Protection of vascular endothelial cells from hydrogen peroxide-induced oxidant injury by gypenosides,saponins of Gynostemma pentaphyllum

Lipid peroxidation and toxicity associated with oxygen radicals have been suggested as major causes of cancer, atherosclerosis and the aging process. Damage of endothelial cells may lead to cardiovascular and cerebrovascular diseases. Endothelial cells are susceptible to oxidant insult. In the present study, the antioxidant effect of a Chinese medicinal herb, Gynostemma pentaphyllum Makino (Chinese name, Jiaogulan), was investigated in vitro using vascular endothelial cells. Confluent monolayers of bovine pulmonary artery endothelial cells (PAEC) were preincubated with different concentrations of gypenosides (GP, total saponins of Gynostemma pentaphyllum) for 16 h, then washed and incubated with hydrogen peroxide (H₂O₂) for 4 h. Cell injury was assessed by measuring the release of intracellular lactate dehydrogenase (LDH), and cell viability with tetrazolium (MTT) assay. Lipid peroxidation products of PAEC were monitored as thiobarbituric acid-reactive substances (TBARS) with a fluorometric assay. The results showed that 62.5 μM H₂O₂ incubated with PAEC for 4 h increased the percentage of LDH release, decreased cell viability manifested by MTT absorbance at 620 nm, and elevated TBARS. Preincubation of GP (25–150 μg/mL) with PAEC for 16 h before H₂O₂ exposure significantly declined LDH release, increased cell viability, and reduced TBARS. These results demonstrate that gypenosides can protect vascular endothelial cells from oxidant injury. The data thus suggest that gypenosides may be beneficial for the prevention and treatment of atherosclerosis and for retardation of the aging process.     

槲皮素对H2O2致内皮细胞损伤的保护作用

目的:探讨槲皮素对血管内皮细胞损伤的保护作用及机制.方法:采用体外培养的人脐静脉内皮细胞株ECV304,观察内皮细胞加入槲皮素8,4,2 mg·L-1培养24 h后,再加入H2O2培养18h后,造成血管内皮细胞损伤模型.用流式细胞仪测定内皮细胞死亡率,用ELISA法检测内皮细胞培养液血栓调节蛋白(TM)的含量;荧光分光光度法测定内皮细胞培养液中乳酸脱氢酶(LDH)的活性.结果:与H2O2损伤后的模型组相比,槲皮素可以减低细胞死亡率,[模型组细胞死亡率为(28.36±0.10)％,槲皮素高、中、低剂量分别为(8.34±0.01)％,(16.58±0.04)％,(10.12±0.02)％],可使培养液中TM蛋白含量减少,[模型组为(58.5±18.8)μg·L-1,槲皮素高、中、低剂量为(32.7±9.7),(27.8±1.9),(32.1±8.6) μg·L-1]和LDH活性减少[模型组为(1 931.9±159.5) U·L-1,槲皮素高、中、低剂量为(1.092±126.2),(1 159.6±274.2),(1 223.5±120.5)U·L-1].结论:槲皮素能明显保护过氧化氢对内皮细胞的损伤,其保护作用与抗脂质过氧化、保护细胞的完整性有关.     

宁夏枸杞总黄酮对H2O2损伤人脐静脉内皮细胞的保护作用

目的: 研究宁夏枸杞总黄酮对过氧化氢(H₂O₂)损伤的人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVEC)的保护作用及可能的机制. 方法: 采用H₂O₂诱导HUVEC氧化应激损伤模型.实验分为正常组、1 mmol·L^-1H₂O₂损伤模型组、枸杞总黄酮保护(100,200,400 mg·L^-1) 预孵育24 h组,以及阳性对照(维生素C 20 mg·L^-1)组,预孵育24 h.采用噻唑蓝(MTT)法检测枸杞总黄酮对1 mmol·L^-1 H₂O₂损伤 4 h细胞活性,测定细胞上清液中丙二醛(MDA),乳酸脱氢酶(LDH),超氧化物歧化酶(SOD),一氧化氮(NO). 结果: 与正常组比较,H₂O₂损伤模型组MDA含量、LDH活性均增高,NO生成量、SOD活性明显下降,其差异均具有显著性(P<0.01).枸杞黄酮保护组MDA含量、LDH活性均下降,NO生成量、SOD活性较H₂O₂损伤模型组明显增高(P<0.01),MDA含量、LDH活性的下降程度,NO生成量、SOD活性的增高程度,与枸杞总黄酮呈剂量依赖性. 结论: 宁夏枸杞总黄酮对H₂O₂所致人血管内皮损伤有保护作用,其机制可能与宁夏枸杞总黄酮抑制损伤细胞的脂质过氧化,以及有效提高机体抗氧化酶的活性、清除自由基,促进一氧化氮(NO)的合成有关.     

