RP-HPLC法测定天葵子中格列风内酯的含量

目的建立使用反相高效液相法测定天葵子药材中苯骈呋喃酮型内酯格列风内酯含量的方法。方法使用迪马Kromasil ODS柱,流动相为甲醇-水(含0·01 %三氟醋酸,0·05 %四氢呋喃) (3∶97),检测波长为260 nm。结果在0·004 -0·4 mg·mL-1的范围内,峰面积与浓度线性良好,相关系数为r=1·000 00;平均回收率为98·77 %; RSD =2·77 %。结论本文对天葵子药材进行了质量控制方面的研究,并首次报道了格列风内酯的含量测定方法。本法快速、准确、灵敏度高,可以作为天葵子药材中格列风内酯含量测定的方法。     

热休克蛋白70在老年性白内障晶状体上皮细胞中的表达及意义

目的:探讨热休克蛋白70(heat shock protein70,HSP70)在老年性白内障晶状体上皮细胞中的表达及意义.方法: 采用PV-6000通用型免疫组织化学染色,检测老年性白内障晶状体前囊膜53例,其中皮质性白内障24例,核性白内障17例,后囊下白内障12例,正常人晶状体前囊膜6例中晶状体上皮细胞中HSP70的表达.并进行阳性细胞计数. 结果:老年性白内障与正常晶状体上皮细胞中均有HSP70表达,其中HSP70在老年性白内障中表达明显高于正常对照组,差异有显著性意义(P＜0.05).老年性白内障组各亚型间有显著性差异(P＜0.05).结论:HSP70可能在老年性白内障的发生、发展中起重要作用.     

Protective effect of docosahexaenoic acid against hydrogen peroxide-induced oxidative stress in human lymphocytes

Oxidatively stressed lymphocytes exhibit decreased proliferative response to mitogenic stimulation. Although several sensitive targets involved in lymphocyte suppression have already been identified, little is known about the influence of oxidative stress on cyclic nucleotide phosphodiesterases (PDE) (EC 3.1.4.17), thought to play a major role in the control of cyclic AMP (cAMP) level, a well-recognized negative effector of lymphoproliferation. Although the polyunsaturated fatty acid content of membrane phospholipids is thought to be directly related to the extent of oxidant-induced lipid peroxidation, some n-3 fatty acids also seem to have antioxidant effects, depending on the concentration used and the overall redox status of the cells in question. Results of the present study showed that human peripheral blood mononuclear cells (PBMC) as well as rat thymocytes were relatively resistant to a short-term exposure (10 min) to hydrogen peroxide (H2O2). Indeed, H2O2-induced lipid peroxidation, estimated by malondialdehyde (MDA) production, was only 2-fold increased by H2O2 concentrations lower than 2 mM, whereas a larger increase (10-fold) could be observed in PBMC at the highest dose (5 mM). Previous enrichment of PBMC with 5 microM docosahexaenoic acid (22:6n-3), brought to the cells as a fatty acid-albumin complex (ratio 1), significantly reduced MDA production induced by low doses of H2O2, the protective effect no longer being observed at the highest doses. In contrast, eicosapentaenoic acid (20:5n-3) did not have any protective effect. Cytosolic PDE activities of both human PBMC and rat thymocytes were significantly inhibited (40-50%) after H2O2 treatment of the cells, whereas particulate PDE activities were not modified. Different responses of PDE activities to H2O2 treatment were observed when PBMC were first enriched with 22:6n-3 prior to H2O2 addition. In 22:6n-3-treated cells, the H2O2-induced inhibition of both cAMP- and cGMP-PDE cytosolic activities was abolished, whereas the particulate activities were increased by the highest H2O2 concentration used (5 mM). At the same time, the glutathione peroxidase (glutathione: oxidoreductase, EC 1.11.1.9) (GSH-Px) activity of PBMC and thymocytes was only marginally inhibited by H2O2 addition (20%), and pretreatment of the cells with 22:6n-3 did not modify the slight inhibitory effect of H2O2. Collectively, these results suggest that lymphocytes are relatively resistant to H2O2-induced lipid peroxidation due to their high GSH-Px content, and that low doses of 22:6n-3 are able to prevent some of the H2O2-induced alterations such as lipid peroxidation and PDE inhibition. Docosahexaenoic acid might thus offer some protection against oxidant-induced lymphocyte suppression.     

