通过噻唑蓝(MTT)法检测细胞增殖活力,并筛选后续实验加药浓度,采用10μmol/L的益母草碱处理HBVAFs,实验分为Control组(正常对照)、Leonurine组...     

牙龈卟啉单胞菌脂多糖对人牙龈成纤维细胞炎症刺激作用的研究*

【摘要】 目的 探讨牙龈卟啉单胞菌(P.g)脂多糖(LPS)刺激人牙龈成纤维细胞(HGFs)分泌炎症细胞因子的作用及其机制。方法 组织块法培养HGFs,用不同浓度(1mg/L、10mg/L)的P.gLPS刺激HGFs后6h和12h,采用酶联免疫法(ELISA)检测细胞分泌肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β),定量real-timePCR检测Toll样受体(TLR)2和TLR4在HGFs中的表达。结果 与非P.gLPS刺激组相比较,P.gLPS刺激HGFs6h和12h后,TLR2的表达和炎症细胞因子TNF-α、IL-1β分泌显著升高,呈浓度依赖性(P<0.05),而且随时间的延长TNF-α、IL-1β分泌明显增加(P<0.05)。TLR4在P.gLPS刺激HGFs6h后的表达明显升高(P<0.05),随着P.gLPS浓度增加其表达量升高更明显,但LPS刺激细胞12h后,TLR4的表达与对照组无明显差别(P>0.05)。结论 P.gLPS能刺激HGFs分泌炎症细胞因子,可能是早期主要通过其表面的TLR2、TLR4来介导炎症细胞因子的分泌,随后主要通过其表面的TLR2来介导炎症反应。      

碱性成纤维细胞生长因子对人牙龈成纤维细胞成骨分化与增殖的影响

目的 观察碱性成纤维细胞生长因子(b FGF)对体外培养的人牙龈成纤维细胞(HGFs)成骨分化能力与细胞增殖的影响,探索b FGF在HGFs体外诱导成骨分化过程中的作用。方法 采用组织块贴壁法体外培养HGFs,取第3代细胞进行如下分组培养。1组为普通培养基组,2组为普通培养基+10μg/L b FGF组,3组为成骨诱导组,4组为成骨诱导+10μg/L b FGF组。应用四甲基偶氮唑蓝比色法检测HGFs增殖状况;用碱性磷酸酶染色法及茜素红染色法检测HGFs的成骨分化能力。结果 在普通培养基和成骨诱导培养基中,10μg/L的b FGF均能促进HGFs的增殖(P<0.01);在成骨诱导培养基中HGFs具有骨向分化能力,形成钙结节;而10μg/L的b FGF对HGFs的碱性磷酸酶活性与矿化结节形成能力均无明显影响。结论 10μg/L的b FGF能促进HGFs的增殖能力,而对其骨向分化无明显影响。     

姜黄素联合白藜芦醇诱导人喉癌细胞Hep-2凋亡的作用机制

目的利用姜黄素及其联合白藜芦醇在体外作用于喉癌细胞Hep-2,观察其对人喉癌细胞的影响,并探讨可能的抗肿瘤作用机制。方法采用MTT法检测各组药物对喉癌细胞增殖的抑制作用;Hoechst 33258染色法观察各组药物对喉癌细胞核的形态影响;流式细胞术检测细胞凋亡率;RT-PCR检测p65和caspase-3的基因表达情况;Western blot法检测各组药物对喉癌细胞p65蛋白和caspase-3蛋白表达情况的影响。结果 MTT结果显示姜黄素联合白藜芦醇组抑制喉癌细胞增殖的作用要明显高于单独姜黄素组和单独白藜芦醇组(P<0.05);Hoechst 33258染色法的结果显示,经各组药物处理后的细胞核形态与对照组相比呈凋亡特征性改变;流式细胞术分析结果显示姜黄素联合白藜芦醇组的细胞凋亡率明显高于单独姜黄素组和单独白藜芦醇组(P<0.05);RT-PCR结果显示姜黄素联合白藜芦醇组的p65基因表达量与二者单独使用时相比明显降低(P<0.05),而姜黄素联合白藜芦醇组的caspase-3基因表达量与二者单独使用时相比明显升高(P<0.05);Western blot结果显示与对照组比较,单独姜黄素组和单独白藜芦醇组的p65蛋白表达明显下调,caspase-3蛋白表达则明显上调,而姜黄素联合白藜芦醇组对p65和caspase-3表达调控的影响与单独姜黄素组和单独白藜芦醇组相比差异有统计学意义(P<0.05)。结论姜黄素联合白藜芦醇在诱导人喉癌细胞Hep-2的凋亡时具有协同效应,其作用机制可能是通过阻断转录因子NF-κB(p65)信号通路的活化,上调caspase-3蛋白的表达来实现的。     

