不同生境人参茎叶总皂苷对气虚血瘀大鼠的作用比较

目的通过相关指标的检测,探究园参茎叶总皂苷和林下山参茎叶总皂苷对气虚血瘀模型大鼠的作用差异,为不同生境人参茎叶资源的开发利用提供理论依据。方法采用游泳力竭联合肾上腺素皮下注射法,构建气虚血瘀模型大鼠。分别给予不同剂量(10、20、40 mg/kg)园参茎叶总皂苷和林下山参茎叶总皂苷干预后,经腹主动脉取血,进行血液流变学检测;通过酶联免疫吸附法检测肌酸激酶(CK)、肌酸激酶同工酶MB(CK-MB)、内皮素-1(ET-1)、一氧化氮(NO)、血栓素B2(TXB2).Na^(+)-K^(+)-ATP酶的表达。结果与正常组相比,模型组的各项指标均有显著升高或降低,具有统计学意义(P<0.01)。与模型组相比,园参茎叶总皂苷和林下山参茎叶总皂苷给药对降低气虚血瘀模型大鼠血清CK CK-MB.ET-1.TXB2水平及全血黏度高切、中切、低切水平.提高气虚血瘀模型大鼠血清NO.Na_(+)-K^(+)-ATP酶水平均具有--定的作用,并且具有统计学差异(P<005,P<0.01)。而园参茎叶总皂苷与林下山参茎叶总皂苷对气虚血瘀模型大鼠的改善作用未见统计学差异(P>0.05)。结论园参茎叶总皂苷和林下山参茎叶总皂苷均能改善气虚血瘀模型大鼠的血液流变学指标,其作用机制可能与保护心肌细胞.改善内皮功能、保证能量代谢等有关;且同等剂量园参茎叶总皂苷与林下山参茎叶总皂苷对气虚血瘀模型大鼠的作用相当。     

淡豆豉提取物对2型糖尿病大鼠主动脉iNOS,eNOS mRNA表达的影响

为观察淡豆豉提取物对NO/NOS系统的影响,探讨其对2型糖尿病大鼠大血管保护作用的机制。采用高糖高脂饲料喂养加小剂量链尿佐菌素腹腔注射的方法复制2型糖尿病大鼠模型,给药56 d后检测大鼠空腹血糖(FBG)、血清胰岛素(FIN),计算胰岛素敏感指数(ISI),放免法检测血清肿瘤坏死因子-α(TNF-α)及一氧化氮(NO)水平,RT-PCR法检测主动脉内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)mRNA表达。结果显示:淡豆豉提取物能显著降低T2DM大鼠FBG、FIN、TNF-α、NO水平,显著提高ISI,显著降低iNOS mRNA表达,对eNOS mRNA表达则无明显影响。淡豆豉提取物可影响2型糖尿病大鼠NO/NOS系统,并可能通过此途径对2型糖尿病大鼠大血管产生保护作用。     

白茶提取物对纳米SiO2诱导的大鼠肺纤维化的抑制作用及机制

硅肺是吸入SiO₂粉尘引起的以肺间质纤维化为主的全身性疾病。探讨了白茶提取物对纳米SiO₂诱导大鼠肺纤维化的抑制作用及机制。54只Wistar大鼠随机分为正常组、模型组、白毫银针提取物组、白牡丹提取物高和低剂量组、EGCG组共6个组,每组9只大鼠。除正常组外的其余5个组采用非暴露式气管插管方法造模纳米SiO₂粉尘(80 mg·mL^-1),每天以灌胃方式给予药物两周之后,检测肺组织中羟脯氨酸(HYP)、一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)和谷光甘肽过氧化物酶(GSH-Px)含量以及肺组织形态学变化。结果显示,与模型组相比,白茶提取物各处理组及EGCG组病理形态改变有不同程度的减轻,其中白毫银针提取物组的效果最佳。白茶提取物各处理组与EGCG组的大鼠肺NO含量和炎症因子IL-6都显著低于模型组(P<0.05),GSH-Px活力高于模型组(P<0.05),高剂量白牡丹提取物对降低NO含量和升高GSH-Px活力效果最好;本研究表明,白茶提取物对于纳米SiO₂引起的大鼠肺纤维化氧化应激损伤具有有效的减缓和修复作用,主要与其抗氧化作用和抑制炎症反应相关。     

