不同时机介入电针对模拟失重大鼠肝脏HSP 70、MDA、SOD和GSH-PX的影响

目的:观察预针刺和针刺治疗对模拟失重大鼠肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)活力,丙二醛(MDA)含量及热休克蛋白70(HSP 70)表达的影响,探讨电针对模拟失重大鼠肝脏损伤改善作用的相关机制。方法:Wistar大鼠随机分为正常组、模型组、预针刺组和针刺组,每组5只。大鼠尾部悬吊4周复制模拟失重模型。预针刺组在尾部悬吊前1周,电针刺激双侧"肾俞""脾俞"和"三阴交"穴,每次30min,每日1次;针刺组大鼠尾部悬吊过程中电针刺激"肾俞""脾俞"和"三阴交"穴,每次30min,隔日治疗1次,共针刺14次。采用免疫组化法检测大鼠肝脏组织HSP 70的表达情况,比色法检测大鼠肝脏组织SOD、GSH-PX活性和MDA含量。结果:与正常组比较,模型组大鼠肝脏HSP 70呈强阳性反应,HSP 70表达量显著增加(P0.01),MDA含量显著升高(P0.01),SOD和GSH-PX活性显著降低(P0.05);与模型组比较,预针刺组大鼠肝脏HSP 70表达量显著降低(P0.01),SOD和GSH-PX活性略有升高(P0.05),MDA含量略有减少(P0.05),针刺组HSP 70表达量略有降低(P0.05),SOD活性和MDA含量略有升高(P0.05),GSH-PX活性略有降低(P0.05);与预针刺组相比,针刺组肝脏GSH-PX活性显著降低(P0.05),MDA含量显著升高(P0.05)。结论:预针刺可以明显抑制大鼠尾部悬吊引起的肝HSP 70表达的上调,从而可能有利于提高肝脏的抗氧化能力。     

幼年大鼠热卡限制对成年后胰岛β细胞功能的影响

将11周龄的SD大鼠随机分为对照组和热卡限制组,干预24周后比较两组大鼠的胰岛β细胞功能及氧化应激指标.结果 显示,从幼年期开始的热卡限制能改善成年大鼠糖负荷后的早期胰岛素分泌相,并减缓氧化应激,这些现象与其体重下降有关.     

六味地黄口服液对冷应激小鼠的保护作用

目的本研究通过冷刺激小鼠模型观察新老两种工艺制备的六味地黄口服液对冷应激损伤的影响及作用比较。方法将80只小鼠随机分成8组（正常组、冷应激组和两种六味地黄口服液不同剂量组）,连续灌胃7d,每日于（10±0.5）℃冷水中游泳5min,于末次实验后,取血清、脑、胸腺及脾组织,分别测定血清和脑组织超氧化物歧化酶（SOD）、乳酸脱氢酶（LDH）活性和丙二醛（MDA）含量,同时计算胸腺、脾脏指数。结果与模型组比较,六味地黄口服液可使冷应激小鼠血清中SOD活性升高;MDA含量和LDH活性降低（P〈0.05）;脑组织中MDA含量降低。两种工艺六味地黄口服液中、大剂量给药组可以增大胸腺和脾脏指数。结论六味地黄口服液对冷刺激引起的氧化应激损伤有明显保护作用。     

男性吸烟者血清SOD及MDA水平的量化研究

目的探讨吸烟对人体内血清超氧化物歧化酶(SOD)和丙二醛(MDA)水平的影响.方法采用横断面调查方法,对226名健康男性吸烟者和非吸烟者测定血清SOD和MDA.结果吸烟组血清SOD和MDA含量均明显高于非吸烟组(P＜0.001);在吸烟者中,随着吸烟年限增加,血清MDA含量增加(P＜0.05),而SOD含量未见显著性差异.结论吸烟对机体抗氧化能力有影响.     

Shikonin ameliorates D-galactose-induced oxidative stress and cognitive impairment in mice via the MAPK and nuclear factor-κB signaling pathway

Oxidative stress acts as the major causative factor for various age‐associated neurodegenerative diseases, triggering cognitive and memory impairments. In the present study, the underlying neuroprotective mechanism governing how shikonin acts against D-galactose (D-gal)-induced memory impairment, neuroinflammation and neuron damage was examined. The results revealed that chronic administration of D-gal [150 mg/kg intraperitoneally (i.p.)] in mice caused cognitive and memory impairments, as determined by Morris water-maze test. Shikonin treatment, however, alleviated D‐gal-induced memory impairment and reversed the D‐gal-induced neural damage and apoptosis. Furthermore, western blotting and the results of morphological analysis revealed that shikonin treatments markedly reduced D‐gal induced neuroinflammation through inhibition of astrocytosis as determined by glial fibrillary acidic protein (GFAP) detection, and downregulating other inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Moreover, shikonin treatment led to inhibition of the activation of nuclear factor‐κB (NF‐κB) and the phosphorylation of mitogen-activated protein kinases (MAPKs), preventing neurodegeneration. Hence, taken together, the results of the present study suggested that shikonin attenuated D‐gal-induced memory impairment, neuroinflammation and neurodegeneration, possibly via the NF‐κB/mitogen-activated protein kinase (MAPK) pathway. Our data suggest that shikonin could be a promising, endogenous and compatible antioxidant candidate for age‐associated neurodegenerative diseases, including Alzheimer's disease.     