体外诱导人牙龈成纤维细胞多向分化潜能的实验研究

目的 探索人牙龈成纤维细胞（hGFs）是否具有多向分化潜能, 为组织工程学提供新的细胞来源。方法 经志愿者知情同意后收集健康牙龈组织, 组织块法培养 hGFs。取第 3 代 hGFs 进行成骨、 成软骨和成脂诱导, 未分化诱导的细胞为对照组。分别用碱性磷酸酶 （ALP） 染色和茜素红染色、 阿利新蓝染色、 油红 O 染色检测细胞成骨、 成软骨和成脂能力。实时定量聚合酶链反应 （PCR） 检测细胞中成骨分化标志基因 ALP、 runt 相关转录因子 2 （Runx2）、成软骨分化标志基因聚集蛋白聚糖（AGR）和成脂分化标志基因过氧化物酶体增殖物激活受体γ2（PPARγ2）的表达。结果 成骨诱导组培养至 7 d 时 ALP 染色可见大量的蓝紫色沉淀, 28 d 时细胞周围有大量红染的钙结节沉积,而对照组无钙结节, 培养至 14 d 细胞中 ALP 和 Runx2 表达明显高于对照组（P < 0.01）。14 d 时成软骨诱导组阿利新蓝阳性, 成脂诱导组可见红色的脂肪滴, 而对照组 2 种染色为阴性, AGR、 PPARγ2 表达均明显高于对照组（P <0.01）。结论 hGFs 具有成骨、 成软骨和成脂分化的多向分化潜能。     

白藜芦醇对人胚肺成纤维细胞株MRC-5生长的抑制作用

目的探讨白藜芦醇(Res)对人胚肺成纤维细胞生长的抑制作用及相关机制。方法以人胚肺成纤维细胞MRC-5为研究对象,分别予20μL二甲基亚砜(DMSO)及0、12.5、25、50、100、200μmol·L-1Res处理细胞24、48、72 h,通过MTT法分析细胞增殖抑制率。另外,以20μL DMSO(溶媒组)及50、100μmol·L-1Res孵育细胞48 h,采用流式细胞术检测细胞周期和凋亡率,行原位缺口末端标记法(TUNEL)测定细胞凋亡指数(AI),应用荧光实时定量PCR和Western blot分别检测细胞周期蛋白D1(cell cycle protein D1,Cyclin D1)、细胞周期蛋白依赖激酶4(cyclin-dependent kinase 4,CDK4)mRNA与蛋白表达,Western blot检测Bcl-2、Bax蛋白表达。结果随着Res浓度的升高和处理时间的延长,细胞增殖抑制率逐渐增加(P<0.01)。在共同培养48h后,50、100μmol·L-1Res处理组S、G2/M期DNA比例及Cyclin D1、CDK4 mRNA与蛋白表达水平、Bcl-2蛋白表达水平降低,而G0/G1期DNA比例、AI、凋亡率及Bax蛋白表达水平增加,与溶媒组比较,差异均有显著性(P<0.01),并且100μmol·L-1Res效果强于50μmol·L-1(P<0.01)。结论Res能抑制MRC-5细胞增殖,其机制可能与阻碍细胞周期进展及促进细胞凋亡有关。     

高糖状态对人牙龈成纤维细胞生物学活性的影响

目的探讨不同浓度葡萄糖对人牙龈成纤维细胞生物学活性的影响。方法将人牙龈成纤维细胞分别接种于5.5,8.8,10,15及20 mmol/L的葡萄糖溶液中培养72 h,观察人牙龈成纤维细胞的形态、增殖以及分泌Ⅰ型胶原的情况。结果当葡萄糖浓度为10 mmol/L以上时,人牙龈成纤维细胞的形态不规则,增殖受到抑制,Ⅰ型胶原分泌减少;随着葡萄糖浓度的增大,人牙龈成纤维细胞的生物学活性受影响愈明显。结论高浓度葡萄糖可以使人牙龈成纤维细胞的形态呈现不规则,并抑制其增殖及Ⅰ型胶原的分泌。     