不同剂型儿茶素对小鼠血清脂质水平的影响

本文探讨了不同剂型儿茶素经不同给予途径对高脂血症小鼠血清脂质水平的影响。结果表明:将儿茶素制成微型胶囊剂型,即经高分子胶体化合物包封后,降低TG、TC、LDL-C和升高HDL-C的作用明显优于游离型儿茶素(P<0.05),静脉注射效果优于口服(P<0.05)。     

乌龙药茶对高脂血症大鼠血脂水平的调节和血管内皮保护作用的研究

采用高脂饲料饲喂法建立高脂血症大鼠模型,通过药、茶和乌龙药茶分别灌胃,实验35d后,检测大鼠血液丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆固醇(TCHO)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、一氧化氮(NO)和内皮素-1(ET-1)的含量,以及观察大鼠的一般情况和肝、肾组织的病理变化,来观察乌龙药茶对实验性高脂血症大鼠血脂水平调节和血管内皮细胞的保护作用。结果表明,药、茶和乌龙药茶均能明显降低模型大鼠血液TCHO、TC、LDL-C和ET-1含量,提高HDL-C和NO含量(P<0.05,P<0.01),其中,乌龙药茶作用显著优于药、茶。研究结论,药、茶和乌龙药茶均能显著调节机体的血脂水平,有效预防高脂血症和保护血管内皮细胞功能;乌龙药茶表现为药与茶两者协同作用、提高功效。     

豆豉对早期动脉粥样硬化大鼠主动脉平滑肌细胞凋亡的影响

观察豆豉对早期动脉粥样硬化大鼠主动脉平滑肌细胞凋亡及相关凋亡基因突变型p53和Fas蛋白表达的调节作用,以探讨其机制.采用高脂饲料喂养法建立大鼠早期动脉粥样硬化模型,同时连续10周灌胃给予豆豉提取物进行干预.末次给药后处死动物,光镜下观察血管平滑肌细胞的形态,透射电镜观察超微结构,采用流式细胞术检测细胞凋亡率以及凋亡相关基因突变型p53和Fas蛋白的表达.模型对照组主动脉平滑肌细胞的凋亡率及增值指数(FI)明显高于正常对照组(P＜0.05),053蛋白表达上调;豆豉干预组(20 g生药·kg-1,dO g生药·kg-1)大鼠主动脉平滑肌细胞的凋亡率明显高于模型对照组(P＜0.05),增殖指数明显低于模型对照组(P＜0.05),Fas蛋白表达上调(P＜0.05),p53蛋白表达下调(P＜0.05),光镜及透射电镜可见主动脉损伤明显较模型对照组改善.豆豉可调节早期动脉粥样硬化大鼠血管平滑肌细胞凋亡与增殖的平衡,其机制可能与调节突变型p53和Fas蛋白的表达有关.     

仙牛腰骶痛颗粒对血瘀证大鼠活血化瘀作用研究

目的对血瘀证大鼠模型相关指标检测,探究仙牛腰骶痛颗粒活血化瘀作用。方法采用冰浴联合皮下注射肾上腺素造成大鼠急性血瘀证模型,连续给药14d,腹主动脉取全血,进行血液流变学检测,并检测大鼠血清中7种相关生化指标CPK、ET-1、Na~+-K~+-ATP、LDH、NO、MDA、SOD的含量。结果与空白比较,模型组全血粘度明显升高(P0.001,P0.01),血清中CPK、ET-1、MDA、NO活性增强(P0.001,P0.01,P0.05);与模型组比较,仙牛腰骶痛颗粒能降低全血黏度(P0.05),血清中CPK、ET-1、MDA、NO、LDH含量降低(P0.01,P0.05),提高SOD、Na~+-K~+-ATP含量(P0.05)。结论仙牛腰骶痛颗粒可能通过降低磷酸肌酸激酶、内皮素改善血管壁弹性;同时,提高钠钾ATP酶活力,降低乳酸脱氢酶生成进而降低血液粘度达到活血化瘀的作用。     