Nrf2-dependent neuroprotective activity of diterpenoids isolated from Sideritis spp

Ethnopharmacological relevance

The species of the genus Sideritis are extensively used in the Mediterranean area in folk medicine for their digestive, antimicrobial, anti-inflammatory and antioxidant properties, among others. Moreover, Sideritis species as tea infusions are popularly known for improving memory function and cognitive ability. Diterpenoids are one of the most abundant and important pharmacological interest of the classes of natural products presented in these medicinal plants.

Aim of the study

To determine for the first time the neuroprotective effects, based on their antioxidant properties, of the three isolated major diterpenoids andalusol, conchitriol and lagascatriol in an oxidative stress model.

Materials and methods

H₂O₂ was used as oxidant inductor and rat adrenal pheochromocytoma PC12 cells as cellular model. Cell viability was measured using MTT and LDH assays, lipid peroxidation was determined by HPLC, GSH and GSSG levels assessed by fluorometric techniques, enzymatic activity and protein expression were determined by spectrofometric techniques and Western blot, respectively.

Results

Pretreatments with the three diterpenoids significantly attenuated H₂O₂-induced changes in mitochondrial integrity and activity (MTT assay), in cell membrane integrity (LDH assay) and in cell morphology. Moreover, these diterpenoids inhibited intracellular ROS production H₂O₂-induced, reduced lipid peroxidation and counteracted GSH/GSSG changes. Furthermore, both activities and protein expression of the endogenous antioxidant enzymes (CAT, SOD, GR, GPx and HO-1) were increased. The Nrf2 pathway was involved, at least in part, in the protective effects of these diterpenoids.

Conclusion

These findings suggest that these natural compounds provide significant antioxidant effects in PC12 under for counteracting the oxidative damage H₂O₂-induced and their potential role as useful agents for the prevention of those oxidative stress-mediated dementia disorders. Andalusol was the most active compound among the studied diterpenoids.     

Ophiopogonin D prevents H2O2-induced injury in primary human umbilical vein endothelial cells

Aim of the study

Vessel endothelium injury caused by reactive oxygen species (ROS) including H₂O₂ plays a critical role in the pathogenesis of cardiovascular disorders. Therefore, drug targeting ROS elimination has highly clinical values in cardiovascular therapy. The plant of Radix Ophiopogon japonicus is a traditional Chinese herbal medicine that has been commonly used for prevention and treatment of cardiovascular diseases for a long history. However, the effective component mediating its beneficial effects remains unknown. In the present study, we investigated the action of Ophiopogonin D (OP-D), one of the most bioactive components of Radix Ophiopogon japonicus, in an endothelial injury model induced by H₂O₂.

Materials and methods

Primarily cultured human umbilical vein endothelial cells (HUVECs) were pretreated with increased doses of OP-D overnight and then challenged with H₂O₂. The protective effects of OP-D against H₂O₂ were evaluated.

Results

We found that OP-D inhibited mRNA levels of antioxidant, inflammatory and apoptotic genes in a dose-dependent manner in HUVECs. H₂O₂-induced lipid peroxidation and protein carbonylation were reduced by OP-D pretreatment. Mitochondrial ROS generation and cell apoptosis were also attenuated in OP-D pretreated cells. In addition, OP-D restored cellular total antioxidative capacity and inhibited the release of inflammatory cytokines. Furthermore, OP-D suppressed the enzymatic activity of catalase, HO-1, and caspases. Finally, OP-D blocked activation of NF-κB and ERK signaling cascades.

