Changes of Selenium Metabolism Glutathione Peroxidase Activity and Lipid Peroxides Content in Severely Scalding-injured Rats

The changes of sclenium metabolism, glutathione peroxidase activity and lipid peroxidescontent in the tissues of rats suffering from 30% TBSA full thickness scalding were observed in thefirst 7 days after injury. It was found that selenium content in the rat tissues decreased remarkably af-ter injury, which in turn resulted in serious reduction of glutathione peroxidasc activity and significantincrease of lipid peroxides in the scrum, crythrocytcs and liver. However the muscular tissue showedno significant changes. These facts imply that after burn injury, the body is in a state of selenium deficiency, the lossof selenium might be responsible for the reduction of anti - peroxidation ability of glutathioneperoxidase, and conscqucntly there is an increase of lipid peroxides in the tissues. Only the musculartissue is insensitive to lipid peroxidation. It is believed that the reduction of anti-peroxidation abilityof glutathione peroxidasc after bum injury might be one of the main causes to intensify, the injury re-suiting from free radicals.

EFFECTS OF COMBINATION OF ACUPUNCTURE AND MOXIBUSTION WITH CHINESE DRUGS ON LIPIDS PEROXIDE AND ANTIOXIDASE IN PATIENTS OF VASCULAR DEMENTIA

In the present paper, blood lipids peroxide(LPO) level and activities of glutathione peroxidase(GSH-Px) and superoxide dismutase(SOD) were investigated before and after combined treatment of acupuncture and moxibustion and Chinese drugs in patients of vascular dementia(VD), and their results were compared with those in healthy persons with the similar ages to the patients. The results showed that the blood LPO level increased significantly, and the activities of SOD and GSH-Px reduced significantly in patients of VD as compared with those in the control group. Degrees of patient’s condition were related with amplitudes of the increase of LPO and the reduction of activities of GSHPx and SOD. Combined treatment of acupuncture and moxibustion and Chinese drugs could raise markedly activitles of blood GSH-Px and SOD, and lowered LPO level in the patients of VD, which are related to clinical therapeutic effects. It is considered that combination of acupuncture and moxibustion with Chinese drugs can increase the action of the antiperoxidative system in the patients of VD, exerting anti-peroxidative ability and clearing LPO and reducing the oxidative injury of the organism by oxygen free radical, which is one of mechanisms of combined treatment of acupuncture and moxibustion with Chinese drugs.

中药调控成骨细胞铁死亡治疗激素性股骨头坏死

背景:有研究发现成骨细胞铁死亡可作为重要的发病机制诱导激素性股骨头坏死的发生与发展。随着祖国医学的发展,有学者发现某些中药单体、中药复方及中成药等可通过多种通路机制调控成骨细胞铁死亡,最终起到治疗激素性股骨头坏死的作用。目的:探讨成骨细胞铁死亡与激素性股骨头坏死的关系及中草药调控成骨细胞铁死亡治疗激素性股骨头坏死的作用机制,为激素性股骨头坏死的诊治提供新的思路。方法:以“铁死亡,激素性股骨头坏死,成骨细胞,中草药,糖皮质激素,铁代谢,活性氧,谷胱甘肽过氧化物酶”为中文检索词,以“ferroptosis,Hormonal necrosis of the femoral head,osteoblast,Chinese herbal medicine,glucocorticoid,iron metabolism,ROS,GPX4”为英文检索词,检索中国知网、Pub Med、万方及维普数据库,筛选各数据库建库至2023年成骨细胞铁死亡与激素性股骨头坏死及中草药干预调控研究相关的文章,最终纳入74篇文献进行综述分析。结果与结论:(1)成骨细胞铁死亡在激素性股骨头坏死发病中起重要作用。(2)成骨细胞铁死亡的发生受到多种机制通路调控,如细胞内铁超载引起铁死亡;细胞发生脂质过氧化损伤细胞膜引起铁死亡;细胞膜上胱氨酸/谷氨酸逆向转运蛋白通过影响谷胱甘肽水平和谷胱甘肽过氧化物酶4活性,从而诱导铁死亡;细胞内发生芬顿反应产生大量活性氧引起铁死亡等。(3)中药单体淫羊藿苷等、中药复方青娥丸等及中成药补肾活血颗粒等均可通过调控成骨细胞铁死亡的发生,有助于防治激素性股骨头坏死。(4)目前关于成骨细胞铁死亡相关机制尚不明确,继续深入探明两者的作用机制,有望为临床治疗激素性股骨头坏死提供新选择。