Oxyresveratrol protects human lens epithelial cells against hydrogen peroxide-induced oxidative stress and apoptosis by activation of Akt/HO-1 pathway

Oxidative stress induced by hydrogen peroxide (H₂O₂) triggers human lens epithelial cell (HLEC) apoptosis and initiates cataract formation. Oxyresveratrol (Oxy) was reported to possess antioxidant and free radical scavenging activities. Herein, we investigated the effects of Oxy on H₂O₂-induced oxidative stress and apoptosis in HLECs and the associated mechanisms. Cell viability was detected by MTT assay. The oxidative damage was assessed by measuring the activities of superoxide dismutases-1 (SOD-1), catalase (CAT), glutathione reductase (GSH), and malondialdehyde (MDA). Apoptosis was analyzed by flow cytometry analysis. The changed expressions of heme oxygenase-1 (HO-1) and protein kinase B (Akt) pathways were evaluated by qRT-PCR and western blot. We found that exposure to H₂O₂ dose-dependently reduced cell viability, and induced oxidative stress and apoptosis in HLECs, which were reversed by pretreatment with Oxy. Oxy increased p-Akt and HO-1 expressions in H₂O₂-stimulated HLECs. Akt and HO-1 expressions form a regulatory axis and Oxy activated the Akt/HO-1 pathway in H₂O₂-stimulated HLECs. Inhibition of the Akt/HO-1 pathway by LY294002 or ZnPP attenuated the effects of Oxy on oxidative stress and apoptosis in H₂O₂-stimulated HLECs. In conclusion, Oxy protected H₂O₂-induced oxidative stress and apoptosis through activating the Akt/HO-1 pathway, suggesting the protective effect of Oxy against H₂O₂-induced cataract.     

榄香烯对晶状体上皮细胞增殖的抑制作用

目的：研究榄香烯（Ele）对重组人表皮生长因子（rhEGF）诱导的晶状体上皮细胞（LEC）增殖的抑制作用及剂量．效应和时间．效应关系，探寻防治后发性白内障的有效方法。方法：四甲基偶氮唑蓝法（MTT）测定不同浓度Ele对增殖状态的牛LEC活性的抑制作用，同时观察时间．效应关系；流式细胞术（FCM）检测不同浓度的Ele对增殖状态的牛LEC增殖细胞核抗原（PCNA）蛋白表达的抑制作用，同时观察时间．效应关系。结果：低、中、高不同浓度的Ele作用24h后，其增殖抑制率随浓度增加而增高，呈明显的剂量．效应关系；中浓度的Ele作用6、12、24、48、72h后，其增殖抑制率随作用时间延长而增高，呈明显的时间．效应关系。Ele对LEC内PCNA蛋白表达有明显的下调作用，低、中、高不同浓度的Ele作用24h后，其PCNA表达率随浓度增加而降低，呈明显的剂量．效应关系；中浓度的Ele作用6、12、24、48、72h后，其PCNA表达率随作用时间延长而降低，呈明显的时间．效应关系。结论：Ele能有效抑制IhEGF诱导的LEC增殖，对防治后发性白内障具有广阔的前景。     

Protective effect of Lepidium sativum seed extract against hydrogen peroxide-induced cytotoxicity and oxidative stress in human liver cells (HepG2)

Context: Garden cress [Lepidium sativum (Brassicaceae)] has been widely used to treat a number of ailments in traditional medicine. The pharmacological and preventive potential of Lepidium sativum, such as anti-inflammatory, antipyretic, antihypertensive, anti-ashthamatic, anticancer, and anti-oxidant, are well known.

Objective: The present investigation was designed to study the protective effects of chloroform extract of Lepidium sativum seed (LSE) against oxidative stress and cytotoxicity induced by hydrogen peroxide (H₂O₂) in human liver cells (HepG2).

Materials and methods: Cytotoxicity of LSE and H₂O₂ was identified by (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), neutral red uptake (NRU) assays, and morphological changes in HepG2. The cells were pre-exposed to biologically safe concentrations (5–25?μg/ml) of LSE for 24 h, and then cytotoxic (0.25 mM) concentration of H₂O₂ was added. After 24 h of the exposures, cell viability by MTT, NRU assays, and morphological changes in HepG2 were evaluated. Further, protective effects of LSE on reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), lipid peroxidation (LPO), and reduced glutathione (GSH) levels induced by H₂O₂ were studied.