大豆异黄酮对奶牛乳腺上皮细胞增殖及泌乳性能的影响

通过体外细胞培养方法研究大豆异黄酮对奶牛乳腺上皮细胞增殖及泌乳性能的影响。取对数生长期的奶牛乳腺上皮细胞,用无血清培养基培养24 h,使细胞同步化后分组试验。试验分空白对照组(0 mg/L大豆异黄酮)和添加不同浓度大豆异黄酮(1、10、100、1 000 mg/L)组,培养48 h后,采用CASY细胞计数仪检测细胞增殖能力与活力,高效液相色谱检测β-酪蛋白和乳糖,甘油三酯检测试剂盒检测甘油三酯的分泌情况。结果表明,与对照组相比,10、100、1 000 mg/L大豆异黄酮组奶牛乳腺上皮细胞的增殖能力与活力显著增强(P<0.05);细胞分泌β-酪蛋白、乳糖和甘油三酯的能力也显著提高(P<0.05)。因此,添加10、100、1 000 mg/L大豆异黄酮均能促进奶牛乳腺上皮细胞增殖及提高其泌乳性能,且呈一定的浓度依赖性。     

儿茶素组成和理化条件对茶黄素酶催化合成的影响

利用梨果实多酚氧化酶,在单因素试验基础上,设计正交试验,进行酶性合成茶黄素,研究儿茶素组成和理化条件对茶黄素合成的影响,以确定最佳反应条件。结果表明,以儿茶素混合物C(EGC>200mg/g,EGCG>200mg/g,儿茶素总量>500mg/g)为材料,茶黄素酶促合成的最佳条件为:反应体系的最佳pH值为5.5,温度为30℃,底物浓度为5mg/ml,酶添加量为75ml/1000mg,最佳反应时间40min。pH值和儿茶素浓度是反应体系中两个重要的影响因子(P<0.05)。     

参红补血颗粒对血虚型血管内皮功能障碍小鼠的作用研究

目的探讨参红补血颗粒(SBG)对血虚型血管内皮功能障碍(VED)小鼠模型的血管内皮保护作用,阐明其相关作用机制。方法通过腹腔注射环磷酰胺联合乙酰苯肼法建立血虚型VED小鼠模型,随机分为VED组、阳性对照组、SBG高剂量组、SBG中剂量组和SBG低剂量组,以腹腔注射等量生理盐水小鼠作为对照组。观察小鼠脏器指数,外周血象指标,HE染色法观察小鼠胸主动脉组织病理形态学,试剂盒检测血清中一氧化氮(NO)含量和胸主动脉组织中谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性,Western blotting法检测胸主动脉组织中TLR4、MyD88、NF-κBp65、ICAM-1蛋白表达量。结果与VED组比较,阳性对照组及SBG高、中、低剂量组小鼠胸腺指数显著升高,脾脏指数明显降低(P<0.01,P<0.05),RBC、HGB、HCT、WBC、PLT水平显著升高(P<0.01,P<0.05),GSH-Px和SOD水平显著升高(P<0.01,P<0.05),TLR4、MyD88、NF-κBp65、ICAM-1明显降低(P<0.01,P<0.05)。结论SBG可以通过抑制TLR4信号通路,降低炎症因子水平,减轻氧化应激损伤,达到保护气滞血瘀型VED小鼠血管内皮的作用。     

Chungtaejeon,a Korean Fermented Tea,Scavenges Oxidation and Inhibits Cytokine Induced Proliferation and Migration of Human Aortic Smooth Muscle Cells

Oxidation susceptibility of serum lipid and the proliferation and migration of vascular smooth muscle cells (VSMC) from tunica media to the sub endothelial region are the key steps in the progression of atherosclerosis. The objective of this study was to determine the effects of Chungtaejeon (CTJ) on oxidation and cytokine induced proliferation and migration of human aortic smooth muscle cells (HASMC). The antioxidative effects of CTJ were evaluated by using 1,1-diphenyl-2-picryl hydrazyl (DPPH) scavenging assay, nitric oxide (NO) scavenging assay and thiobarbituric acid reactive substance (TBARS) assay. Similarly, the proliferation, migration and expression of matrix metalloproteinases (MMPs) in HASMC were assessed by MTT assay, transwell Boyden chamber assay and gelatin zymography, respectively. Western blotting was done to determine the protein expression of MMP-9, phospho extracellular regulated kinase (pERK1/2) and phospho c-Jun N-terminal kinase (pJNK). In results, the IC₅₀ values for DPPH and NO scavenging activities were 8.91 μg/ml and 14.32 μg/ml, respectively. Furthermore, CTJ inhibited TBARS formation dose dependently. The pretreatment of CTJ dose dependently inhibited the tumor necrosis factor-α (TNF-α) induced proliferation and MMP-9 expression and platelet derived growth factor (PDGF) induced migration of HASMC. Thus, CTJ can be suggested to have beneficial effect in the prevention of atherosclerosis.     