Conclusion

Our findings provide the first evidence that OP-D plays a protective role as an effective antioxidant in H₂O₂-induced endothelial injury. Ophiopogonin D can be therefore developed as a novel drug for the therapy of cardiovascular disorders.     

大黄清除活性氧的作用

 目的：检测和确定大黄(Rheum officinale Baill.)清除活性氧的作用。方法：利用多种产生和检测活性氧的化学发光体系来检测大黄清除多种活性氧的作用，并以抑制各体系发光强度50%的大黄浓度(IC₅₀值)作指标。结果：在O₂、H₂O₂、全血吞噬细胞、亚油酸脂质过氧化发光体系中，大黄的IC₅₀值分别为6.0 μg/ml，95 μg/ml，7.5 mg/ml和28 μg/ml。然而，大黄对OH·无清除作用。结论：大黄能清除O₂、H₂O₂和其它活性氧,抑制脂质过氧化，是一种有效的抗氧化剂。     

Protective effect of GCSB-5, an herbal preparation, against peripheral nerve injury in rats

Aim of the study

GCSB-5 (traditional name: Chungpa-Juhn), an herbal medicine composed of 6 crude herbs (Saposhnikovia divaricata Schiskin, Achyranthis bidentata Blume, Acanthopanax sessiliflorum Seem, Cibotium baromets J. Smith, Glycine max Meriill, and Eucommia ulmoides Oliver), has been widely used in Asia for treatment of neuropathic and inflammatory diseases. This study investigated the protective effect of GCSB-5 against peripheral nerve injury in vitro and in vivo.

Materials and methods

After left sciatic nerve transection, rats received oral administration of GCSB-5 (30, 100, 300, and 600 mg/kg), or saline (vehicle), respectively, once daily for 8 weeks. Motor functional recovery and axonal nerve regeneration were evaluated by measurement of sciatic functional index (SFI), sensory regeneration distance, and gastrocnemius muscle mass ratio. The myelinated axon number was counted by morphometric analysis. In the in vitro study, the effects of GCSB-5 on H₂O₂-induced oxidative damage in SH-SY5Y cells were investigated by measurement of cell viability, production of reactive oxygen species (ROS), lipid peroxidation, release of lactate dehydrogenease (LDH), and cellular glutathione contents. Neurite outgrowth was also determined.

Results

After 8 weeks of nerve transection, SFI, regeneration distance, and gastrocnemius muscle mass ratio and myelinated axon number showed a significant decrease and these decreases were attenuated by GCSB-5. GCSB-5 significantly inhibited H₂O₂-induced cell death and oxidative stress, as evidenced by decreases in production of ROS and lipid peroxidation and release of LDH, and by increase in total GSH content.

Conclusions

The neuroprotective effect afforded by GCSB-5 is due in part to reduced oxidative stress.     

基于中药血清药物化学及血清药理学方法探讨荭草保护心肌细胞氧化损伤的物质基础

目的:应用中药血清药物化学及血清药理学方法探讨荭草保护H9c2心肌细胞氧化损伤的物质基础。方法:通过比较荭草提取液、给药后含药血清和空白血清的超高效液相色谱(UPLC)指纹图谱,寻找荭草的入血成分;建立体外培养的H9c2心肌细胞H2O2氧化损伤模型,以荭草含药血清对氧化损伤心肌细胞存活率、乳酸脱氢酶(LDH)漏出率、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力的影响为评价指标,并采用吖啶橙(AO)和溴化乙锭(EB)双荧光染色法观察荭草含药血清对H2O2氧化损伤的心肌细胞形态学的影响,研究荭草含药血清对氧化损伤心肌细胞的保护作用。结果:灌胃给予荭草提取液后,从大鼠血清中发现25个移行成分,其中有9个为荭草中的原型成分,16个可能为其在体内转化的代谢产物;与模型组相比,荭草含药血清各剂量组能明显降低氧化损伤心肌细胞LDH漏出率、MDA含量(P<0.05),显著升高T-SOD活性和细胞存活率(P<0.05或P<0.01),有效抑制细胞凋亡。结论:荭草含药血清中的移行成分及其代谢产物可能是荭草保护心肌细胞氧化损伤的物质基础。     

Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2

Aim of the study

Vessel endothelium injury caused by reactive oxygen species (ROS) including H₂O₂ plays a critical role in the pathogenesis of cardiovascular disorders. Therefore, agents or antioxidants that can inhibit production of ROS has highly clinical values in cardiovascular therapy. Curculigoside is the major bioactive compounds present in Curculigo orchioides, and possess potent antioxidant properties against oxidative stress insults through undefined mechanism(s). The present study was designed to test the hypothesis that curculigoside can inhibit H₂O₂-induced injury in human umbilical vein endothelial cells.

Materials and methods

Human umbilical vein endothelial cells (HUVECs) were treated with curculigoside in the presence/absence of hydrogen peroxide (H₂O₂). The protective effects of curculigoside OP-D against H₂O₂ were evaluated.

Results

HUVECs incubated with 400 μM H₂O₂ had significantly decreased the viability of endothelial cells, which was accompanied with apparent cells apoptosis, the activation of caspase-3 and the upregulation of p53 mRNA expression. In addition, H₂O₂ treatment induced a marked increase of MDA, LDH content and in intracellular ROS, decreased the content of nitric oxide (NO) and GSH-Px activities in endothelial cells. However, pretreatment with 0.5.5,10 μM curculigoside resulted in a significant recovery from H₂O₂-induced cell apoptosis. Also, it decreased other H₂O₂-induced damages in a concentration-dependent manner. Furthermore, pretreatment with curculigoside decreased the activity of caspase-3 and p53 mRNA expression, which was known to play a key role in H₂O₂-induced cell apoptosis.

Conclusion

The present study shows that curculigoside can protect endothelial cells against oxidative injury induced by H₂O₂, suggesting that this compound may constitute a promising intervention against cardiovascular disorders.     

赤芍总苷、川芎总酚酸组分组成结构对缺氧损伤人脐静脉内皮细胞的影响

目的: 研究赤芍总苷、川芎总酚酸组分不同组成结构对连二亚硫酸钠(Na₂S₂O₄)诱导的人脐静脉内皮细胞(HUVEC)缺氧损伤模型的保护作用,并参照基线等比增减法,设计不同组分组成结构,优化出最佳的组分结构。 方法: 采用 Na₂S₂O₄ 体外诱导HUVEC,建立细胞损伤模型。采用MTT比色法测定细胞活力,试剂盒测定细胞内超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量、乳酸脱氢酶(LDH)含量、一氧化氮(NO)含量,通过Western blot检测了各组细胞Bcl-2,Bax蛋白的表达量。 结果: 与模型组比较,赤芍总苷组分、川芎总酚酸组分不同组成结构可显著提高SOD活力,降低MDA,LDH,NO含量 (P<0.01,P<0.05)。芍芎组分可以下调Bax蛋白的表达量,上调Bcl-2蛋白的表达量,Bcl-2/Bax显著升高(P<0.01,P<0.05),抑制细胞凋亡。结果显示赤芍总苷、川芎总酚酸组分组成结构比例为8:2时,对缺氧损伤的内皮细胞保护作用最好。 结论: 芍芎组分可以减轻HUVEC的缺氧损伤,8:2组分组成时保护作用最为明显,其机制可能与其抗氧化和抑制细胞凋亡 有关。     