Results: Pre-exposure of LSE significantly attenuated the loss of cell viability up to 48% at 25?µg/ml concentration against H₂O₂ (LD₅₀ value?=?2.5?mM). Results also showed that LSE at 25?µg/ml concentration significantly inhibited the induction of ROS generation (45%) and LPO (56%), and increases the MMP (55%) and GSH levels (46%).

Discussion and conclusion: The study suggests the cytoprotective effects of LSE against H₂O₂-induced toxicity in HepG2. The results also demonstrate the anti-oxidative nature of LSE.     

Protective effect of erdosteine metabolite I against hydrogen peroxide-induced oxidative DNA-damage in lung epithelial cells

It has been shown that the mucolytic agent erdosteine (N-carboxymethylthio-acetyl-homocysteine thiolactone, CAS 84611-23-4) has anti-inflammatory and anti-oxidant properties, and an active metabolite I (MET I) containing pharmacologically active sulphydryl group has been found to have a free radical scavenging activity. The aim of this study was to assess the ability of erdosteine metabolite I to protect A549 human lung adenocarcinoma cell against hydrogen peroxide (H2O2)-mediated oxidative stress and oxidative DNA damage. When A549 cells were pre-treated with the active metabolite I (2.5-5-10 microg/ml) for 10-30 min and then exposed to H2O2 (1-4 mM) for two additional hours at 37 degrees C, 5% at CO2, the intracellular peroxide production, reflected by dichlorofluorescein (DCF) fluorescence, decreased in a concentration-dependent manner. Furthermore, using a comet assay as an indicator for oxidative DNA damage, it was found that the metabolite I prevented damage to cells exposed to shortterm H2O2 treatment. The data suggest that this compound is effective in preventing H2O2-induced oxidative stress and DNA damage in A549 cells. The underlying mechanisms involve the scavenging of intracellular reactive oxygen species (ROS).     

Protective effects of kahweol and cafestol against hydrogen peroxide-induced oxidative stress and DNA damage

There is an increasing evidence that oxidative stress is implicated in the processes of inflammation and carcinogenesis. It has been shown that kahweol and cafestol, coffee-specific diterpenes, exhibit chemoprotective effects. This study investigated the effects of kahweol and cafestol, coffee-specific diterpenes, on the hydrogen peroxide (H(2)O(2))-induced oxidative stress and DNA damage in NIH3T3 cells. When the cells were treated with kahweol or cafestol, cytotoxicity, lipid peroxidation, and reactive oxygen species production induced by H(2)O(2) were markedly reduced in a dose-dependent manner. Moreover, kahweol and cafestol were shown to be highly protected against H(2)O(2)-induced oxidative DNA damage as determined by the Comet (single cell gel electrophoresis) assay and the measurement of 8-oxoguanine content in NIH3T3 cells. Kahweol and cafestol also protected hydroxyl radical-induced 2-deoxy-d-ribose degradation by ferric ion-nitrilotriacetic acid and H(2)O(2). In addition, kahweol and cafestol efficiently removed the superoxide anion generated from the xanthine/xanthine oxidase system. These results suggest that kahweol and cafestol are effective in protecting against H(2)O(2)-induced oxidative stress and DNA damage, probably via scavenging free oxygen radicals, and that kahweol and cafestol act as antioxidants.     

兔晶体上皮细胞的体外培养

目的 建立兔晶体上皮细胞体外培养的简便方法并观察原代和传代细胞的生物学特征和组织学变化。方法将家兔晶体前囊经消化、离心,以获取分散的晶体上皮细胞,在MEM培养基中培养2周,采用倒置显微镜观察活体细胞的增殖活动和形态学变化。结果兔晶体上皮细胞在体外培养时可以存活并传代,晶体上皮细胞在体外的增殖力与兔龄呈负相关性。结论本方法简便,有效,可用于实验研究。     

Benomyl-induced effects of ORMDL3 overexpression via oxidative stress in human bronchial epithelial cells