Marine cyclotripeptide X-13 promotes angiogenesis in zebrafish and human endothelial cells via PI3K/Akt/eNOS signaling pathways

Cyclotripeptide X-13 is a core of novel marine compound xyloallenoide A isolated from mangrove fungus Xylaria sp. (no. 2508). We found that X-13 dose-dependently induced angiogenesis in zebrafish embryos and in human endothelial cells, which was accompanied by increased phosphorylation of eNOS and Akt and NO release. Inhibition of PI3K/Akt/eNOS by LY294002 or L-NAME suppressed X-13-induced angiogenesis. The present work demonstrates that X-13 promotes angiogenesis via PI3K/Akt/eNOS pathways.     

Xyloketal B Attenuates Atherosclerotic Plaque Formation and Endothelial Dysfunction in Apolipoprotein E Deficient Mice

Our previous studies demonstrated that xyloketal B, a novel marine compound with a unique chemical structure, has strong antioxidant actions and can protect against endothelial injury in different cell types cultured in vitro and model organisms in vivo. The oxidative endothelial dysfunction and decrease in nitric oxide (NO) bioavailability are critical for the development of atherosclerotic lesion. We thus examined whether xyloketal B had an influence on the atherosclerotic plaque area in apolipoprotein E-deficient (apoE^−/−) mice fed a high-fat diet and investigated the underlying mechanisms. We found in our present study that the administration of xyloketal B dose-dependently decreased the atherosclerotic plaque area both in the aortic sinus and throughout the aorta in apoE^−/− mice fed a high-fat diet. In addition, xyloketal B markedly reduced the levels of vascular oxidative stress, as well as improving the impaired endothelium integrity and NO-dependent aortic vasorelaxation in atherosclerotic mice. Moreover, xyloketal B significantly changed the phosphorylation levels of endothelial nitric oxide synthase (eNOS) and Akt without altering the expression of total eNOS and Akt in cultured human umbilical vein endothelial cells (HUVECs). Here, it increased eNOS phosphorylation at the positive regulatory site of Ser-1177, while inhibiting phosphorylation at the negative regulatory site of Thr-495. Taken together, these findings indicate that xyloketal B has dramatic anti-atherosclerotic effects in vivo, which is partly due to its antioxidant features and/or improvement of endothelial function.     

L-arginine supplementation influenced nitrite but not nitrate and total nitrite in rabbit model of hypercholesterolemia

Background: The assessment of altered nitric oxide (NO) availability is of potentially important diagnostic and prognostic significance. The present study is aimed to investigate the effect of L-arginine (as a natural NO donor) supplementation on NO metabolite in a rabbit model of hypercholesterolemia to find a reliable marker for endothelial NO production. Methods: White male rabbits (n = 30) randomly assigned to 2 groups. Rabbits were fed 1% high-cholesterol diet (HC group, n = 15), or HC diet with oral L-arginine (3% in drinking water) (HC + L-arginine group, n = 15) for 4 weeks. The serum levels of lipids, L-arginine, total NO metabolites (NOx), nitrite and nitrate were measured before and after the study. Results: In this study, L-arginine supplementation led to a significant increased plasma level of L-arginine. The serum level of nitrite was significantly higher in L-arginine treated group while serum level of nitrate and NOx was significantly lower than HC group. Conclusion: As the result of our study showed, nitrite is a useful marker of endogenous endothelial NO production and although frequently used, neither nitrate nor NOx are reliable markers of acute changes in endothelial NO synthase activity.     