Effects of resveratrol on hydrogen peroxide-induced oxidative stress in embryonic neural stem cells

Resveratrol, a natural phenolic compound, has been shown to prevent cardiovascular diseases and cancer and exhibit neuroprotective effects. In this study, we examined the neuroprotective and antJoxJdant effects of resveratrol against hydrogen peroxide in embryonic neural stem cells. Hydrogen peroxide treatment alone increased catalase and glutathione peroxidase activities but did not change superoxide dismutase levels compared with hydrogen peroxide ＋ resveratrol treatment. Nitric oxide synthase activity and concomitant nitric oxide levels increased in response to hydrogen peroxide treatment. Conversely, resveratrol treatment decreased nitric oxide synthase activity and nitric oxide levels. Resveratrol also attenuated hydrogen peroxide-induced nuclear or mitochondrial DNA damage. We propose that resveratrol may be a promising agent for protecting embryonic neural stem cells because of its potential to decrease oxidative stress by inducing higher activity of antioxidant enzymes, decreasing nitric oxide production and nitric oxide synthase activity, and alleviating both nuclear and mitochondrial DNA damage.

Impact of dietary oils and fats on lipid peroxidation in liver and blood of albino rats

Objective:To investigate the effects of different dietary fat and oils(differing in their degree of saturation and unsaturation)on lipid peroxidation in liver and blood of rats.Methods:The study was conducted on SO albino rats that were randomly divided into 5 groups of 10 animals.The groups were fed on dietary butter(Group I),margarine(Croup II),olive oil(Group III),sunflower oil(Group IV)and com oil(Group V)for 7 weeks.After 12 h of diet removal,livers were excised and blood was collected to measure malondialdehyde(MDA)levels in the supernatant of liver homogenate and in blood.Blood superoxide dismutase activity(SOD),glutathione peroxidase activity(GPx),serum vitamin E and total antioxidant capacity(TAC)levels were also measured to determine the effects of fats and oils on lipid peroxidation.Results:The results indicated that no significant differences were observed in SOD activity,vitamin E and TAC levels between the five groups.However,there was significant decrease of GPx activity in groups IV and V when compared with otlier groups.The results indicated that feeding corn oil caused significant increases in liver and blood MDA levels as compared with other oils and fats.There were positive correlations between SOD and GPx,vitamin E and TAC as well as between GPx and TAC(r:0.743;P<0.001)and between blood MDA and liver MDA(r:0.897;P<0.00l).The results showed also negative correlations between blood MDA on one hand and SOD,GPx,vitamin E and TAC on the other hand.Conclusions:The results demonstrated that feeding oils rich in polyunsaturated fatly acids(PUFA)increases lipid peroxidation significantly and may raise the susceptibility of tissues to free radical oxidative damage.

Dynamic Changes in Lipid Peroxidation and Antioxidant Level in Rat’s Tissues with <i>Macrovipera</i><i>lebetina</i><i>obtusa</i>and <i>Montivipera</i><i>raddei</i>Venom Intoxication