The respiratory system is a major site of exposure route during pesticide use. Although pesticide exposure is associated with chronic respiratory diseases including asthma, the underlying pathophysiological mechanism remains to be elucidated. In this study, we investigated the in vitro effects of benomyl-induced ORMDL3 overexpression on the toxicological mechanism using the human bronchial epithelial cell line 16HBE14o-. Benomyl increased reactive oxygen species and Ca²⁺ levels, and asthma-related ADAM33 and ORMDL3 expression in 16HBE14o− cells. Considering the change in Ca²⁺ level and protein expression, we focused on ORMDL3 to elucidate the mechanism of benomyl-induced asthma. Antioxidant treatment showed that benomyl-induced ORMDL3 and endoplasmic reticulum stress could be triggered by oxidative stress. Furthermore, ORMDL3 knockdown alleviated the effects of benomyl on intracellular Ca²⁺, and the expression of metalloproteinases, and proinflammatory cytokines involved in the pathogenesis of asthma. In conclusion, our results suggest that benomyl-induced ORMDL3 overexpression via oxidative stress might be a mechanism involved in asthma. Moreover, antioxidants and alleviating mechanisms that reduce ORMDL3 levels could serve as promising therapeutic targets for pesticide-induced asthma.     

促红细胞生成素对人视网膜色素上皮细胞氧化损伤的保护作用

目的探讨促红细胞生成素对过氧化氢氧化损伤人视网膜色素上皮细胞的保护作用及其机制。方法采用600μmol.L-1的过氧化氢造成体外培养的人视网膜色素上皮细胞氧化损伤模型。实验设计分为5组:对照组,过氧化氢模型组,过氧化氢+10 kIU.L-1EPO组,过氧化氢+20 kIU.L-1EPO组和过氧化氢+40 kIU.L-1EPO组。MTT法检测细胞活性,测定细胞内超氧化物歧化酶(SOD)和丙二醛(MDA)含量,Annexin V-FITC/PI双染色流式细胞法测定细胞的凋亡率。结果过氧化氢模型组RPE细胞的活性明显降低,不同浓度的EPO药物干预组的细胞活性较模型组明显升高,并随着EPO浓度的升高而升高。过氧化氢模型组RPE细胞SOD活性降低,MDA的含量增加;而EPO药物干预组SOD活性较模型组明显升高,MDA含量减少,差异有显著性。过氧化氢模型组RPE细胞的凋亡率升高,而不同浓度的EPO药物干预组降低RPE的凋亡率,凋亡率随着EPO浓度的升高而降低。结论促红细胞生成素对过氧化氢诱导的人RPE细胞的氧化损伤有保护作用,其机制可能与抑制氧化反应、提高抗氧化酶活性、减少细胞凋亡有关。     

Cytoprotective effect of green tea extract and quercetin against hydrogen peroxide-induced oxidative stress

In this study, we evaluated the cytoprotective effects of antioxidative substances in hydrogen peroxide (H2O2) treated Mel-Ab melanocytes. Tested substances include selenium, quercetin, green tea (GT) extract, and several vitamins (ascorbic acid, Trolox, and folic acid). Of these, both quercetin and GT extract were found to have strong cytoprotective effects on H2O2-induced cell death. We also examined additive effects, but no combination of two of any of the above substances was found to act synergistically against oxidative damage in Mel-Ab cells. Nevertheless, a multi-combination of GT extract, quercetin, and folic acid appeared to prevent cellular damage in a synergistic manner, which suggests that combinations of antioxidants may be of importance, and that co-treatment with antioxidants offers a possible means of treating vitiligo, which is known to be related to melanocyte oxidative stress.     

Honokiol inhibits H(2)O(2)-induced apoptosis in human lens epithelial cells via inhibition of the mitogen-activated protein kinase and Akt pathways

Oxidative stress-induced apoptosis in lens epithelial cells plays an important role in cataract formation, and its prevention may be of therapeutic interest. This study was performed to investigate the protective effect and mechanisms of honokiol on H₂O₂-induced apoptosis in human lens epithelial (HLE) cells. HLE cells (SRA01-04) were pretreated with honokiol at concentrations of 5 μM, 10 μM and 20 μM before 50 μM H₂O₂ treatment. The results demonstrated that pretreatment of honokiol inhibited the activation of caspase-3 and caspase-9 and downregulated the expression of Bcl-2. Mechanistically, honokiol suppressed H₂O₂-induced phosphorylation of ERK1/2, p38 mitogen-activated protein kinase (MAPK), JNK and Akt. Honokiol also inhibited H₂O₂-induced nuclear factor-κB (NF-κB)/p65 phosphorylation and translocation in HLE cells. These results demonstrate that honokiol suppresses H₂O₂-induced HLE cell apoptosis via interference with the MAPKs, Akt and NF-κB signaling, suggesting that honokiol might have a potential effect against cataract formation.     