纤维连接蛋白诱导人胚肺成纤维细胞增殖的信号转导通路研究

目的探讨纤维连接蛋白(FN)诱导人胚肺成纤维细胞(HFL-1)增殖的信号转导通路。方法采用不同浓度FN刺激HFL-1并观察磷酸酰基醇-3-激酶(PI3K)信号转导通路抑制剂wortmannin(WMN)、细胞外信号调节蛋白激酶(ERK)信号转导通路抑制剂PD98059和P38蛋白激酶信号转导通路抑制剂SB203580对FN诱导HFL-1增殖作用的影响。用四甲基偶氮唑蓝(MTT)法检测各组细胞增殖情况。结果FN对HFL-1诱导增殖作用呈剂量依赖性升高趋势,在50ng/mL时作用显著;WMN,PD98059和SB203580均可抑制FN诱导的HFL-1细胞增殖。结论FN诱导HFL-1的细胞增殖可以通过PI3K和丝裂原活化蛋白激酶(MAPK)信号转导途径实现。     

甘草总黄酮通过调控MAPK/NF-κB信号通路对脂多糖诱导的人牙龈成纤维细胞炎症反应的抑制作用

目的:探讨甘草总黄酮通过调控丝裂原活化蛋白激酶(MAPK)/核转录因子κB(NF-κB)信号通路对脂多糖(LPS)诱导的人牙龈成纤维细胞(HGF)炎症反应的抑制作用。方法:体外分离培养原代HGF,以5μg·ml^-1 LPS处理后,采用CCK-8实验检测0,1.5,3,6,12,24μg·ml^-1甘草总黄酮对HGF细胞活力的影响,筛选出甘草总黄酮适合的剂量和作用时间。体外培养原代HGF,随机分为对照组(不进行任何药物处理)、LPS组(5μg·ml^-1)、甘草总黄酮低剂量(6μg·ml^-1)+LPS(5μg·ml^-1)组、甘草总黄酮高剂量(12μg·ml^-1)+LPS(5μg·ml^-1)组、甘草总黄酮高剂量(12μg·ml^-1)+LPS(5μg·ml^-1)+C16-PAF(MAPK激活剂,4μmol·L^-1)组。采用CCK-8实验、划痕实验分别检测各组细胞活力和迁移率;酶联...     

白藜芦醇对于小鼠败血症休克的保护作用及其作用机制的研究

目的从动物休克模型和细胞水平上研究白藜芦醇(resveratrol,Res)对败血症的调节作用及其分子药理学作用机制。方法通过建立小鼠盲肠结扎穿孔诱导的败血症休克模型(CLP),研究白藜芦醇给药后的小鼠的存活率。然后利用体外培养的心肌细胞建立LPS损伤模型,采用反转录PCR(RT-PCR)、Real-time PCR检测细胞内源性TNF-α、SIRT1等的mRNA的表达水平,Western blot分析NF-κB重要亚基的蛋白表达水平。结果与单纯休克模型组相比较,腹腔注射白藜芦醇(1和5 mg·kg-1·d-1)治疗明显增加败血症休克小鼠的存活率;白藜芦醇处理明显促进SIRT1、SIRT6和SIRT7的mRNA表达,抑制LPS诱导的NF-κB核转位。结论适当剂量的白藜芦醇可能通过上调SIRT家族成员,并抑制NF-κB炎症反应通路,对败血症休克具有潜在的药理学保护作用。     

Impact of oxidative stress on neuronal survival

1. Reactive oxygen species and oxidative state are slowly gaining acceptance in having a physiological relevance rather than just being the culprits in pathophysiological processes. The control of the redox environment of the cell provides for additional regulation in relation to signal transduction pathways. Conversely, aberrant regulation of oxidative state manifesting as oxidative stress can predispose a cell to adverse outcome. 2. The phosphatidylinositol 3-kinase/akt pathway is one such pathway that is partially regulated via oxidative state and, in an oxidative stress paradigm such as ischaemic-reperfusion injury, may be inactivated, which can lead to exacerbation of cell death. 3. Activation of nuclear factor (NF)-kappaB has been associated with oxidative stress. The role of NF-kappaB in neuronal cell death is widely debated, with major studies highlighting both a pro- and anti-apoptotic role for NF-kappaB, with the outcome being region, stimulus, dose and duration specific. 4. Oxidative state plays a key role in the regulation and control of numerous signal transduction pathways in the cell. Elucidating the mechanisms behind oxidative stress-mediated neuronal cell death is important in identifying potential putative targets for the treatment of diseases such as stroke.     

