Circulating markers of oxidative stress and liver fibrosis in Sudanese subjects at risk of schistosomiasis and hepatitis

Epidemiological studies in the developing world are frequently biased by the simultaneous presence of several infectious pathogens. In the present study, we examined the usefulness of circulating markers of oxidative stress and liver fibrosis to investigate the distinct forms of chronic liver inflammations associated with schistosomiasis and viral hepatitis, respectively. The study was performed in a Sudanese population exposed to Schistosoma. Circulating hyaluronic acid (HA) was used as a marker of liver fibrosis; the severity of schistosomiasis was determined by ultrasonic examination; viral hepatitis infection was ascertained by circulating anti-hepatitis antibodies. Serum markers were examined also in Sudanese subjects not exposed to Schistosoma infection and in French control subjects. We found a drastic decrease of lycopene levels in the subjects exposed to schistosomiasis in comparison with non-exposed Sudanese and French control subjects. Retinol, alpha-tocopherol and five carotenoids were unchanged. Lycopene depletion was unlikely to be due to variations of nutritional origin, since the lycopene/beta-carotene ratio was five-fold lower in the population at risk of schistosomiasis than in the other groups. We found that high HA serum levels were associated with severe periportal fibrosis but not with viral infection. Conversely, levels of the oxidized lipid malondialdehyde (MDA) were associated with viral infection but not with the severity of schistosomiasis, even though the two infections had additive effects. We concluded that serum markers are valuable tools for investigating the complex effects of co-existing factors of chronic liver inflammation.     

Short exposure of albumin to high concentrations of malondialdehyde does not mimic physiological conditions

Malondialdehyde (MDA), a major lipid peroxidation product, spontaneously binds to, and modifies proteins. In vivo, proteins are physiologically exposed to micromolar MDA concentrations for long periods. In order to mimic this process in vitro, protein modification is often performed by short exposure to millimolar MDA concentrations, also in order to generate antigenic structures for antibody production.     

艾灸足三里和梁门穴诱导热休克蛋白70抗大鼠胃黏膜氧化损伤作用

目的:观察艾灸足三里和梁门穴对应激性溃疡大鼠胃黏膜热休克蛋白70(HSP70)表达的影响,探讨艾灸足阳明经穴抗胃黏膜氧化损伤的作用机制.方法:将SD大鼠60只完全随机平均分为空白组、模型组、艾灸足三里等穴组和艾灸非穴对照点组,采用水浸-束缚应激法制备应激性溃疡模型.按Guth法计算胃黏膜损伤指数(UI),用激光多普勒血流仪测定胃黏膜血流量(GMBF),用免疫组织化学法和硫代巴比妥酸染色法对处理后大鼠检测其胃黏膜HSP70的表达和丙二醛(MDA)的含量.结果:与模型组和艾灸非穴组比较,艾灸足三里等穴可使应激性溃疡大鼠胃黏膜损伤指数明显下降(14.100±5.425vs26.800±9.807,26.200±7.729,P<0.01),HSP70表达上调(0.133±0.035vs0.077±0.057,0.059±0.038,P<0.01)、血流量增高(279.827±172.862mL/minvs139.489±33.133,141.512±58.450mL/min,P<0.05)、MDA含量减少(2.586±0.252μmol/Lvs3.906±0.768,3.464±1.502μmol/L,P<0.05).结论:艾灸足三里和梁门穴能诱导胃黏膜HSP70高表达并降低MDA含量,以达到其抗氧化损伤作用,并有相对的穴位特异性.     

Effect of DASH diet on oxidative stress parameters: A systematic review and meta-analysis of randomized clinical trials