总丹酚酸和银杏叶提取物对血管平滑肌细胞保护作用的比较

 目的对丹参水溶液提取物总丹酚酸和银杏叶提取物EGb761对血管平滑肌细胞损伤的保护作用进行了比较研究。方法选用培养的10～20代大鼠血管平滑肌细胞用于实验研究。细胞用H₂O₂2(100μmol·L^-1)处理1h造成细胞氧化损伤模型，采用MTT方法观察总丹酚酸和EGb761对H₂O₂损伤细胞生存率的影响，同时以乳酸脱氢酶(LDH)、丙二醛(MDA)、一氧化氮(NO)3种物质变化作为指标，观察了总丹酚酸和EGb761对H₂O₂损伤血管平滑肌细胞的保护作用。结果总丹酚酸100，10 μg·mL^-1能显著提高细胞的存活率，而总丹酚酸1μg·mL^-1和EGb761 100，10，1μg·mL^-1对细胞的存活率没有明显的升高作用；总丹酚酸100 μg·mL^-1，EGb761 100，10，1 μg·mL^-1均能显著降低H₂O₂损伤细胞上清液中LDH 的量，总丹酚酸10，1 μg·mL^-1作用不显著；EGb761 100，10 μg·mL^-1能明显降低细胞上清中MDA的量，EGb761 1 μg·mL^-1及总丹酚酸100，10，1μg·mL^-1作用不明显；总丹酚酸100，10，1 μg·mL^-1和EGb761 100，10 μg·mL^-1明显降低H₂O₂损伤引起NO的释放。结论总丹酚酸和EGb761对H₂O₂损伤的血管平滑肌有保护作用，但作用机制似乎有所不同，需要做进一步研究。     

菟丝子总黄酮对过氧化氢损伤的血管内皮细胞的保护作用

目的:探讨菟丝子总黄酮对H202损伤的人脐静脉内皮细胞(HUVECs)的保护作用.方法:于37℃、5％ CO2、95％空气饱和湿度的培养箱内体外培养内皮细胞,将细胞分为4组,即正常对照组:加入DMEM培养液(pH 7.2 ～7.4)、菟丝子对照组(菟丝子0.5mg·L-1)、模型组(过氧化氢终浓度为200 mmol·L-)、菟丝子+过氧化氢组(菟丝子0.5mg· L-1,过氧化氢200 mmol·L-),研究菟丝子总黄酮对受损血管内皮细胞内超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、乳酸脱氢酶(LDH)释放情况、谷胱甘肽过氧化物酶(GSH-Px)活性及对细胞形态学的影响.结果:菟丝子总黄酮(0.5 mg·L-1)能明显减轻H2O2对HUVECs所致的氧化损伤,可明显改善氧化损伤的HUVECs形态学变化,H2O2模型组(200 mmol·L-)与空白组比较,LDH释放和MDA含量显著升高(P＜0.01,P＜0.05),SOD释放水平和GSH-Px活力显著下降(P＜0.01),菟丝子(0.5mg·L-1)+ H2O2(200 mmol·L-1)组与H2O2模型组(200 mmol·L-1)比较,LDH释放和MDA含量显著下降(P＜0.01,P＜0.05),SOD释放水平和GSH-Px活力显著升高(P＜0.01).结论:菟丝子总黄酮对H202诱导的HUVECs的损伤具有保护作用.     

木豆叶提取物对H_2O_2诱导的H9c2细胞氧化损伤的保护作用及机制研究

目的研究木豆叶提取物(ECCL)对H2O2诱导的H9c2细胞氧化应激损伤的保护作用及其机制。方法建立H2O2诱导的H9c2细胞氧化损伤模型,于H2O2刺激前加入PI3K信号通路阻断剂LY294002(LY)预处理10 min,加入20、50μg/m L ECCL预处理24 h。MTT法检测细胞存活率,比色法测定上清液中乳酸脱氢酶(LDH)、丙二醛(MDA)水平和超氧化物歧化酶(SOD)的活性,Western blotting检测细胞内p-Akt、p-e NOS蛋白表达。结果与模型组比较,ECCL可明显增加H9c2细胞H2O2损伤后细胞存活率(P0.01),增加SOD活力,降低MDA、LDH水平,增加p-Akt和p-e NOS蛋白表达(P0.05、0.01),LY可阻断ECCL对H9c2的上述作用。结论 ECCL能够减轻H2O2所致的H9c2细胞损伤,可能是通过激活PI3K通路促进其下游因子Akt和e NOS磷酸化发挥作用。     