Nitric Oxide Synthase in the Central Nervous System and Peripheral Organs of Stramonita haemastoma: Protein Distribution and Gene Expression in Response to Thermal Stress

Nitric oxide (NO) is generated via the oxidation of l-arginine by the enzyme NO synthase (NOS) both in vertebrates and invertebrates. Three NOS isoforms, nNOS, iNOS and eNOS, are known in vertebrates, whereas a single NOS isoform is usually expressed in invertebrates, sharing structural and functional characteristics with nNOS or iNOS depending on the species. The present paper is focused on the constitutive Ca²⁺/calmodulin-dependent nNOS recently sequenced by our group in the neogastropod Stramonita haemastoma (ShNOS). In this paper we provide new data on cellular distribution of ShNOS in the CNS (pedal ganglion) and peripheral organs (osphradium, tentacle, eye and foot) obtained by WB, IF, CM and NADPHd. Results demonstrated that NOS-like proteins are widely expressed in sensory receptor elements, neurons and epithelial cells. The detailed study of NOS distribution in peripheral and central neurons suggested that NOS is both intracellular and presynaptically located. Present findings confirm that NO may have a key role in the central neuronal circuits of gastropods and in sensory perception. The physiological relevance of NOS enzymes in the same organs was suggested by thermal stress experiments demonstrating that the constitutive expression of ShNOS is modulated in a time- and organ-dependent manner in response to environmental stressors.     

Dihydroaustrasulfone Alcohol Inhibits PDGF-Induced Proliferation and Migration of Human Aortic Smooth Muscle Cells through Inhibition of the Cell Cycle

Dihydroaustrasulfone alcohol is the synthetic precursor of austrasulfone, which is a marine natural product, isolated from the Taiwanese soft coral Cladiella australis. Dihydroaustrasulfone alcohol has anti-inflammatory, neuroprotective, antitumor and anti-atherogenic properties. Although dihydroaustrasulfone alcohol has been shown to inhibit neointima formation, its effect on human vascular smooth muscle cells (VSMCs) has not been elucidated. We examined the effects and the mechanisms of action of dihydroaustrasulfone alcohol on proliferation, migration and phenotypic modulation of human aortic smooth muscle cells (HASMCs). Dihydroaustrasulfone alcohol significantly inhibited proliferation, DNA synthesis and migration of HASMCs, without inducing cell death. Dihydroaustrasulfone alcohol also inhibited platelet-derived growth factor (PDGF)-induced expression of cyclin-dependent kinases (CDK) 2, CDK4, cyclin D1 and cyclin E. In addition, dihydroaustrasulfone alcohol inhibited PDGF-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), whereas it had no effect on the phosphorylation of phosphatidylinositol 3-kinase (PI3K)/(Akt). Moreover, treatment with PD98059, a highly selective ERK inhibitor, blocked PDGF-induced upregulation of cyclin D1 and cyclin E and downregulation of p27^kip1. Furthermore, dihydroaustrasulfone alcohol also inhibits VSMC synthetic phenotype formation induced by PDGF. For in vivo studies, dihydroaustrasulfone alcohol decreased smooth muscle cell proliferation in a rat model of restenosis induced by balloon injury. Immunohistochemical staining showed that dihydroaustrasulfone alcohol noticeably decreased the expression of proliferating cell nuclear antigen (PCNA) and altered VSMC phenotype from a synthetic to contractile state. Our findings provide important insights into the mechanisms underlying the vasoprotective actions of dihydroaustrasulfone alcohol and suggest that it may be a useful therapeutic agent for the treatment of vascular occlusive disease.     

接种茄病镰刀菌(Fusarium solani f.sp.glycines)对不同基因型大豆植株和须根的影响

摘要：茄病镰刀菌（Fusarium solani f．sp．glydne）是一种土生细菌,通过侵染大豆根系引发猝死综合症。利用温室盆栽试验和须根培养试验研究了接种茄孢镰刀菌对13个不同基因型大豆的影响。结果表明：接种后所有盆栽大豆主根都有明显深褐色的侵染病斑;移植后21d测定了盆栽植株叶部发病程度,Peking表现最为严重,然后依次为Spencer,Ripley,P3981,Williams82,Essex,Forrest,Iroquois,PI520733,Hartwig,PI567650B,Jack,和PI567374。叶部发病程度与冠高（r=-0．422,P=0．0018）、冠重（r=-0．857,P〈0．0001）和根重（r=-0．732,P〈0．0001）呈显著负相关。主根病斑长度与叶部发病程度没有相关性,表明大豆对病原菌的抗性不能仅通过根系得到充分控制。对培养的大豆须根接种茄病镰刀菌菌丝体10d后,不同基因型大豆的菌落直径的变化范围为17—40mm,差异显著（P=0．05）,其中Spencer和Peking须根上的菌落直径显著（P=0．05）大于PI567374和PI520733。对Spencer和PI567374的须根接种10灿茄病镰刀菌常量成分悬浮液,10d后菌落直径分别为50和38mm,差异显著（P=0．05）。通常,不同基因型大豆间茄病镰刀菌在培养须根上的生长与整株的症状间有一定的相关性,但不总是这样,这是因为即使根系对毒素产生抗性来减少叶部病害症状,但并不是所有的大豆都表现出明显的根系抗性。     