Background and aimsOxidative stress (OS) is one of the main risk factors for several chronic diseases. The Dietary Approaches to Stop Hypertension (DASH) contain many antioxidants and may contribute to managing OS.ObjectiveTo perform a systematic review and meta-analysis to examine the impacts of the DASH diet on OS parameters.MethodsA comprehensive electronic search in MEDLINE, Scopus, EMBASE, and the Cochrane Central Register of Controlled Trials was performed through September 2020 to find related studies evaluating the impact of the DASH diet on OS parameters. Standardized mean differences were pooled using random-effects meta-analysis.ResultsEight studies with a total of 317 subjects met our inclusion criteria. Four studies included in meta-analysis model with 200 participants (100 in treatment and 100 in control group). The DASH diet was associated with a statistically significant decrease in malondialdehyde (MDA) (SMD: −0.53; 95% CI: −0.89, −0.16; I² = 42.1%), and a significant increase in glutathione (GSH) (SMD: 0.83; 95% CI: 0.36, 1.03; I² = 42.1%). Meta-analysis found no statistically significant effect of DASH diet on nitric oxide (NO) (SMD: −1.40; 95% CI: −0.12, 1.93; I² = 92.6%) or total antioxidant capacity (TAC) levels (SMD: 0.95; 95% CI: −0.10, 1.99; I² = 87.6%).ConclusionOur results demonstrated that a DASH diet could significantly increase GSH and decrease MDA levels. Furthermore, there is a trend to improve TAC, NO, and f2-isoprostanes by the adherence to the DASH diet. However, long-term, large sample size and well-designed randomized clinical trials are still needed to draw concrete conclusions about DASH diet’s effects on OS parameters.     

Histopathologic,biochemical and genotoxic investigations on chronic sodium nitrite toxicity in mice

The aim of this study was to investigate the effects of long term Sodium nitrite (NaNO₂) consumption. Swiss albino mice were given NaNO₂ (0, 10 and 20 mg/kg/day) as mixed in feed for 8 months. At the end of treatments, animals were sacrificed and selected organs were processed for histopathologic, imunohistochemical, biochemical and genotoxic investigations. Mild to moderate degenerative changes were observed in liver, kidney, intestine, lung and spleen of NaNO₂-given mice. Inducible nitric oxide synthase and nitrotyrosine activities increased in liver and kidney of NaNO₂-given mice. Proliferating cell nuclear antigen activity increased in liver. Apoptotic cell death was observed in livers of the treatment groups. Liver malondialdehyde level was higher in the treatment groups while no change was seen in kidney. Nitric oxide levels in both liver and kidney of the treatment groups were lower than those of the control group. In genotoxic investigations, the number of chromosome and chromatid breaks, chromatid association, and polyploidy increased while mitotic index decreased in NaNO₂-given mice. The results showed that NaNO₂ would cause histopathologic changes, nitrosative tissue damage, and lipid peroxidation in liver and kidney, as well as induce chromosomal aberrations even if it was given at low levels for long time.     

迎春花总黄酮对小鼠抗氧化作用的影响

目的研究迎春花总黄酮对小鼠抗氧化作用的影响。方法取小鼠32只,随机分为生理盐水组、50．0mg／kg迎春花总黄酮组、100．0mg／kg迎春花总黄酮组、200．0mg／kg迎春花总黄酮组。给药10d,颈椎脱臼处死小鼠。取心、脑、肝等组织,分别检测其心、脑、肝等组织中的超氧化物歧化酶（SOD）的活性、丙二醛（MDA）的含量和总抗氧化能力（TAOC）。结果与生理盐水组比较,100．0、200．0mg／kg的迎春花总黄酮能显著升高小鼠心、脑、肝等组织中的SOD活性和TAOC含量（P〈0．05,P〈0．01）,显著降低心、脑、肝等组织中MDA含量（P〈0．05,P〈0．01）。结论迎春花总黄酮具有清除体内脂质过氧化物和减轻机体的过氧化损伤的作用。     