We investigated the balance of free radicals in different tissues (liver, heart, brain and muscle) of rats in course of in vivo and in vitro processing by Macrovipera lebetina obtusa (MLO) and Montivipera raddei (MR) snake venoms. Chemiluminescence (ChL) levels were examined in tissue assays after incubation (at 37 &#176C for a period of 10 min) with venom for in vitro experiments and in tissue assays isolated of 10 min after venom injection for in vivo experiments. The TBA-test was also performed to confirm the free radical expression. The activities of antioxidant enzymes (such as superoxide dismutase and glutathione peroxidase) in isolated tissues were detected by spectro-photometry. During the in vitro processing chemiluminescence levels of tissue homogenates significantly decreased, while in course of in vivo intoxication the level of ChL was elevated in brain and liver;lipid peroxidation also increased in brain tissue, but there was no significant balance change in other tissues;the activity of superoxide dismutase mainly correlated with changes of free radical balance during intoxication. On the contrary, the activity of glutathione peroxidase showed the reverse tendencies to change. We suggest that free radicals and their oxidative stresses may play a role in the early stage of intoxication causing the so-named “spreading-effect”, which is very characteristic for the venom of vipers.

Alterations of Antioxidative Enzymes Activities and Induction of Lipid Peroxidation in Germinating Wheat Seeds Subjected to Cadmium Stress

Germinating wheat （Triticum aestivum L.） seeds were exposed to CdCI2 （50, 100 and 200 μM） for 48 h and some aspects of oxidative metabolism was assessed in the embryonic tissues. The germination percentage and the soluble protein content of the embryonic tissues were found to decrease with increasing of Cd concentration. There was elevation in superoxide dismutase （SOD） and decline in catalase （CAT） and peroxidase （POX） activities. The increasing of lipid peroxidation levels indicated the prevalence of oxidative stress in the tissues which was probably due to the alteration of antioxidative enzymes activities. The adding of ascorbate, along with CdCl2, has resulted in restoration of the Cd induced decline in CAT activity. Weakening in H2O2 detoxification system seems to be the principal reason behind Cd induced oxidative stress in germinating seeds. Thus, imposition of oxidative stress might be the consequence of cadmium stress and this finding may help in elucidating the mechanisms underlying cadmium mediated toxicity in germinating seeds.

CLINICAL SIGNIFICANCE OF VITAMIN C TO AMELIORATE LIPID PEROXIDATION DAMAGE IN CORONARY ARTERY DISEASE

The activities of superoxide dismutase (SOD). glutathione peroxidase (GSH-PX) in blood and the content of melondialdehyde (MDA) in plasma of 30 Fatients (male 17, female 13) with coronary artery disease (CAD) were determined in this study. It was shown that SOD and GSH-PX activities were decreased and the content of MDA was increased in the Patients comparative with the healthy controls (P<0.001). Vitamin C, the free radical scavenger, was then administered intravenously with a daily dose of 2g for 2 weeks. The activities of SOD and GSB-PX were significantly elevated (P<0.01, and P<0.05, respectively). and the level of MDA was obviously declined (P<0.01). Thus,the lipid peroxidation is involved in the pathogenesis of CAD,and vitamin C possessing some effects to ameliorate the lipid peroxidation damage could be helpful in the treatment of CAE.

