荷丹片对动脉粥样硬化大鼠氧化应激的影响

目的:观察不同剂量荷丹片对动脉粥样硬化大鼠氧化应激的影响。方法:48只雄性SD大鼠随机分为正常组,模型组,荷丹片高(3g·kg-1·d-1)、中(1.5g·kg-1·d-1)、低(0.5g·kg-1·d-1)剂量组及辛伐他汀组,每组8只。正常组给予普通鼠饲料喂养,其余各组使用高脂饲料造模。12周后取各组大鼠腹主动脉电子显微镜下观察主动脉形态学变化;腹静脉取血测定各组大鼠超氧化物歧化酶(SOD)、丙二醛(MDA)及NO含量。结果:高剂量荷丹片可以升高血清SOD、NO水平,降低血清MDA水平,与模型组相比差异有统计学意义(P0.05)。荷丹片高剂量组与辛伐他汀组比较差异无统计学意义(P0.05)。荷丹片组镜下表现主动脉粥样硬化组织损伤明显减轻。结论:高剂量荷丹片通过减轻AS大鼠氧化应激发挥其抗动脉粥样硬化的作用。     

荷丹片对冠心病合并2型糖尿病患者血脂、炎症因子及氧化应激水平的影响

目的:探究荷丹片对冠心病合并2型糖尿病患者血脂、炎症因子及氧化应激水平的影响及安全性。方法:收集2013年7月-2015年11月我院收治的冠心病合并2型糖尿病患者118例,按随机数字表法分为观察组(63例)和对照组(55例)。对照组患者给予控制血糖、调节血脂、扩张血管、抗凝等常规治疗;观察组患者在对照组基础上餐前口服荷丹片1.46 g,tid。两组患者均连续治疗6个月。比较两组患者治疗前后血脂[总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)]、血清炎症因子[肿瘤坏死因子α(TNF-α)、白细胞介素10(IL-10)、IL-6、超敏C反应蛋白(hs-CRP)]、血清氧化应激指标[丙二醛(MDA)、超氧化物歧化酶(SOD)、一氧化氮(NO)]水平及不良反应发生情况。结果:治疗前,两组患者血脂、炎症因子及氧化应激指标水平比较,差异均无统计学意义(P>0.05);治疗后,两组患者TC、TG、LDL-C、TNF-α、IL-6、hs-CRP、MDA水平显著降低,IL-10、SOD、NO水平显著升高,且观察组上述指标均显著优于对照组,差异均有统计学意义(P<0.05)。两组患者不良反应发生率比较,差异无统计学意义(P>0.05)。结论:荷丹片能有效改善冠心病合并2型糖尿病患者血脂及血清炎症因子水平,减轻炎性损伤,降低氧自由基水平,增强机体抗氧化能力,减轻氧化应激损伤,且安全性较高。     

黄芪多糖对荷腹水瘤小鼠氧化应激功能的影响

目的 探讨黄芪多糖（APS）如何影响荷腹水瘤小鼠的氧化应激功能。方法 取生长良好的S180细胞配成瘤细胞悬液接种于小鼠腹腔内,建立腹水瘤模型。将荷瘤小鼠随机分为模型组（腹腔注射0.9%NaCl 100 mL）、对照组(腹腔注射100 mg·kg^-1环磷酰胺100 mL)和低、中、高剂量实验组(分别腹腔注射20,40和60 mg·mL^-1 APS 100 mL),每组30只;另取18只正常小鼠作为空白组（腹腔注射0.9%NaCl 100 mL）。6组小鼠均每天给药1次,连续给药28 d。用比色法测定血清、肝和脑组织中超氧化物歧化酶（SOD）、丙二醛（MDA）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）、一氧化氮（NO）、髓过氧化物酶（MPO）和总抗氧化能力（T-AOC）的含量。结果 干预28 d后,APS使血清SOD水平由模型组中的（64.78±3.92）U·mL^-1升高至高剂量实验组的（102.35±9.84）U·mL^-1,其余CAT、GSH-Px、T-AOC水平同样明显升高,使MDA...     

