鼠神经生长因子、亚低温联合甲强龙在急性脊髓损伤中的应用及对氧化应激水平的影响

目的 探讨鼠神经生长因子、亚低温联合甲强龙治疗急性脊髓损伤的临床疗效及对氧化应激水平的影响。方法 选取2016年5月—2018年6月延安大学附属医院收治的急性脊髓损伤患者132例作为研究对象。按随机数字表法分为对照组和观察组,每组66例。对照组静脉滴注甲强龙,初始剂量为30 mg/kg,随后以5.4 mg/（kg·h）的速度持续静脉滴注23 h,同时给予亚低温治疗,降温同时给予静脉滴注冬眠合剂维持24 h;观察组在对照组的基础上,肌内注射鼠神经生长因子30 g/d,持续给药2个月。观察两组患者脊髓功能恢复情况,包括：ADL、运动、触觉及针刺觉检查评分;观察血清GSH-Px和SOD的变化,追踪两组患者的并发症。结果 两组患者治疗后ADL、运动、触觉及针刺觉检查评分较治疗前升高（P <0.05）;观察组的评分高于对照组（P <0.05）;两组患者治疗后血清GSH-Px和SOD水平较治疗前升高（P <0.05）;观察组的氧化应激水平高于对照组（P <0.05）;两组患者并发症发生率差异无统计学意义（P >0.05）。结论 在甲强龙背景治疗下,鼠神经生长因子联合亚低温能促进急性脊髓损伤患者的神经功能恢复,提高患者的生活质量。     

云母颗粒对无水乙醇诱导大鼠胃黏膜损伤的影响及机理探讨

[目的]研究云母颗粒对无水乙醇诱导大鼠胃黏膜损伤的保护作用及其机理。[方法]将48只健康雄性SD大鼠随机分为云母颗粒高、中、低剂量组,思密达组,模型对照组,空白对照组6组。分别将云母颗粒和思密达预先灌胃于相应各组大鼠,3h后以1ml／100g无水乙醇灌胃致胃黏膜损伤,45min后下腔静脉取适量血,处死取胃,然后分别检测各组的胃黏膜损伤指数、血清和胃黏膜组织中超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-Px）含量,并观察病理学变化,以评价胃黏膜损伤程度及药物的作用。[结果]云母各剂量组中SOD、GSH-Px含量均显著高于模型对照组,而MDA含量则明显低于模型对照组（P〈0．05）。[结论]云母颗粒对无水乙醇诱导的大鼠胃黏膜损伤具有预防与保护作用,其保护作用是通过增加大鼠血清和胃黏膜组织中SOD、GSH-Px含量并减少MDA的生成来实现的,即云母颗粒具有抗脂质过氧化作用。     

黄花棘豆醇提物的抗缺氧作用研究

目的 研究黄花棘豆的抗缺氧作用.方法 实验分为常压密闭抗缺氧、减压密闭抗缺氧及亚硝酸中毒实验3部分,每部分60只小鼠,予各组小鼠连续ig7 d,于末次灌胃1h后分别记录小鼠的生存时间,并测定、分析各组小鼠心脏和大脑中的SOD、MDA、Bcl-2、Bax和GSH-Px.结果 与空白对照组比较,黄花棘豆高剂量组小鼠的缺氧暴露时间明显延长,各项生化指标均有改善(P＜0.05).结论 黄花棘豆醇提物能够提高小鼠缺氧耐受力,具有一定的抗缺氧作用.     

Assessment of oxidative stress responses and the cytotoxic and genotoxic potential of the herbicide tembotrione in HepG2 cells

Tembotrione is a triketone herbicide, usually used for post-emergence weed control in corn. Currently, there is little or no published data on its genotoxicity to human cells either in vitro or in vivo. This study evaluated the impact of acute (4 and 24 h) exposure to low concentrations of tembotrione [corresponding to the acceptable daily intake (0.17 μg/mL), residential exposure level (0.002 μg/mL) and acceptable operator exposure level (0.0012 μg/mL)] on human hepatocellular carcinoma cell line HepG2, using biomarkers of oxidative stress, CCK-8 colorimetric assay for cell viability, alkaline comet assay, and cytokinesis-block micronucleus “cytome” assay. Tembotrione applied at concentrations likely to be encountered in occupational and residential exposures induced cytogenetic outcomes in non-target cells despite non-significant changes in the values of oxidative stress biomarkers. We assume that the observed effects were mainly the consequence of impaired metabolic pathways in HepG2 cells due to the inhibition of the enzyme 4-hydroxyphenyl-pyruvate-dioxygenase by tembotrione, which possibly caused a depletion of folate levels leading to excess formation of nuclear buds in the affected cells. Regardless of the fact that tembotrione was previously reported negative for mutations and chromosome aberrations in vitro, our findings call for more precaution in its use.     