血清谷胱甘肽过氧化物酶、脂质过氧化物水平与妊娠期糖尿病及其糖脂代谢异常、胰岛素抵抗和母婴结局的关系

目的探讨血清谷胱甘肽过氧化物酶(GSH-PX)、脂质过氧化物(Lpo)水平与妊娠期糖尿病(GDM)及其糖脂代谢异常、胰岛素抵抗和母婴结局的关系。方法选择2020年6月至2022年6月重庆大学附属黔江医院收治的120例GDM病人(GDM组)和同期收治的120例糖耐量正常的孕产妇(对照组)。检测血清GSH-Px、Lpo水平以及糖脂代谢、胰岛素抵抗指标,追踪母婴结局。Pearson分析GSH-Px、Lpo与糖脂代谢、胰岛素抵抗之间相关性,多因素logistic回归分析GDM母婴结局不良的因素。结果GDM组血清GSH-Px水平[(21.05±3.46)U/g比(30.42±5.09)U/g]低于对照组(P<0.05),Lpo水平[(15.95±3.17)μmol/L比(10.61±2.33)μmol/L]高于对照组(P<0.05)。GDM病人血清GSH-Px水平与总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、空腹血糖(FPG)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)呈负相关(P<0.05),与高密度脂蛋白胆固醇(HDL-C)呈正相关(P<0.05);Lpo水平与TC、TG、LDL-C、FPG、FINS、HOMA-IR呈正相关(P<0.05),与HDL-C呈负相关(P<0.05)。120例GDM病人中45例发生母婴结局不良,母婴结局不良组血清GSH-Px水平低于母婴结局良好组(P<0.05),Lpo水平高于母婴结局良好组(P<0.05)。多因素logistic回归分析结果显示年龄、HOMA-IR、Lpo是GDM病人母婴结局不良的危险因素(P<0.05),GSH-Px是GDM病人母婴结局不良的保护因素(P<0.05)。结论GDM病人血清GSH-Px水平降低,Lpo水平增高,且与糖脂代谢紊乱、胰岛素抵抗以及母婴结局不良有关,检测血清GSH-Px、Lpo水平有助于评估GDM胰岛素抵抗状态和母婴结局风险。

Ferroptosis mechanism and Alzheimer's disease

Regulated cell death is a genetically determined form of programmed cell death that commonly occurs during the development of living organisms.This process plays a crucial role in modulating homeostasis and is evolutionarily conserved across a diverse range of living organisms.Ferroptosis is a classic regulatory mode of cell death.Extensive studies of regulatory cell death in Alzheimer’s disease have yielded increasing evidence that fe rroptosis is closely related to the occurrence,development,and prognosis of Alzheimer’s disease.This review summarizes the molecular mechanisms of ferroptosis and recent research advances in the role of ferro ptosis in Alzheimer’s disease.Our findings are expected to serve as a theoretical and experimental foundation for clinical research and targeted therapy for Alzheimer’s disease.

Metformin alleviates spinal cord injury by inhibiting nerve cell ferroptosis through upregulation of heme oxygenase-1 expression

Previous studies have reported upregulation of heme oxygenase-1 in different central nervous system injury models.Heme oxygenase-1 plays a critical anti-inflammatory role and is essential for regulating cellular redox homeostasis.Metformin is a classic drug used to treat type 2 diabetes that can inhibit ferroptosis.Previous studies have shown that,when used to treat cardiovascular and digestive system diseases,metformin can also upregulate heme oxygenase-1 expression.Therefore,we hypothesized that heme oxygenase-1 plays a significant role in mediating the beneficial effects of metformin on neuronal ferroptosis after spinal cord injury.To test this,we first performed a bioinformatics analysis based on the GEO database and found that heme oxygenase-1 was upregulated in the lesion of rats with spinal cord injury.Next,we confirmed this finding in a rat model of T9 spinal cord compression injury that exhibited spinal cord nerve cell ferroptosis.Continuous intraperitoneal injection of metformin for 14 days was found to both upregulate heme oxygenase-1 expression and reduce neuronal ferroptosis in rats with spinal cord injury.Subsequently,we used a lentivirus vector to knock down heme oxygenase-1 expression in the spinal cord,and found that this significantly reduced the effect of metformin on ferroptosis after spinal cord injury.Taken together,these findings suggest that metformin inhibits neuronal ferroptosis after spinal cord injury,and that this effect is partially dependent on upregulation of heme oxygenase-1.

铁死亡及其在实验性急性肺损伤中的作用

作为一种非凋亡性细胞死亡方式,铁死亡的特征是铁依赖性脂质过氧化物积累引起的膜脂质过氧化、线粒体萎缩等,在形态和生化特性上与其他细胞程序性死亡不同。铁死亡受多种代谢通路调控,参与了失血性休克、缺血再灌注、脓毒症、放射等引起的急性肺损伤。本文综述了铁死亡的主要调控机制及其在多种动物模型急性肺损伤发病机制中的作用,以期为防治急性肺损伤提供新的策略。