Vasorelaxant and hypotensive effects of Allium cepa peel hydroalcoholic extract in rat

The aim of present study was to investigate the effect of onion (Allium cepa) peel hydroalcoholic extract (OPE) on rat hypertension induced by high-fructose diet and aorta contractility. The OPE was prepared by maceration method using 70% ethanol. The thoracic aorta from male adult rat (Wistar) was dissected and suspended in Krebs-Henseleit solution under 1 g resting tension. Tissue preparation was contracted by KCl (80 mM) or phenylephrine (Phe, 1 microM) and then the extract was applied cumulatively (0.0625-2 mg mL(-1)). Hypertension was induced in negative control and three groups of rats by adding fructose (10% WN/V) in drinking water for 6 weeks but control group received tap water. Hypertensive groups received saline or OPE at 200, 400 and 800 mg kg(-1) daily for last 3 weeks by gavage. Results showed that OPE reduces aorta contractions induced by KCl or Phe in a concentration-dependent manner (p < 0.001). Removing aorta endothelium did not attenuate the OPE activity. Inhibition of nitric oxide, cGMP and prostaglandin synthesis by L-NAME (100 microM), methylene blue (10 microM) and indomethacin (10 microM), respectively, did not attenuate OPE activity. Atropine abolished ACh-induced relaxation in Phe precontracted aorta but not the OPE-induced relaxation. Although the extract did not change heart rate but after 3 weeks reduced the hypertension induced by fructose (p < 0.001). Present results indicated that OPE reduces aortic contractions possibly via inhibition of calcium influx but without involving NO, cGMP, endothelium and prostaglandins. The OPE hypotensive effect could be due to extract quercetin content, antioxidant activity and inhibiting vascular smooth muscle cells Ca2+ influx.     

茶黄素激活Nrf2/HO-1通路保护血管内皮细胞氧化应激损伤

为探讨茶黄素（Theaflavin,TF）对过氧化氢（H₂O₂）诱导的血管内皮细胞氧化应激损伤的保护效应及作用机制,将人脐静脉血管内皮细胞HUVEC分为对照组、损伤组（0.2 mmol·L^-1 H₂O₂处理）和TF预处理组（2.0、5.0、10.0 μmol·L^-1 TF和0.2 mmol·L^-1 H₂O₂处理）。损伤组和TF组均以H₂O₂处理24 h,其中TF组先以不同浓度TF预处理2 h,对照组均以定量溶剂处理。以MTT法测定细胞活力,DCFH-DA探针测定活性氧（ROS）水平,流式细胞术检测细胞凋亡,Western blot测定蛋白表达水平,相应试剂盒测定乳酸脱氢酶（LDH）、一氧化氮（NO）、丙二醛（MDA）含量及超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化氢酶（GSH-Px）活性。结果显示,与对照组相比,损伤组细胞活力显著降低,LDH释放量增加,NO水平降低,胞内ROS水平升高,MDA增加,抗氧化酶活力降低,细胞凋亡升高;TF预处理能够显著提高细胞活力,降低LDH水平,维持NO水平,降低胞内ROS水平及MDA的产生,提高抗氧化酶活力,并抑制细胞凋亡;进一步研究显示,TF能够激活Nrf2/HO-1通路,且Nrf2抑制剂会显著降低TF的内皮细胞保护效应。可见,TF能够有效抑制H₂O₂诱导的血管内皮细胞氧化应激损伤,其机制至少部分是通过激活Nrf2/HO-1通路实现的。