C-Phycocyanin prevents acute myocardial infarction-induced oxidative stress,inflammation and cardiac damage

ContextC-Phycocyanin is a protein with anti-scavenger, antioxidant and anti-inflammatory actions against agents that cause cellular damage. The cardioprotective action of C-phycocyanin against acute myocardial infarction (AMI) has not been studied in animal models.ObjectiveTo investigate C-phycocyanin’s effect on oxidative stress, inflammation and cardiac damage in a model of isoproterenol-induced AMI.Materials and methodsWistar rats were divided into four groups: (1) sham + vehicle (0.9% saline solution by oral gavage, OG); (2) sham + C-phycocyanin (50 mg/kg/d, OG); (3) AMI + vehicle, and (4) AMI + C-phycocyanin. AMI was induced by administering isoproterenol (20, 10, 5 and 3 mg/kg each dose per day), and serum cardiac enzymes were quantified. After five days, the animals were euthanized; the heart was dissected to determine oxidative stress, redox environment, inflammation and cardiac damage markers.ResultsWe observed that C-phycocyanin reduced AMI-increased cardiac enzymes (CK by about 53%, CKMB by about 60%, AST by about 16% and ALT by about 21%), lipid peroxidation (57%), reactive oxygen species (50%), nitrites (46%), oxidized glutathione (41%), IL1β (3%), INFγ (5%), TNFα 3%), Bcl2 (37%), Bax (43%), COX2 (21%) and caspase 9 (61%). Finally, C-phycocyanin reduced AMI-induced aberrant histological changes related to myonecrosis, interstitial oedema and inflammatory infiltration in the heart muscle.ConclusionsC-Phycocyanin prevents AMI-induced oxidative stress, inflammation and heart damage. This study is the first report that employed C-phycocyanin in an animal model of AMI and supports the potential use of C-phycocyanin in the management of AMI.     

Erythropoietin prevents vascular inflammation and oxidative stress in subtotal nephrectomized rat aorta beyond haematopoiesis

1. Recombinant human erythropoietin (rHuEPO) has been used for the management of renal anaemia. Recent studies suggest pleiotropic properties of rHuEPO in various tissues. The aim of the present study was to investigate the vasoprotective effects of rHuEPO in renal failure rats. 2. Rats subjected to 5/6 and 17/18 nephrectomy (5/6Nx and 17/18Nx rats, respectively) were treated with rHuEPO (75 U/kg, s.c.) three times a week for 2 weeks. 3. Administration of rHuEPO to 5/6Nx or 17/18Nx rats had no effect on systolic blood pressure or decreased haematocrit. However, rHuEPO treatment normalized proteinuria and creatinine clearance in 5/6Nx, but not in 17/18Nx, rats. 4. Vasodilation in response to acetylcholine in aortic rings was impaired in 5/6Nx and 17/18Nx rats and improved by rHuEPO in both groups. Immunohistochemical analysis revealed that macrophage infiltration into adventitial areas and the expression of osteopontin were enhanced in aortas from 5/6Nx and 17/18Nx rats, but that rHuEPO suppressed these effects. In addition, rHuEPO attenuated medial hyperplasia and NADPH oxidase‐derived superoxide production in 5/6Nx and 17/18Nx rats. 5. Activation of the Akt signalling pathway was evident in rHuEPO‐treated rats as the increased expression of phosphorylated Akt and glycogen synthase kinase‐3β. Treatment with rHuEPO restored the expression of phosphorylated endothelial nitric oxide synthase in the aorta and urinary excretion of NO_x in nephrectomized rats. 6. These results suggest that a low dose of rHuEPO results in the normalization of endothelial function, vascular inflammation and oxidative stress in rats with renal ablation beyond haematopoiesis. In addition, these vasoprotective effects are observed even in a state of deteriorating renal dysfunction.     