铁死亡在急性肾损伤中作用及机制的研究进展

铁死亡是一种新型的调节细胞死亡的策略,其发生过程与细胞内的铁代谢、脂质代谢、氨基酸代谢以及多种信号通路有密切联系。铁死亡在急性肾损伤(AKI)的发病机制中起关键作用。铁死亡可能是治疗缺血再灌注损伤、肾毒性药物、横纹肌溶解综合征、脓毒症等多种原因引起的AKI的重要靶点。本文就铁死亡的调控机制及其在AKI中作用的研究进展予以综述。

铁死亡与动脉粥样硬化的联系

铁死亡(Ferroptosis)是新近发现的细胞死亡形式,其特征是细胞内铁离子异常积聚和致死性脂质过氧化。这种调节性细胞死亡与铁代谢、氨基酸代谢、脂质代谢等多种代谢途径有着较为密切的联系。动脉粥样硬化是多种心血管疾病发病的基础之一。近期研究表明,除了凋亡、坏死、自噬等经典死亡途径外,铁死亡也参与了动脉粥样硬化的发生发展。本文阐述了铁死亡机制及其对动脉粥样硬化病变相关细胞及因子的影响。

铁死亡在牙周炎中的研究进展

牙周炎是由菌斑微生物引起的慢性炎症性疾病,是目前导致我国成人失牙的首要原因。由于牙周炎发病机制复杂,目前发病机制仍不清楚。铁死亡(ferroptosis)是一种铁依赖性调节细胞死亡的形式,通过不同的信号途径影响细胞内谷胱甘肽过氧化物酶4(glutathione peroxidase 4,GPX4)功能,进而抗氧化能力下降,活性氧积累,脂质过氧化,最终造成细胞和组织损伤。最近研究发现,铁超载、氧化应激和脂质过氧化与牙周炎的发生、发展过程密切相关。铁死亡主要表现为机体的氧化还原稳态被破坏,抗氧化能力降低,损伤相关的分子模式被激活,促炎介质释放,炎症被诱导或加重。铁依赖性氧化应激与脂质过氧化同时参与铁死亡与炎性疾病的调控,牙周炎致病菌能诱导牙周韧带干细胞的铁死亡,从而激活炎症因子如白细胞介素⁃17、肿瘤坏死因子⁃α、缺氧诱导因子⁃1α等的释放,加重牙周炎;另外铁死亡所激活的炎症因子在牙槽骨稳态中发挥重要作用,铁死亡参与脂多糖诱导牙龈成纤维细胞炎症的过程。未来的研究可着重于探讨铁死亡在牙周炎中作用的分子机制及其治疗靶点,为牙周病的防治提供新的策略。

“脾失健运-铁死亡”在阿尔茨海默病中的机制探析

阿尔茨海默病(Alzheimer′s Disease,AD)以进行性记忆力减退为主要特点,主要发病学说有β-淀粉样蛋白(β-Amyloid,Aβ)瀑布假说和tau蛋白假说。AD的中医认识中多重肾而轻脾,脾胃是其他脏腑功能的基础,脾气健运对治疗AD有重要意义。现代研究发现,铁死亡通过铁代谢紊乱、脂质过氧化、谷胱甘肽耗竭、谷胱甘肽过氧化物酶4失活影响AD的发生发展。脾失健运与铁死亡导致AD的机制有所类似。该文以脾胃为重要切入点,从铁死亡的角度论述“脾失健运-铁死亡”在AD中的机制,强调了脾胃在AD中的重要性,旨在为脾胃治疗AD提供铁死亡方向的理论支持。

铁死亡的分子机制及其对膀胱癌的影响

膀胱癌(bladder cancer,BC)是泌尿系统三大常见恶性肿瘤之一,具有发病率高、易转移、治疗效果不佳、预后较差的特点,严重威胁着全人类的健康。肿瘤细胞表现出强烈的需铁现象,而铁超载会诱导细胞发生铁死亡,即一种由脂质过氧化和细胞膜损伤引起的铁依赖性细胞死亡。因此,铁死亡具有很强的抗肿瘤潜力。铁死亡的分子机制与细胞磷脂代谢异常、铁代谢异常、抗氧化和非抗氧化系统Xc-/谷胱甘肽(glutathione,GSH)/谷胱甘肽过氧化物酶4(glutathione peroxidase 4,GPX4)的失调有关。铁死亡相关分子在BC的发生和发展、转移、耐药及免疫反应等方面发挥着重要的作用,有望成为治疗BC的靶点。