Protective effects of dehydrocostus lactone against hydrogen peroxide-induced dysfunction and oxidative stress in osteoblastic MC3T3-E1 cells

Oxidative stress regulates cellular functions in multiple pathological conditions, including bone formation by osteoblasic cells. To elucidate the protective effects of dehydrocostus lactone on the response of osteoblast to oxidative stress, osteoblastic MC3T3-E1 cells were incubated with 0.3 mM hydrogen peroxide (H₂O₂) and/or dehydrocostus lactone (0.1–10 μg/ml), and markers of osteoblast function and oxidative damage were examined. Dehydrocostus lactone (0.1–10 μg/ml) significantly increased osteoblast growth compared with control (P < 0.05). H₂O₂-induced reduction of differentiation markers such as alkaline phosphatase (ALP), collagen content, and calcium deposition was recovered in the presence of dehydrocostus lactone (0.4–2 μg/ml). Treatment with dehydrocostus lactone (10 μg/ml) decreased the production of osteoclast differentiation-inducing factors such as interleukin (IL)-6 and receptor activator of nuclear factor-kB ligand (RANKL) in the presence of H₂O₂. Moreover, dehydrocostus lactone (0.4–2 μg/ml) decreased the formation of protein carbonyl (PCO) and malondialdehyde (MDA) induced by H₂O₂ in osteoblasts. Taken together, these results demonstrate that dehydrocostus lactone can protect osteoblasts against H₂O₂-induced cellular dysfunction. These results also suggest that dehydrocostus lactone may be valuable as a protective agent against oxidative damage in osteoblasts.     

Protective effects of flavonoids in the roots of Scutellaria baicalensis Georgi against hydrogen peroxide-induced oxidative stress in HS-SY5Y cells.

Oxidative stress plays an important role in the pathological process of neurodegenerative diseases. The effects of four major flavonoids present in Scutellaria baicalensis Georgi on hydrogen peroxide-induced neuronal cell damage are studied in this paper. When human neuroblastoma SH-SY5Y cells were incubated in Hanks' solution with the addition of 400 microM hydrogen peroxide for 2 h, the viability of cells was decreased remarkably, while the cell lipid peroxidation and the percentage of lactose dehydrogenase released into the culture medium was significantly increased. Addition of 10 microM of baicalein and baicalin significantly attenuated the cellular injury induced by hydrogen peroxide, while the effect of wogonin was marginal and wogonoside showed no effect at the tested concentration. In a separate experiment, 10 microM of baicalein and baicalin also antagonized the intracellular free-calcium concentration ([Ca2+]i) increase caused by 1 mM hydrogen peroxide. The effects of baicalein in both experiments were similar to those of quercetin, a well-studied antioxidant flavonoid. These results demonstrated the protective effects of flavonoids originating from Scutellaria baicalensis Georgi on the oxidative injury of neuronal cells.     

Cadmium-induced induction of cell death in human lens epithelial cells: Implications to smoking associated cataractogenesis

Cadmium is reported to accumulate in human eye tissues suggesting its implication in diverse ocular pathology. Using an in vitro cell culture model we investigated the effects of cadmium on human lens epithelial cells (HLECs) (HLE-B3). We observed cadmium-induced dose- as well as time-dependent decline in HLECs viability which was exacerbated significantly upon reduction of intracellular glutathione levels by buthionine sulfoximine (BSO). There was a dose-dependent significant increase in lactate dehydrogenase (LDH) release from HLECs suggesting cadmium-induced alteration of membrane integrity as well as necrotic cell death. The decline in cell viability was also due to apoptosis of the HLECs as determined by quantifying % apoptotic cells as well as PARP cleavage. Moreover, release of apoptosis inducing factor (AIF) into the cytosol was also detected. Cadmium was also observed to increase oxidative stress, lipid peroxidation and activation of MAPK pathway in HLECs. Antioxidants like N-acetylcysteine (NAC) and α-Tocopherol significantly prevented cadmium-induced toxicity in HLECs. Our findings suggest that cadmium-induced elevated oxidative stress as well as activation of MAPK signaling cascade eventually led to cell death of HLECs through apoptosis as well as necrosis. The loss of HLECs by cadmium could possibly explain its implication in cataract development particularly associated with smoking.     