阻塞性睡眠呼吸暂停低通气综合征及其相关高血压患者血清过氧化氢酶、谷胱甘肽过氧化物酶和丙二醛水平的变化

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)及阻塞性睡眠呼吸暂停低通气综合征相关高血压(obstructive sleep apnea-hypopnea associated hypertension,OSAHAHT)患者血清过氧化氢酶(catalase,CAT)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-PX)和丙二醛(malonaldehyde,MDA)水平的变化.方法 选择OSAHS患者24例,OSAHAHT患者21例;正常对照组23名,测定血清CAT、GSH-PX、MDA水平.并与睡眠呼吸监测指标进行相关分析.结果 与正常对照组比较,OSAHS组及OSAHAHT组血清CAT、GSH-PX活性均降低(P<0.01),MDA浓度均升高(P<0.01).OSAHS及OSAHAHT患者血清CAT、GSH-PX、MDA水平与反映睡眠呼吸暂停严重程度的指标有相关性(P<0.01).结论 OSAHS患者存在CAT、GSH-PX、MDA水平的变化,且与OSAHS的病情严重程度相关;氧化应激及氧化损伤在OSAHAHT患者中更明显.     

Hepatoprotective potential of Tecomella undulata stem bark is partially due to the presence of betulinic acid

Ethnopharmacological relevance

Tecomella undulata (TU;` Family Bignoniaceae) is used in Indian Ayurvedic system of medicine for treating various diseases including hepatic ailments. It is also incorporated in various marketed hepatoprotective polyherbal formulations.

Aim

The present study was aimed at evaluating possible hepatoprotective role of isolated compounds from TU stem bark (TSB) using in vitro and in vivo experimental models.

Methods

In vitro cytotoxicity and hepatoprotective potential of various extract, fractions and isolated compounds from TU stem bark were evaluated using HepG2 cells. Rats were pre-treated with TU methanolic extract (TSB-7) or betulinic acid (MS-2) or silymarin for 7 days followed by a single dose of CCl₄ (0.5 ml/kg, i.p.). Plasma markers of hepatic damage, hepatic antioxidants and indices of lipid peroxidation along with microscopic evaluation of liver were assessed in control and treatment groups.

Results

TSB-2 and MS-1 accounted for significant cell death whereas; TSB-1, TBS-7, TSB-9, TSB-10 and, MS-2 did not register significant cytotoxicity. Further, non-cytotoxic components exhibited ascending grade of hepatoprotection in vitro (TSB-10<TSB-1<TSB-7<TSB-9<MS-2). Pre-treatment of TSB-7 or MS-2 to CCl₄ treated rats prevented hepatocyte damage as evidenced by biochemical and histopathological observations.

Conclusion

It can be concluded that, hepatoprotective potential of Tecomella undulata stem bark is partially due to the presence of betulinic acid.     

Acute acidosis elevates malonaldehyde in rat brain in vivo

Oxidative stress in brain tissue was measured experimentally in situ using microdialysis to sample the extracellular environment for a lipid peroxidation breakdown product and antioxidants. The extracellular concentrations of the lipid peroxidation product malonaldehyde (MDA) and the antioxidants ascorbic acid (AA) and uric acid (UA) were measured in rat cortex and striatum in vivo using microdialysis coupled to HPLC with UV detection. Tissue acidosis following ischaemia and epileptic seizures may contribute to neuronal damage, which may be mediated by reactive oxygen species. Perfusion of microdialysis probes with acidic artificial cerebrospinal fluid (pH 6) led to a significant increase in the sampled concentration of MDA and the antioxidant ascorbic acid. Simultaneous perfusion of ascorbate (5 mM) with acidic ACSF (pH 6) completely attenuated the rise in lipid peroxidation. This study provides in vivo evidence for acidosis induced oxidative stress in brain tissue and an antioxidant action of ascorbate. The methodology described here can provide direct in vivo information in respect of oxidative stress in experimental situations. The method could equally be applied to the assessment of oxidative stress in a number of pathological models not necessarily confined to the CNS     

职业性铝接触对红细胞膜Na—K—ATP酶活性的影响

为探讨铝的毒作用机制．本研究选择某铝厂铝作业工人72名作为研究对象，以同一地区非铝作业工人41名作为对照人群，观察铝对职业人群红细胞膜Na-K－ATP酶活性的影响。结果显示，各年龄段铝作业工人的尿铝含量均明显高于对照组；丙二醛（MDA）含量无显著性差异；Na－K－ATP酶活性铝接触组与对照组之间有明显差异，以35～44岁年龄段铝作业工人为最高，并与同年龄段对照工人存在显著性差异。长期职业性铝接触可以引起红细胞膜Na－K－ATP酶活性升高，这一结果可能是由于铝的直接作用，而与机体脂质过氧化作用无关．