维生素C多聚磷酸酯对小鼠肝脏脂质过氧化物和抗氧化物酶的影响

为研究维生素C多聚磷酸酯对小鼠肝脏脂质过氧化物和抗氧化物酶的影响 ,我们设置了 4个实验组 ,采用 2 4只小鼠 ,饵料中 35 %维生素C多聚磷酸酯的添加量依次为 0、 5 0 0、 2 5 0 0和 5 0 0 0mg/kg ,喂食 4周后取其肝脏 ,用硫代巴比妥酸分光光度测脂质过氧化物的含量 ,用亚硝酸盐形成法测定超氧化物歧化酶的活性 ,用分光光度法测过氧化氢酶和谷胱甘肽过氧化物酶的活性。结果表明 ,维生素C多聚磷酸酯对小鼠肝脏脂质过氧化物没有明显影响 ,但随着维生素C多聚磷酸酯添加量的增加 ,脂质过氧化物有减少的趋势。维生素C多聚磷酸酯添加量为 2 5 0 0和 5 0 0 0mg/kg的两组 ,其超氧化物歧化酶的活性明显高于对照组和维生素C多聚磷酸酯添加量为 5 0 0mg/kg组 ;过氧化氢酶的活性明显高于对照组。维生素C多聚磷酸酯添加量为5 0 0 0mg/kg组 ,其谷胱甘肽过氧化物酶的活性明显高于其它三组。表明高剂量的维生素C多聚磷酸酯能促进小鼠抗氧化物酶的活性 。

籽粒苋延缓衰老作用的研究

本文以BALB／C小鼠为对象，研究籽粒苋对小鼠七项衰老指标的影响，结果表明籽粒苋可以使血清及肝脏中过氧化脂质（LPO）分别降低12．9％及12．1％（P＜0．01）；显著降低心肌脂褐素（LF）含量达25．4％（P＜0．01）；显著升高血红细胞及肝中超氧化物歧化酶（SOD）活性分别为12．1％和14．5％（P＜0．05或P＜0．01）；还可以明显提高血中谷胱甘肽过氧化物酶（GSH-Px）活性达39．4％（P＜0．01）；显著增加皮肤羟脯氨酸（Hyp含量18．1％（P＜0．01）；对血中过氧化氢酶（CAT）活性可以提高11．8％，与老龄对照组比较，尚未有显著差异。籽粒苋还能显著抑制脑中B型单胺氧化酶（MAO－B）活性29．8％（P＜0．01），同时对肝内MAO－B活性无影响。以上结果证明，籽粒苋能提高体内抗氧化酶活性，抑制脂质的过氧化反应，具有良好的抗衰老作用，是一种理想的功能性食品。

柔嫩艾美耳球虫感染雏鸡LPO含量和抗自由基酶活性的动力学

通过测定柔嫩艾美耳球虫 (Eimeria tenella)感染鸡的盲肠、肝脏、脾脏和法氏囊组织中脂质过氧化物 (L PO)含量和超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GXH- Px)及过氧化氢酶 (CAT)活性 ,研究雏鸡感染球虫后机体内自由基生成和抗自由基反应。结果表明 ,雏鸡感染 E.tenella后 ,盲肠、肝脏和脾脏组织中的 L PO含量在感染后显著 (P<0 .0 5 )或极显著 (P<0 .0 1)升高 ,T- SOD、Mn- SOD、Cu、Zn- SOD、GSH- Px和 CAT活性水平不同程度下降。试验结果说明在 E.tenella感染后 ,鸡体内的氧自由基生成反应加剧 ,氧自由基参与了球虫的致病过程。