Resveratrol prevents the expression of glaucoma markers induced by chronic oxidative stress in trabecular meshwork cells

Elevated intraocular pressure (IOP) constitutes the best characterized risk for primary open-angle glaucoma (POAG). Elevated IOP is believed to result from an increase in aqueous humor outflow resistance at the level of the trabecular meshwork (TM)/Schlemm’s canal. Malfunction of the TM in POAG is associated with the expression of markers for inflammation, cellular senescence, oxidative damage, and decreased cellularity. Current POAG treatments rely on lowering IOP, but there is no therapeutic approach available to delay the loss of function of the TM in POAG patients. We evaluated the effects of chronic administration of the dietary supplement resveratrol on the expression of markers for inflammation, oxidative damage, and cellular senescence in primary TM cells subjected to chronic oxidative stress (40% O₂). Resveratrol treatment effectively prevented increased production of intracellular reactive oxygen species (iROS) and inflammatory markers (IL1α, IL6, IL8, and ELAM-1), and reduced expression of the senescence markers sa-β-gal, lipofuscin, and accumulation of carbonylated proteins. Furthermore, resveratrol exerted antiapoptotic effects that were not associated with a decrease in cell proliferation. These results suggest that resveratrol could potentially have a role in preventing the TM tissue abnormalities observed in POAG.     

Resveratrol attenuates hyperoxia‐induced oxidative stress,inflammation and fibrosis and suppresses Wnt/β‐catenin signalling in lungs of neonatal rats

Although survival rate of infants born prematurely has been raised by supplemental oxygen treatment, it is followed by high morbidity of hyperoxia‐induced bronchopulmonary dysplasia. In this study, the effect of resveratrol on the lung injury was evaluated in hyperoxia‐exposed rats of preterm birth. The results demonstrated that hyperoxia led to thickened alveolar wall, simplified alveolar architecture and fibrosis. In addition, elevated methane dicarboxylic aldehyde level, decreased glutathione level and superoxide dismutase activity were also found in hyperoxic lungs, as well as the increased tumor necrosis factor‐α, interleukin‐1β and interleukin‐6 in the bronchoalveolar lavage fluid. Fibrotic‐associated proteins transforming growth factor‐β1, α‐smooth muscle actin, collagen I and fibronectin deposition were also found in interstitial substance of lungs. Furthermore, Wnt/β‐catenin signalling was found to be active in hyperoxia‐induced lungs. In addition, expression of SP‐C was increased and T1α was decreased in hyperoxia‐exposed lungs. Resveratrol intraperitoneal administration alleviated hyperoxia‐induced histological injury of lungs, regulated redox balance, decreased pro‐inflammatory cytokine release, and down‐regulated expression of fibrotic‐associated proteins. Furthermore, Wnt/β‐catenin signalling was also suppressed by resveratrol, as represented by diminished expression of lymphoid enhancer factor‐1, Wnt induced signalling protein‐1 and cyclin D1. In addition, the increase of SP‐C and decrease of T1α expression was prevented as well. The present study showed that resveratrol could protect lungs from hyperoxia‐induced injury through its antioxidant, anti‐inflammatory and anti‐fibrotic effects. The transdifferentiation of alveolar epithelial type II cells to alveolar epithelial type I cells promotion and Wnt/β‐catenin signalling suppression are also involved in the protective effect.     

Angiotensin-converting enzyme inhibitor prevents oxidative stress,inflammation, and fibrosis in carbon tetrachloride-treated rat liver

Hepatic fibrosis is a common feature of chronic liver injury, and the involvement of angiotensin II in such process has been studied earlier. We hypothesized that anti-angiotensin II agents may be effective in preventing hepatic fibrosis. In this study, Long Evans female rats were used and divided into four groups such as Group-I, Control; Group-II, Control?+?ramipril; Group-III, CCl₄; and Group-IV, CCl_4?+_?ramipril. Group II and IV are treated with ramipril for 14 d. At the end of treatment, the livers were removed, and the level of hepatic marker enzymes (aspartate aminotransferase, Alanine aminotransferase, and alkaline phosphatase), nitric oxide, advanced protein oxidation product , catalase activity, and lipid peroxidation were determined. The degree of fibrosis was evaluated through histopathological staining with Sirius red and trichrome milligan staining. Carbon-tetrachloride (CCl₄) administration in rats developed hepatic dysfunction and raised the hepatic marker enzymes activities significantly. CCl₄ administration in rats also produced oxidative stress, inflammation, and fibrosis in liver. Furthermore, angiotensinogen-inhibitor ramipril normalized the hepatic enzymes activities and improved the antioxidant enzyme catalase activity. Moreover, ramipril treatment ameliorated lipid peroxidation and hepatic inflammation in CCl₄-treated rats. Ramipril treatment also significantly reduced hepatic fibrosis in CCl₄-administered rats. In conclusion, our investigation suggests that the antifibrotic effect of ramipril may be attributed to inhibition of angiotensin-II mediated oxidative stress and inflammation in liver CCl₄-administered rats.     