PM2.5-induced oxidative stress triggers autophagy in human lung epithelial A549 cells

Exposure to higher levels of air pollution particulate matter (PM) with an aerodynamic diameter of less than 2.5 μm (PM_2.5) links with an increased risk of cardiovascular and respiratory deaths and hospital admission as well as lung cancer. Although the mechanism underlying the correlation between PM_2.5 exposure and adverse effects has not fully elucidated, PM_2.5-induced oxidative stress has been considered as an important molecular mechanism of PM_2.5-mediated toxicity. In this work, human lung epithelial A549 cells were used to further investigate the biological effects of PM_2.5 on autophagy. The cell viability showed both time- and concentration-dependent decrease when exposure to PM_2.5, which can be attributed to increase of the levels of extracellular lactate dehydrogenase (LDH) release and intracellular reactive oxygen species (ROS) generation in A549 cells. Moreover, PM_2.5-induced oxidative damage in A549 cells was observed through the alteration of superoxide dismutase (SOD) and catalase (CAT) activities compared to the unexposed control cells. PM_2.5-induced autophagy was indicated by an increase in microtubule-associated protein light chain-3 (LC3) puncta, and accumulation of LC3 in both time- and concentration-dependent manner. PM_2.5-induced mRNA expression of autophagy-related protein Atg5 and Beclin1 was also observed compared with those of the unexposed control cells. These results suggest the possibility that PM_2.5-induced oxidative stress probably plays a key role in autophagy in A549 cells, which may contribute to PM_2.5-induced impairment of pulmonary function.     

盐酸戊乙奎醚对肺泡Ⅱ型上皮细胞氧化损伤的影响

目的 探讨盐酸戊乙奎醚对肺泡Ⅱ型上皮细胞氧化损伤的保护作用。方法 用过氧化氢（H2O2）加入A549 细胞培养液中制成 A549 细胞氧化损伤模型, 实验分为空白对照组（C 组）、 H2O2处理组（H 组）和盐酸戊乙奎醚-过氧化氢处理组 （P 组）。用 MTT 方法测 A549 细胞存活率, 用 TUNEL 方法测定细胞凋亡指数, 并测定细胞内的丙二醛（MDA）、 超氧化物歧化酶（SOD）、 还原型谷胱甘肽（GSH）、 烟酰胺腺嘌呤二核苷磷酸（NADPH）含量。结果 与 C 组比较, H 组的细胞存活率下降, 凋亡指数增加, MDA 含量上升, SOD、 GSH、 NADPH 的含量下降 （P＜0.05）。与H 组比较, P 组的细胞存活率增加, 凋亡指数下降, MDA 含量下降, SOD、 GSH、 NADPH 的含量增加（P＜0.05）。结论 盐酸戊乙奎醚对A549 细胞过氧化损伤具有保护作用。     

阿魏酸钠防护晶状体上皮细胞氧化损伤的信号转导机制

目的:探讨阿魏酸钠对氧化损伤的晶状体上皮细胞内Ca2 、环磷酸腺苷(cAMP)、环磷酸鸟苷(cGMP)的影响,从细胞信号转导角度揭示天然药物防治白内障的细胞和分子学机制。方法:采用牛晶状体上皮细胞进行晶状体上皮细胞(LEC)原代和传代培养,以含有过氧化氢(H2 O2 )的培养液孵育LEC复制氧化损伤模型,并加入阿魏酸钠单体共同孵育。分别采用四甲基偶氮唑兰(MTT)比色测定法观察在不同时间和浓度条件下LEC活性变化,采用荧光分光光度计测定不同时间细胞内钙离子浓度([Ca2 ]i)以及放射免疫分析法测定不同时间LEC内cAMP、cGMP的含量变化。结果:H2 O2 组可引起LEC吸光度值(A)明显下降(P <0 .0 1) ,阿魏酸钠能明显增强氧化损伤的LEC活性,并呈剂量 效应关系和时间 效应关系。氧化损伤的LEC[Ca2 ]i 升高(P<0 .0 1) ;阿魏酸钠可以降低由H2 O2 引起的细胞[Ca2 ]i 的升高,并呈时间 效应关系。H2 O2 组cAMP浓度升高;cGMP浓度下降(P <0 .0 1) ;阿魏酸钠使cAMP水平下调,cGMP水平上升(P <0 .0 1) ,并呈时间 效应关系。结论:阿魏酸钠可明显抑制LEC氧化损伤及凋亡,其作用机制可能是通过钙信号系统、cAMP信号系统、cGMP信号系统及其相互作用来调节生物学效应。