Protective effects of steroids from Allium chinense against H2O2‐induced oxidative stress in rat cardiac H9C2 cells

Allium chinense, a traditional herbal medicine, has been used for the treatment of cardiovascular diseases for hundreds of years. In this study, A. chinense steroids (ACSs) including three steroidal glycosides and their parent aglycones were isolated from the bulbs of A. chinense. For the first time, their cardioprotective effects were evaluated in cultured rat cardiac H9C2 cells by pretreatment with ACSs for 24 h before exposure to 0.2 mm H₂O₂. The results showed the cell viability decreased markedly when H9C2 cells were incubated with 0.2 mm H₂O₂ alone for 2 h, while the cell lipid peroxidation (estimated by the excessive production of nitric oxide and malondialdehyde) and intracellular free calcium concentration ([Ca²⁺]_i) increased significantly. The addition of 20 μm (below the toxic concentration) of ACSs notably attenuated the cellular injury induced by H₂O₂. The effects of ACSs in our experiments were similar to those of nimodipine, a clinically applied calcium channel blocker. Preliminary analysis of the structure–activity relationship indicated that ACSs with a spirostane‐type skeleton exhibited stronger protection than that with a furostane‐type skeleton, and glycosylation of the steroids could substantially lower the protective activities. The above results suggested the protective effects of steroids originated from A. chinense on the oxidative injury of H9C2 cells and ACSs may have potential for preventing cardiac injuries induced by oxidative stress. Copyright © 2009 John Wiley & Sons, Ltd.     

竹节参总皂苷对H2 O2致乳鼠心肌细胞氧化应激损伤的保护作用

目的:通过建立H2O2诱导心肌细胞氧化应激损伤模型,观察竹节参总皂苷(SPJ)对心肌细胞的保护作用.方法:将原代培养的乳鼠心肌细胞随机分为正常组,模型组(H2O2),SPJ低剂量组(50 mg·L-1),SPJ高剂量组(100 mg·L-1).H2O2诱导心肌细胞氧化损伤2h后SPJ孵育24 h,显微镜下观察细胞搏动频率,MTT法测定细胞存活率,比色法测定细胞培养上清液中乳酸脱氢酶( LDH)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)的活性及丙二醛( MDA)含量.结果:SPJ(50,100 mg·L-1)可明显增加心肌细胞搏动频率,降低H2O2所致乳鼠心肌细胞LDH释放量,升高SOD,CAT,GSH-Px活性,降低MDA含量(P＜0.01或P＜0.05).结论:SPJ对H2O2所致乳鼠心肌细胞氧化应激损伤有明显保护作用.     

补肾抗衰片对EA.hy 926细胞过氧化损伤的影响

目的：观察补肾抗衰片对EA.hy 926细胞氧化应激损伤的影响。方法：采用过氧化氢（H₂O₂）诱导EA.hy 926细胞损伤建立EA.hy 926细胞过氧化模型,以CCK-8法评价模型。实验分为空白对照组、实验对照组、H₂O₂过氧化损伤模型组以及补肾抗衰片干预组,利用CCK-8法测定各组细胞活力,采用流式细胞术检测EA.hy 926细胞内的总氧化水平（ROS）,采用免疫荧光法检测HO-1蛋白水平。结果：补肾抗衰片具有抗H₂O₂诱导的EA.hy 926细胞过氧化损伤,维持细胞氧化还原平衡状态的效应。结论：补肾抗衰片抗氧化损伤,维持细胞氧化还原平衡可能与调节HO-1蛋白水平有关。     

海带褐藻多糖硫酸酯的抗氧化活性研究

目的 研究海带褐藻多糖硫酸醋的抗氧化作用。方法 采用体外实验研究海带褐藻多糖硫酸醢对超氧阴离子、羟自由基、DPPH的清除作用以及对H2O2诱导的红细胞氧化溶血和大鼠肝匀浆脂质过氧化的保护作用。结果 海带褐藻多糖硫酸醋对超氧阴离子具有良好的清除作用，IC50为20．3μg／mL，其对羟自由基的清除作用较弱，对有机自由基DPPH的作用很弱。褐藻多糖硫酸醋能够抑制H2O2诱导的红细胞氧化溶血，对FeSO4-抗坏血酸体系造成的脂质过氧化具有良好的保护作用。结论 海带褐藻多糖硫酸醋具有显著的体外抗氧化活性。     