真武汤加味治疗糖尿病肾病脾肾气虚证临床研究

目的:观察真武汤加味对糖尿病肾病脾肾气虚证患者血清转化生长因子-β(transforming growth factor beta,TGF-β)和谷胱甘肽过氧化物酶(glutathion peroxidase,GSH-Px)水平的影响,并观察其治疗该病的临床疗效。方法:将114例患者按随机数字表法分为对照组和观察组各57例。对照组患者给予氯沙坦钾片,每次100 mg,1次·d~(-1),口服。观察组在对照组治疗基础上加用真武汤加味,1剂·d~(-1)。两组疗程均为24周,并进行24周随访。记录治疗期间和随访期间病情进展至Ⅴ期的患者,或肌酐翻倍等终点事件发生情况;检测治疗前后糖化血红蛋白(glycosylated hemoglobin,HbAlc)、尿素氮、血肌酐、24小时尿蛋白定量检测;进行治疗前后脾肾气虚证评分;检测治疗前后TGF-β、GSH-Px水平。结果:观察组临床疗效有效率为84.21%,高于对照组的64.91%,差异有统计学意义(χ~2=5.573,P0.05)。观察组中医证候有效率为91.23%,高于对照组的75.44%,差异有统计学意义(χ~2=5.116,P0.05)。对照组终点事件发生率为43.86%,高于观察组的24.56%,差异有统计学意义(χ~2=4.715,P0.05)。治疗后两组Hb Alc水平均较治疗前下降(P0.01),两组24小时尿蛋白定量、尿素氮和肌酐水平均较治疗前升高(P0.01);治疗后观察组HbAlc、24小时尿蛋白定量、尿素氮和肌酐水平均低于对照组(P0.01)。治疗后观察组TGF-β水平均低于对照组,GSH-Px水平高于对照组(P0.01)。结论:真武汤加味治疗糖尿病肾病脾肾气虚证能改善临床症状、降低蛋白尿、调节血糖,从而降低终点事件的发生率,对DN病情起到延缓作用,其作用机制可能是下调TGF-β、升高GSH-Px等细胞因子来实现的。     

乌药醚内酯对肝损伤模型大鼠的保护作用

目的 考察不同剂量乌药醚内酯对大鼠肝损伤模型的保护作用。 方法 60只健康雄性SD大鼠随机均分为空白对照组、模型组、乌药醚内酯低、中、高剂量组及阳性药物对照组,除空白对照组外,其余5组采用四氯化碳腹腔注射建立肝损伤大鼠模型,造模期间各组给予相应的药物或等体积的水,造模6w后处死大鼠取血清,测ALT、AST、MDA含量及SOD、GSH-Px的活性,取肝脏组织染色切片观察病理变化。 结果 与模型组对比,乌药醚内酯各剂量组能降低模型大鼠血清ALT、AST且呈剂量依赖性;高剂量组还能显著升高模型大鼠血清SOD、GSH-Px活性,降低MDA含量,显著降低肝脏组织的病理变化评分。 结论 乌药醚内酯可能通过提高抗氧化能力来降低肝损伤模型大鼠的ALT和AST水平及肝脏病理变化。     

Effects of enoxaparin in the rat hippocampus following traumatic brain injury

Purpose of this study was to investigate the effects of low molecular weight heparin, enoxaparin, on different parameters of the hippocampal damage following traumatic brain injury (TBI) in the rat. TBI of moderate severity was performed over the left parietal cortex using the lateral fluid percussion brain injury model. Animals were s.c. injected with either enoxaparin (1 mg/kg) or vehicle 1, 7, 13, 19, 25, 31, 37, and 43 h after the TBI induction. Sham-operated, vehicle-treated animals were used as the control group. Rats were sacrificed 48 h after the induction of TBI. Hippocampi were processed for spectrophotometric measurements of the products of oxidative lipid damage, thiobarbituric acid-reactive substances (TBARS) levels, as well as the activities of antioxidant enzymes, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). Moreover, the Western blotting analyses of the oxidized protein levels, expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), pro- and mature-interleukin-1β (pro-, and mature-IL-1β), and active caspase-3 were performed. COX-2 expressions were also explored by using immunohistochemistry. Glial fibrillary acidic protein immunochistochemistry was performed with the aim to assess the level of astrocytic activity. Fluoro-Jade B staining was used to identify the level and extent of hippocampal neuronal injury. TBI caused statistically significant increases of the hippocampal TBARS and oxidized protein levels as well as COX-2, pro-IL-1β, and active caspase-3 overexpressions, but it did not significantly affect the SOD and GSH-Px activities, the iNOS, and mature-IL-1β expression levels. TBI also induced hippocampal reactive astrocytosis and neurodegeneration. Enoxaparin significantly decreased the hippocampal TBARS and oxidized protein levels, COX-2 overexpression and reactive gliosis, but it did not influence the SOD and GSH-Px activities, pro-IL-1β and active caspase-3 overexpressions as well as neurodegeneration following TBI. These findings demonstrate that enoxaparin may reduce oxidative damage, inflammation and astrocytosis following TBI in the rat and could be a candidate drug for neuroprotective treatment of this injury.     