N-acetylcysteineamide (NACA) prevents inflammation and oxidative stress in animals exposed to diesel engine exhaust

Diesel exhaust particles (DEPs), a by-product of diesel engine exhaust (DEE), are one of the major components of air borne particulate matter (PM) in the urban environment. DEPs are composed of soot, polycyclic aromatic hydrocarbons (PAHs), redox active semi-quinones, and transition metals, which are known to produce pro-oxidative and pro-inflammatory effects, thereby leading to oxidative stress-induced damage in the lungs. The objective of this study was to determine if N-acetylcysteineamide (NACA), a novel thiol antioxidant, confers protection to animals exposed to DEPs from oxidative stress-induced damage to the lung. To study this, male C57BL/6 mice, pretreated with either NACA (250 mg/kg body weight) or saline, were exposed to DEPs (15 mg/m³) or filtered air (1.5–3 h/day) for nine consecutive days. The animals were sacrificed 24 h after the last exposure. NACA-treated animals exposed to DEP had significant decreases in the number of macrophages and the amount of mucus plug formation in the lungs, as compared to the DEP-only exposed animals. In addition, DEP-exposed animals, pretreated with NACA, also experienced significantly lower oxidative stress than the untreated group, as indicated by the glutathione (GSH), and malondialdehyde (MDA) levels and catalase (CAT) activity. Further, DEP-induced toxicity in the lungs was reversed in NACA-treated animals, as indicated by the lactate dehydrogenase levels. Taken together, these data suggest that the thiol-antioxidant, NACA, can protect the lungs from DEP-induced inflammation and oxidative stress related damage.     

白藜芦醇对焦虑模型小鼠行为的改善及对氧化应激因子的影响

目的：观察白藜芦醇对氧化应激小鼠焦虑样行为的改善作用及对其体内氧化应激因子的影响。方法：将小鼠随机分为正常组、模型组和给药组,给予小鼠L-丁硫氨酸-亚砜亚胺（BSO）造模后分别给予不同剂量白藜芦醇（10,20,40,80 mg·kg^-1）,采用明暗箱行为学实验观察药物对小鼠焦虑样行为的影响,通过检测小鼠杏仁核及海马中氧化应激相关因子SOD及MDA水平,采用Western blot检测小鼠杏仁核以及海马中NADPH氧化酶亚基gp91phox的表达变化来研究白藜芦醇抗焦虑作用与氧化应激的关系。结果：行为学实验结果显示,给予白藜芦醇（80 mg·kg^-1）48 h后能明显改善BSO引起的焦虑样行为,主要表现在明暗箱实验中小鼠穿梭明暗箱次数增多（P<0.05）以及停留在明箱中时间比变大（P<0.01）,给予白藜芦醇（40,80 mg·kg^-1）小鼠杏仁核（P<0.01,P<0.01）及海马中SOD活力明显增加（P<0.05,P<0.01）,此外给予白藜芦醇（40,80 mg·kg^-1）小鼠杏仁核（P<0.01,P<0.01）及海马中（P<0.05,P<0.01）MAD含量明显减少。Western blot实验结果显示给予白藜芦醇（20,40,80 mg·kg^-1）能明显降低BSO引起的杏仁核gp91phox表达增加（P<0.05,P<0.01,P<0.01）,同时给予白藜芦醇（20,40,80 mg·kg^-1）能明显降低海马中gp91phox表达（P<0.05,P<0.01,P<0.01）。结论：白藜芦醇能逆转氧化应激引起的小鼠焦虑样行为,其机制可能和其改善小鼠体内氧化应激能力有关。