人工模拟干旱胁迫下金银花幼苗的生理适应性反应

目的研究人工模拟干旱胁迫条件下金银花幼苗的生理适应性反应,为揭示金银花植株的抗旱机制以及抗旱品种的选育提供理论依据。方法采用聚乙二醇（PEG-6000）模拟干旱胁迫处理金银花幼苗,检测幼苗体内的丙二醛（MDA）含量;超氧化物歧化酶（SOD）、过氧化物酶（POD）、过氧化氢酶（CAT）、抗坏血酸过氧化物酶（APX）等保护酶活性,渗透调节物质脯氨酸（Pro）和可溶性糖含量。结果 10%、20%和30%PEG处理幼苗后120 h MDA含量分别高出对照组20.31%、28.12%和36.72%,随着PEG浓度升高,MDA含量逐渐增加。SOD、POD、CAT和APX活性总体呈现先升高后降低的趋势,各种酶对干旱胁迫的响应速率不同,CAT于干旱胁迫后立即开始启动,SOD、POD于干旱胁迫后24 h启动,而APX于干旱胁迫后48 h开始启动。Pro和可溶性糖含量均于处理后24 h开始增高,于处理后72 h达到峰值。结论随着干旱程度的增加和胁迫的延长,金银花体内膜质过氧化严重,通过增加Pro、可溶性糖的含量以及保护酶系统来抵御干旱胁迫,保护酶启动顺序为CAT、SOD、POD、APX。     

番茄红素对兔动脉粥样硬化形成和氧化损伤的影响

目的观察番茄红素对兔实验性动脉粥样硬化形成和氧化损伤的影响。方法采用高胆固醇喂饲模型;将21只新西兰家兔随机分为3组:对照组、高脂组和番茄红素组,分别给予普通饲料和高胆固醇饮食喂养,番茄红素组另加用番茄红素;于实验开始前1天和开始后第4、8、10周末取空腹血,测定血清超氧化物歧化酶活性、丙二醛含量。第10周末,测定血清一氧化氮合酶活性及一氧化氮含量。实验结束后,观察主动脉血管病理变化。结果与高脂组相比,番茄红素组主动脉脂质斑块面积减少;血超氧化物歧化酶活性明显增加;血清丙二醛含量减少,一氧化氮含量增加。结论研究结果提示,番茄红素具有较好的抗动脉粥样硬化作用,抗氧化损伤及保护血管内皮功能可能是番茄红素产生抗动脉粥样硬化作用的重要机制之一。     

应激性溃疡的发生及川芎嗪的防治效应

本实验观察了家兔创伤后胃粘膜损伤情况及川芎嗪的防治效应。发现动物创伤后目粘膜损伤严重．出现应激性溃疡．同时血浆和胃粘膜组织中脂质过氧化物商二醇含量增加，且胃粘膜细胞有明显的钙积聚。而应用川芎嗪防治的动物．脂质过氧化反应被明显地抑制，钙超载现象显著减轻．胃粘膜损伤轻微。提示，应激性溃疡的发生与自由基反应和细胞内钙超载有关，川芎嗪对应激性溃疡具有防治作用。     

Aging aggravates long-term renal ischemia-reperfusion injury in a rat model

Aim

Ischemia-reperfusion injury (IRI) has been considered as the major cause of acute kidney injury and can result in poor long-term graft function. Functional recovery after IRI is impaired in the elderly. In the present study, we aimed to compare kidney morphology, function, oxidative stress, inflammation, and development of renal fibrosis in young and aged rats after renal IRI.

Materials and methods

Rat models of warm renal IRI were established by clamping left pedicles for 45 min after right nephrectomy, then the clamp was removed, and kidneys were reperfused for up to 12 wk. Biochemical and histologic renal damage were assessed at 12 wk after reperfusion. The immunohistochemical staining of monocyte macrophage antigen-1 (ED-1) and transforming growth factor beta 1 (TGF-β1) and messenger RNA level of TGF-β1 in the kidney were analyzed.

Results

Renal IRI caused significant increases of malondialdehyde and 8-hydroxydeoxyguanosine levels and a decrease of superoxide dismutase activity in young and aged IRI rats; however, these changes were more obvious in the aged rats. IRI resulted in severe inflammation and tubulointerstitial fibrosis with decreased creatinine (Cr) clearance and increased histologic damage in aged rats compared with young rats. Moreover, we measured the ratio of Cr clearance between young and aged IRI rats. It demonstrated that aged IRI rats did have poor Cr clearance compared with the young IRI rats. ED-1 and TGF-β1 expression levels in the kidney were significantly higher in aged rats than in young rats after IRI.

Conclusion

Aged rats are more susceptible to IRI-induced renal failure, which may associate with the increased oxidative stress, increased histologic damage, and increased inflammation and tubulointerstitial fibrosis. Targeting oxidative stress and inflammatory response should improve the kidney recovery after IRI.