左金丸对胃热证大鼠炎症因子、氧化应激因子及凋亡因子的影响

目的:探讨左金丸干预大鼠胃热证的作用机制。方法:将大鼠随机分成正常组、模型组和左金丸组,通过灌胃辣椒煎液和无水乙醇建立大鼠胃热证模型,采用酶联免疫吸附法(ELISA)和化学比色法测定各组大鼠血清中的炎症因子如白细胞介素(IL)-2、IL-6、IL-10、IL-1β和髓过氧化物酶(MPO);氧化应激因子如还原型谷胱甘肽(GSH)、谷胱甘肽-S-转移酶(GST)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、一氧化氮(NO)、丙二醛(MDA)和凋亡因子如B细胞淋巴瘤因子-2(Bcl-2)的活性或含量。结果:左金丸能显著减少胃热证大鼠胃黏膜损伤面积,显著升高胃热证大鼠血清中GST、GSH-Px、CAT、SOD活性和GSH、IL-10、Bcl-2的含量,显著降低胃热证大鼠血清中MPO活性和IL-2、IL-6、IL-1β、MDA的含量。结论:左金丸可通过抗炎、抗氧化应激和抗凋亡作用干预胃热证。     

荷丹片对三酰甘油胆固醇和高密度脂蛋白的影响

目的：观察荷丹片降低血脂的疗效与安全性.方法：治疗组30例口服荷丹片5片,tid×8周,对照组30例口服血脂康2片,bid×8周,治疗前、治疗后4和8周分别抽血检查血脂和肝肾功能.结果：两组分别降低血胆固醇(TC)19.8%和21.3%, 升高高密度脂蛋白(HDL)10.5%和5.7%, 三酰甘油(TG)分别降低了38.1%和32.2%；荷丹片降低TC和TG的总有效率均为90.0%,升高HDL的总有效率为86.7%；血脂康降低TC和TG的总有效率分别为93.3%和86.7%,升高HDL的总有效率为83.3%；两者均无明显的肝、肾功能损害等副作用.结论：荷丹片是一种安全、有效的降脂药,特别适合于高TG、低HDL血症患者.     

达格列净对应激性心肌病小鼠炎症及氧化应激的影响

目的 探讨达格列净对应激性心肌病(SCM)小鼠炎症及氧化应激的影响。方法 21只小鼠随机均分为假手术组(C组)、SCM模型组(A组)和达格列净预处理组(B组)。采用心脏超声检测左心室射血分数(LVEF)和左心室缩短分数(LVFS),ELISA法检测心肌肌钙蛋白T(cTnT)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、IL-6、IL-18和TNF-α水平,微孔板法检测丙二醛(MDA)、SOD、谷胱甘肽过氧化物酶(GSH-Px)水平,HE染色观察心肌细胞形态学变化,TUNEL染色观察心肌细胞凋亡情况,Wsetern blot法检测磷脂酰肌醇3-激酶(PI3K)、Akt、Bcl-2、Bax蛋白表达。结果 与C组相比,A组LVEF、LVFS、SOD水平和Bcl-2蛋白表达更低(P<0.05),心肌细胞凋亡率、cTnT、CK-MB、LDH、IL-6、IL-18、TNF-α、MDA、GSH-Px水平及PI3K、Akt、Bax蛋白表达更高(P<0.05),心肌细胞排列紊乱,细胞核萎缩,细胞间质略水肿;B组经达格列净预处理后各指标均较A组有不同程度的改善(P<0.05)。结...     

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。     

丁苯酞对慢性应激大鼠海马组织氧化应激及炎症因子的影响

目的探讨丁苯酞对由应激引起的海马组织氧化应激及炎症因子的影响及其可能的作用机制。方法SD大鼠随机分为4组:对照组、丁苯酞组、模型组、抑郁+丁苯酞组。模型组和抑郁+丁苯酞组给予慢性应激造模,丁苯酞组单独给予20 mg/(kg·d)的丁苯酞,对照组给予相同体积的玉米油。7周后,对大鼠的行为学进行考察,并观察海马组织IL-6、TNF-α、IL~(-1)β的表达及SOD、MDA的变化。结果丁苯酞改善了应激对大鼠行为学的改变,同时也抑制了抑郁模型大鼠海马组织IL-6、TNF-α、IL~(-1)β的表达,缓解了氧化应激。结论本研究首次在抑郁摸型大鼠中直接证明了丁苯酞有潜在的抗抑郁作用,且其机制可能与其抗氧化及免疫调节作用有关。     