羟乙葛根素对过氧化氢致牛脑微血管内皮细胞损伤的保护作用

 目的研究过氧化氢损伤牛脑微血管内皮细胞(BCMEC_s)的机制及羟乙葛根素的保护作用。方法比色法测定培养液中乳酸脱氢酶(LDH)活性,硫代巴比妥酸法测定细胞内和培养液中脂质过氧化产物丙二醛(MDA)含量,黄嘌呤氧化酶法检测细胞内和培养液中超氧化物歧化酶(SOD)的活性,放射性免疫法检测细胞培养液中血栓素A₂的最终代谢产物血栓素B₂(TXB₂)的水平和前列环素最终代谢产物6-酮基前列腺素1α(6-keto-PGF1α)的含量。结果H₂O₂(200μmol·L^-1)损伤后,BCMEC_sLDH释放水平、MDA含量呈时间依赖性增加,SOD活性呈时间依赖性降低,羟乙葛根素能够呈浓度依赖性降低LDH水平和MDA含量,提高SOD活性;H₂O₂(200μmol·L^-1)损伤BCMEC_s后,细胞培养液中TXB₂含量显著升高、6-keto-PGF1α含量显著降低,羟乙葛根素能够呈浓度依赖性降低TXB₂含量、升高6-keto-PGF1α水平。结论羟乙葛根素对过氧化氢损伤BCMEC_s后的脑血管内皮细胞功能具有保护作用,其机制与抗氧化作用有关。     

Effect of Cinnamoyl and Flavonol Glucosides Derived from Cherry Blossom Flowers on the Production of Advanced Glycation End Products (AGEs) and AGE‐induced Fibroblast Apoptosis

Cherry blossom flowers are familiar to the Japanese, and some species of the flowers soaked in salty vinegar are used as processed foods. The constituents of aqueous ethanol extract from cherry blossom (Prunus lannesiana) flowers (CBE) were examined and cinnamoyl and flavonol glucosides were isolated. To elucidate the pharmacological functions of CBE and its constituents, their effects on the production of advanced glycation end products (AGEs) and on AGE‐induced fibroblast damage were examined. CBE and 1‐O‐(E)‐caffeoyl‐β‐d ‐glucopyranoside (CaG), a principal compound in CBE, significantly suppressed the production of AGEs derived from glucose and albumin at 100 μg/mL. Among the flavonol glucosides, quercetin 3‐O‐β‐d ‐glucopyranoside (QG) exhibited potent suppressive activity (IC₅₀: 30 μg/mL). CBE and CaG suppressed glyoxal‐induced AGE production in fibroblasts at 10 μg/mL, but QG did not. In addition, CBE and CaG recovered collagen lattice formation consisting of collagen and glycated fibroblasts at 10 μg/mL. Moreover, CBE and its constituents, except kaempferol 3‐O‐(6″‐malony)‐β‐d ‐glucopyranoside, significantly suppressed fibroblast apoptosis induced by carboxymethyl lysine‐collagen at 10 μg/mL. These results show that cinnamoyl and flavonol glucosides of cherry blossom flowers suppress AGE production and AGE‐induced fibroblast apoptosis. Cherry blossom flowers may be effective against skin AGE production and fibroblast damage by AGEs. Copyright © 2011 John Wiley & Sons, Ltd.     

黄芪活性提取成分对膜脂质过氧化损伤的防护作用

采用3种活性氧产生体系诱发膜脂质过氧化为实验模型,观察了黄芪活性提取成分对膜脂质过氧化作用的防护效能。结果表明,黄芪活性提取成分对多种自由基均有良好的清除作用,其中黄芪总黄酮和黄芪总皂甙的作用最佳。