Acute and chronic effects of electroconvulsive treatment on oxidative parameters in schizophrenia patients

Electroconvulsive therapy (ECT) is an effective treatment alternative for schizophrenia. Previous studies have already indicated the possible effects of oxidative stress in this disorder. However, there have been no previous studies evaluating the effects of ECT on the oxidative stress in these patients. We therefore aimed to investigate the acute and chronic effects of ECT on serum levels of oxidant and antioxidant molecules in schizophrenia patients (n = 28). The serum MDA and CAT levels of the patients with schizophrenia were higher than that of the controls before ECT (n = 20) but there was no significant difference in the serum NO and GSH levels of the patient groups compared to the controls. We found that the NO levels of the patients were higher than the controls in the group experiencing their first episode but not in the chronic group. There was a significant clinical improvement in the patients in terms of BPRS, SANS and SAPS reduction after the 9th ECT, but not the 1st ECT. Serum MDA levels were significantly reduced compared to the baseline after the 9th ECT session although there was no significant difference after the 1st session. Separate evaluation of the patient groups revealed that the significant MDA decrease following ECT was in the patients experiencing their first episode and not in the chronic group. No significant difference was noted in the serum levels of other oxidant and antioxidant molecules after either the 1st or 9th ECT session. These results suggest that ECT does not produce any negative effect on oxidative stress in patients with schizophrenia.     

Cardioprotective effects of saponins from Panax japonicus on acute myocardial ischemia against oxidative stress-triggered damage and cardiac cell death in rats

Aim

To study the cardioprotective effects of saponins from Panax japonicus (SPJ) on acute myocardial ischemia injury rats induced by ligating of the left anterior descending branch (LAD), on the basis of this investigation, the possible mechanism of SPJ was elucidated.

Materials and methods

SPJ was identified by high performance liquid chromatography-evaporative light scattering detection. Male Sprague-Dawley rats (200–220 g) were randomly divided into four groups: sham-operated, LAD, LAD + l-SPJ (SPJ, 50 mg/kg/day, orally) and LAD + h-SPJ (SPJ, 100 mg/kg/day, orally). Before operation, the foregoing groups were pretreated with homologous drug once a day for 7 days, respectively. After twelve hours in LAD, the cardioprotective effects of SPJ were evaluated by infarct size, biochemical values, hemodynamic, and histopathological observations and the antioxidative and antiapoptotic relative gene expressions.

Results

SPJ significantly improved heart function and decreased infarct size; remarkably decreased levels of serum lactate dehydrogenase, creatine kinase, xanthine oxide and malondialdehyde content, increased contents of serum total antioxidant capacity, superoxide dismutase (SOD), glutathione peroxidase, catalase; quantitative real-time PCR results showed that SPJ might markedly reverse the down-regulated mRNA expressions of the SOD1, SOD2 and SOD3, ameliorate the increased Bax and caspase-3 mRNA expressions and decreased Bcl-2 mRNA expression and ratios of Bcl-2 to Bax. Histopathological observations provided supportive evidence for biochemical analyses, and with the dose of SPJ increasing, the aforesaid improvement became more and more strong.

Conclusions

The studies demonstrated that in ischemic myocardium, oxidative stress caused the overgeneration and accumulation of reactive oxygen species (ROS), which was central of cardiac ischemic injury. SPJ exerted beneficially cardioprotective effects on myocardial ischemia injury rats, mainly scavenging oxidative stress-triggered overgeneration and accumulation of ROS, alleviating myocardial ischemia injury and cardiac cell death.     

茵芩清肝汤对酒精性肝病大鼠血清NO,GSH-Px的影响

目的:研究茵芩清肝汤对酒精性肝病大鼠血清一氧化氮(N0)、谷胱甘肽过氧化物酶(GSH-Px)的影响.方法:按每天8～12 mL·kg-1ig 52度白酒(随时间延长而递增,第1周为8 mL·kg-1,第2周10 mL-kg-1,第3周起12 mL·kg-1,以后继续维持此量,直至实验结束)配合高脂肪饲料喂养,造成大鼠酒精性肝病模型.随机分为模型组、正常组、茵芩清肝汤(20 9·kg-1 ig)组,硫普罗宁(5 mg· kg-1ig)组、水飞蓟宾(5 mg·kg-1ig)组进行比较.每组30只,分别于实验第4周、第8周、第12周每组各取大鼠10只,称重后以乙醚麻醉动物,迅速断头取血,按常规方法分离血清,测量NO,GSH-Px含量.结果:模型组大鼠血清NO各阶段水平较正常组(15.36±7.2) μmol· L-1明显升高(P＜0.01),第12周达到(40.8±7.5)μmol· L-(P ＜0.01),GSH-Px各阶段水平较正常组(146.3±51.9) U·mg-1明显降低(P＜0.01),第12周达到(86.4±6.4) U·mg-1 (P ＜0.01).各治疗组大鼠血清NO各阶段水平较模型组均降低(P＜0.05),菌芩清肝汤组第12周达到(31.12±4.7)μmol·L-1(P ＜0.01);GSH-Px水平(107.7±31.1) U·mg-1较模型组均明显升高(P＜0.01).结论:茵芩清肝汤可降低血清NO含量、提高GSH-Px活性,抑制脂质过氧化反应,这可能是它防治酒精性肝病的机制之一.