用HPLC-TOF-MS法分析荷丹片的化学成分

目的:用高效液相色谱-飞行时间质谱(HPLC-TOF-MS)联用技术对荷丹片中化学成分进行鉴别与结构解析。方法:色谱分离采用Agilent Zorbax SB-Aq柱(250mm×4.6mm,5μm),流动相为乙腈(A相)-1%乙酸水溶液(B相),梯度洗脱:0～50min,0%～30%B相,50～90min,30%～75%B相;流速为1ml/min。质谱定性分析采用TOF-MS,在正离子模式下进行扫描,参比离子m/z分别为121.05和922.01。结果:在液质联用条件下,通过TOF-MS以及碎片离子裂解分析,鉴定了荷丹片中的33种化学成分和5组同分异构体。结论:HPLC-TOF-MS联用技术是鉴定荷丹片中化学成分的一种简单、有效的方法。     

中枢神经体液因子和氧化应激对心绞痛的影响

<正>心绞痛是心血管系统中最常见的疾病之一,严重危害人类的健康,深入研究心绞痛发生、发展机制,并采取有效的措施延缓或逆转心绞痛的病理过程,一直受到人们的关注。丘脑是机体内重要的痛觉     

影响贝诺酯片溶出度的因素探讨

贝诺酯片是解热、消炎镇痛药,以前该品种只进行崩解度检查,但从《中国药典》2000年版开始要求进行溶出度的检查。但该品种在放置一段时间后容易出现溶出度降低的问题,通过对辅料的种类、制备方法等方面来讨论贝诺酯片溶出度的因素,选出合适的条件,切实提高贝诺酯溶出度从而保证其质量。     

等离子射频髓核成形术复合臭氧髓核消融术治疗间盘源性疼痛

摘要 目的：探讨等离子髓核消融术复合臭氧髓核消融术治疗间盘源性疼痛的疗效及安全性。方法：对影像CT或MRl检查、临床症状、体征及间盘造影均符合腰椎间盘源性疼痛诊断的患者,在西门子Powermobile C型臂X线引导下,对责任间盘行等离子髓核消融术复合臭氧髓核消融术,术前及术后2个月内进行VAS评分及改良MacNab标准疗效评价。结果：术后7天VAS评分与术前比较显著降低（P＜0.05),术后随访2个月,改良Macnab疗效评价有效率93%（53/57）,优良率87.7％(50／57例);所有患者均未出现椎间隙感染、神经根及脊髓损伤等严重并发症。结论：等离子髓核成消融复合臭氧髓核消融术治疗椎间盘源性疼痛疗效确切,并发症少,但须严格掌握适应症。     

Resveratrol toxicity: Effects on risk factors for atherosclerosis and hepatic oxidative stress in standard and high-fat diets

The beneficial action of moderate wine consumption is increasingly being attributed to resveratrol (trans-3,4′,5-trihydroxystilbene). To test the safety of resveratrol use as a dietary supplement, 24 male Wistar rats were initially divided into three groups: (C, n = 6) was given standard chow and water; (R, n = 6) received standard chow and 6 mg/l resveratrol in its drinking water (1 mg/kg/day), and (HFD, n = 12) received high-fat diet and water. In order to more appropriately study the effects of resveratrol on high-fat diet, after 30 days of treatments, HFD-rats were divided into two subgroups (n = 6/group):(HFD) remained receiving high-fat diet and water; (HFD-R) given high-fat diet and 6 mg/l resveratrol in its drinking water (1 mg/kg/day). The total experimental period was 45 days. The resveratrol dose took into account its average concentration in wine, the time variability of wine ingestion, and so of resveratrol consumption in humans. HFD-rats had hyperglycaemia, dyslipidemia, increased serum oxidized-LDL (ox-LDL) and hepatic oxidative stress. Comparing HFD-R and HFD-rats, resveratrol improved lipid profile and glucose level, enhanced superoxide dismutase, thus reducing ox-LDL and hepatic oxidative stress. Resveratrol, in standard-fed-rats reduced glutathione-antioxidant defense system and enhanced hepatic lipid hydroperoxide. In conclusion, based on the results of this single dose preliminary study with resveratrol in the drinking water of male Wistar rats for 30 days, it may be concluded that resveratrol may have beneficial effects in high-fat diets (e.g. ox-LDL, decreased serum and hepatic oxidative stress), but not in standard-fed diets (effects produced include enhanced hepatic oxidative stress). Further studies are indicated.     

小檗碱对胰岛素抵抗大鼠氧化应激和内质网应激的影响

目的观察小檗碱对胰岛素抵抗大鼠氧化/抗氧化状态和内质网应激(endoplasmic reticulum stress,ERstress)的影响,并探讨其改善胰岛素抵抗的分子机制。方法采用高脂高热卡饮食饲养8wk制备胰岛素抵抗大鼠模型,成模后随机分为小檗碱组(BER组)、Alpha-硫辛酸组(ALA组)和模型组(MOD组),各组以相应的药物干预4wk。另设正常组(NOR组),予普通饲料喂养,不予药物干预。比较各组大鼠空腹血糖(FBG)、空腹胰岛素水平(Fins)和胰岛素敏感性(ISI)。血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性以观察药物对大鼠氧化和抗氧化的影响。Westernblot方法测定肝脏组织中的ER应激标志物c-Jun氨基端激酶(c-junNH2-terminal kinase,JNK)和Phospho-c-Jun(Ser73)(p-c-Jun)的含量变化。RT-PCR方法测定肝脏组织ER应激标志物葡萄糖调节蛋白GRP78(glucose regulated protein78,GRP78)mRNA表达水平,以观察小檗碱对胰岛素抵抗大鼠ER应激的影响。结果与NOR组比较,MOD组大鼠血清中MDA含量明显升高,SOD、GSH-Px活性明显降低(P均<0.05)。BER组大鼠SOD、GSH-Px的活性较MOD组明显升高(P<0.01,P<0.05),MDA含量较模型组明显下降。比较各组肝组织p-c-Jun/JNK的水平,MOD组较NOR组明显升高(P<0.01),BER组及ALA组较MOD组均明显下降(P均<0.01)。比较各组肝组织中GRP78mRNA水平,MOD组较NOR组明显升高(P<0.05),BER组及ALA组较MOD组均明显下降。结论小檗碱能提高胰岛素抵抗大鼠的胰岛素敏感性,增加其抗氧化能力,改善其ER应激状态,其作用机制可能与改善ER应激有关。     

Effects of Daflon on oxidative stress induced by hindlimb ischemia/reperfusion.

The objective of this study was to investigate the effects of Daflon 500 mg on tissue damage in kidney after ischemia/reperfusion hindlimb, by assessing blood biochemical assay and histopathological analysis. Rats were given Daflon 80 mg x kg(-1) x day(-1) for 10 days. On 11th day of treatment, 4h ischemia followed by 4 h reperfusion period was performed on right hind limb of the rats. Control groups were given only arabic gum and were subjected to same ischemia/reperfusion period.At the end of reperfusion period, erythrocyte superoxide dismutase, Na(+)-K(+) ATPase and reduced glutathione levels were increased in the rats erythrocytes in Daflon group (P<0.01, for all). On the other hand, serum myeloperoxidase and malondialdehyde levels were significantly lower in the Daflon-received rats (P<0.01, for all). Histopathological studies demonstrated that, there was a prominent tubulointerstitial injury with loss of brush border and this degeneration was accompanied by segmental glomerular degeneration also for both control and Daflon group. Daflon-received group animals displayed significantly less periglomerular and perivascular leukocytic infiltration (P=0.015).These overall results suggest that Daflon contributes renal protection from hind limb ischemia/reperfusion injury in some degree, by decreasing systemic oxidative stress.     

Effects of sodium tungstate on oxidative stress enzymes in rats

Abstract

Tungsten, due to its distinguished physical properties, has wide industrial and military applications. Environmental exposure to tungsten, which mainly occurs through various sources like food, water, soil, etc., is of growing concern as various toxic effects have recently been reported. In this study, we investigated the effects of oral and intraperitoneal (i.p.) administration of sodium tungstate on various biochemical variables indicative of oxidative stress in erythrocytes and soft tissue damage in rats. Male rats were administered to 119?mg, 238?mg/kg of sodium tungstate orally or 20?mg and 41?mg/kg through i.p. route, for 14 consecutive days. The results demonstrated a significant increase in Reactive Oxygen Species (ROS) and an increase in catalase and glutathione peroxidase antioxidant enzymes activities in erythrocytes. Erythrocyte glutathione-S-transferase (GST) activity showed significant inhibition, while tissue ROS and thiobarbituric acid reactive substance levels increased accompanied by a decreased reduced glutathione, oxidized glutathione (GSH:GSSG) ratio. These changes were supported by an increase in plasma transaminases activities, creatinine, and urea levels, suggesting hepatic and renal injury. These biochemical alterations were prominent in rats intraperitoneally administrated with sodium tungstate than oral administration, suggesting more pronounced toxicity. The study also suggests oxidative stress as one of the major mechanism involved in the toxic manifestations of sodium tungstate.     

Effects of ascorbic acid and alpha-tocopherol on arsenic-induced oxidative stress

Arsenic is an ubiquitous element in the environment causing oxidative burst in the exposed individuals leading to tissue damage. Antioxidants have long been known to reduce the free radical-mediated oxidative stress. Therefore, the present study was designed to determine whether supplementation of alpha-tocopherol (400 mg/kg body weight) and ascorbic acid (200 mg/kg body weight) to arsenic-intoxicated rats (100 ppm in drinking water) for 30 days affords protection against the oxidative stress caused by the metalloid. The arsenic-treated rats showed elevated levels of lipid peroxide, decreased levels of non-enzymatic antioxidants and activities of enzymatic antioxidants. Administration of alpha-tocopherol and ascorbic acid to arsenic-exposed rats showed a decrease in the level of lipid peroxidation (LPO) and enhanced levels of total sulfhydryls, reduced glutathione, ascorbic acid and alpha-tocopherol and so do the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase to near normal. These findings suggest that alpha-tocopherol and ascorbic acid prevent LPO and protect the antioxidant system in arsenic-intoxicated rats.     

Effects of pH on nicotine-induced DNA damage and oxidative stress

Epidemiological evidence suggests that chewing betel quid and smoking have synergistic potential in the development of oral squamous-cell carcinoma in Taiwan. Chewing betel quid produces alkalization of saliva. This study investigated the response of human oral cancer OEC-M1 cells to nicotine in different pH environments (6.5 and 8) by examining its effects on DNA damage as evidenced by single-cell gel electrophoresis. Nicotine (1 and 10 muM) significantly induced DNA strand breakage when cultured at pH 8 for 6 h but did not induce DNA damage at pH 6.5. Nicotine-induced DNA damage was also time dependent. When cells were pretreated with catalase or N-acetylcysteine, a significant reduction in nicotine-induced DNA damage was observed. Flow cytometric analyses showed that the production of 8-oxoguanine was significantly increased following nicotine (10 muM) treatment. Posttreatment of nicotine-damaged DNA by endonuclease III and formamidopyrimidine-DNA glycosylase, recognizing oxidized DNA bases, increased the extent of DNA damage. These results suggest that nicotine-induced DNA strand breakage is pH dependent, and oxidative stress might be involved in nicotine-induced DNA damage. Finally, cigarette smoke condensate (equivalent to 8 muM nicotine) induced significant DNA strand breaks in OEC-M1 cells at pH 8 and correlated with the generation of oxidative DNA damage. Thus, alkaline saliva generated by chewing betel quid plays an important role in cigarette-related nicotine-induced DNA damage, and reactive oxygen species may be involved in generating this DNA damage.     

Glutathione-related factors and oxidative stress in autism, a review

Autism spectrum disorders are complex neuro-developmental disorders whose neurobiology is proposed to be associated with oxidative stress which is induced by reactive oxygen species. The process of oxidative stress can be a target for therapeutic interventions. In this study, we aimed to review the role of oxidative stress, plasma glutathione (GSH), and related factors as the potential sources of damage to the brain as well as the possible related factors which reduce the oxidative stress. Methylation capacity, sulfates level, and the total glutathione level are decreased in autism. On the other hand, both oxidized glutathione and the ratio of oxidized to reduced glutathione are increased in autism. In addition, the activity of glutathione peroxidase, superoxide dismutase, and catalase, as a part of the antioxidative stress system are decreased. The current literature suggests an imbalance of oxidative and anti-oxidative stress systems in autism. Glutathione is involved in neuro-protection against oxidative stress and neuro-inflammation in autism by improving the anti-oxidative stress system. Decreasing the oxidative stress might be a potential treatment for autism.