Dip2a regulates stress susceptibility in the basolateral amygdala

Dysregulation of neurotransmitter metabolism in the central nervous system contributes to mood disorders such as depression, anxiety, and post–traumatic stress disorder. Monoamines and amino acids are important types of neurotransmitters. Our previous results have shown that disco-interacting protein 2 homolog A(Dip2a) knockout mice exhibit brain development disorders and abnormal amino acid metabolism in serum. This suggests that DIP2A is involved in the metabolism of amino acid–associated neurotransmitters. Therefore, we performed targeted neurotransmitter metabolomics analysis and found that Dip2a deficiency caused abnormal metabolism of tryptophan and thyroxine in the basolateral amygdala and medial prefrontal cortex. In addition, acute restraint stress induced a decrease in 5-hydroxytryptamine in the basolateral amygdala. Additionally, Dip2a was abundantly expressed in excitatory neurons of the basolateral amygdala, and deletion of Dip2a in these neurons resulted in hopelessness-like behavior in the tail suspension test. Altogether, these findings demonstrate that DIP2A in the basolateral amygdala may be involved in the regulation of stress susceptibility. This provides critical evidence implicating a role of DIP2A in affective disorders.

Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

Fe^(2+)/Mn^(2+)活化亚硫酸盐降解盐酸土霉素的机理研究

盐酸土霉素常被用于治疗畜禽疾病,但是它不能被畜禽完全代谢,残留的盐酸土霉素进入水体危害水环境的健康。铁锰作为常见的过渡金属,通常以二价态活化亚硫酸盐来降解有机污染物,反应条件温和、操作简单,但是单独的二价铁与二价锰氧化还原电势低,活化亚硫酸盐效果较差。本研究采用Fe^(2+)/Mn^(2+)共活化Na_(2)SO_(3)降解水中的盐酸土霉素,考察药剂用量、pH、溶解氧、氯离子、碳酸根及腐殖酸对Fe^(2+)/Mn^(2+)/Na_(2)SO_(3)体系降解盐酸土霉素的影响;通过焦磷酸盐实验、自由基淬灭实验和EPR实验分析Fe^(2+)/Mn^(2+)/Na_(2)SO_(3)体系中的活性物种;利用紫外可见光谱、傅里叶红外光谱、气相色谱-质谱联用仪识别盐酸土霉素的官能团及其降解中间产物的变化,推断盐酸土霉素的降解途径。结果表明:当Fe^(2+)/Mn^(2+)/Na_(2)SO_(3)浓度比为1∶4∶20(浓度分别为0.1、0.4和2 mmol/L)时,在反应45 min、pH为9.0条件下,盐酸土霉素的去除率和矿化率最高,分别达到94%和49%。随着溶解氧从9 mg/L下降至1.89 mg/L,盐酸土霉素去除率从94%下降至17%;氯离子、腐殖酸和碳酸根均对盐酸土霉素的降解产生抑制作用。Mn(Ⅲ)和SO_(4)·^(-)是降解盐酸土霉素的主要活性氧化剂,盐酸土霉素的降解经过电子转移、开环与酰基化等过程。

电协同Fe^(2+)活化过硫酸盐处理偶氮染料废水的研究

偶氮染料废水会对自然环境和人类健康产生巨大危害。文章研究电协同Fe^(2+)活化过硫酸盐体系高效处理偶氮染料废水,以金橙G废水为处理对象,考察不同反应条件例如pH、Fe^(2+)投加量、过二硫酸盐(PDS)投加量、电流密度等因素对处理效果的影响,采用响应曲面法优化反应条件并确定最佳反应条件下的处理效果。结果表明,在pH为3、极板间距为9 cm、电流密度为15 mA/cm^(2)、PDS投加量为6.66 mmol/L、Fe^(2+)投加量为2 mmol/L、Na_(2)SO_(4)投加量为89.39 mmol/L的条件下,金橙G废水色度平均去除率为93.03%,COD平均去除率为85.80%。分析电协同Fe^(2+)活化过硫酸盐体系起主要作用的自由基及降解机理,证实了电和Fe^(2+)的协同作用。该研究可为电协同Fe^(2+)活化过硫酸盐体系在偶氮染料废水处理领域的应用提供技术支撑。

Fe^(2+)、Cu^(2+)诱导工艺对柞木表板颜色变化规律的影响

木材中的木质素、抽提物等物质具有能与金属盐溶液产生颜色反应的特性。利用这一特性以硫酸亚铁、硫酸铜溶液作为诱导剂,通过正交试验得到色差最大时的工艺参数,探究金属Fe^(2+)、Cu^(2+)的诱导剂质量分数、诱导时间、干燥时间、干燥温度对实木复合地板柞木表板颜色变化的影响。结果表明:Fe^(2+)、Cu^(2+)的诱导剂质量分数对柞木表板色彩色调的影响极为显著(F值分别为20.4453、8.8442);柞木表板的明度色品指数(L^(*))、红绿轴色品指数(a^(*))、黄蓝轴色品指数(b^(*))均随着Fe^(2+)、Cu^(2+)的诱导剂质量分数、诱导时间、干燥时间的增加而逐渐减少,总色差(ΔE^(*))逐渐增大,最大为31.53、9.90,表板色调逐渐偏暗、偏绿、偏蓝;随着干燥温度的增加,Fe^(2+)、Cu^(2+)诱导时的柞木表板总色差都逐渐减小。

外源Fe^(2+)浓度和矿物粒径对生物浸铀的影响

为改善以往生物浸铀效率不高的缺陷,通过添加外源Fe^(2+)及改变矿物粒径来提高生物对铀的浸出率。研究结果表明:外源Fe^(2+)浓度分别为0、0.5、1.0和2.0 g/L时,铀浸出率分别为87.34%、88.27%、91.23%、89.13%,当浸出体系中Fe^(2+)浓度为1.0 g/L时,铀矿石会产生部分溶解且表面粗糙孔隙明显,有利于铀的浸出,溶浸液中存在适量的Fe^(2+)对生物浸铀的能力具有提升效果。另外,外源Fe^(2+)对铀矿生物浸出符合固体产物层控制模型,浸出过程主要受扩散控制。当粒径<-2 mm和-5 mm时铀浸出率分别为91.23%和83.70%,矿物粒径适当减小可增大颗粒比表面积,同样利于铀的浸出。

Upregulation of α-ENaC induces pancreatic β-cell dysfunction,ER stress,and SIRT2 degradation

Islet beta cells(β-cells)produce insulin in response to high blood glucose levels,which is essential for preserving glucose homeostasis.Voltage-gated ion channels inβ-cells,including Na+,K+,and Ca2+channels,aid in the release of insulin.The epithelial sodium channel alpha subunit(α-ENaC),a voltage-independent sodium ion channel,is also expressed in human pancreatic endocrine cells.However,there is no reported study on the function of ENaC in theβ-cells.In the current study,we found thatα-ENaC was expressed in human pancreatic glandule and pancreatic isletβ-cells.In the pancreas of db/db mice and high-fat diet-induced mice,and in mouse isletβ-cells(MIN6 cells)treated with palmitate,α-ENaC expression was increased.Whenα-ENaC was overexpressed in MIN6 cells,insulin content and glucose-induced insulin secretion were significantly reduced.On the other hand,palmitate injured isletβ-cells and suppressed insulin synthesis and secretion,but increasedα-ENaC expression in MIN6 cells.However,α-ENaC knockout(Scnn1a−/−)in MIN6 cells attenuatedβ-cell disorder induced by palmitate.Furthermore,α-ENaC regulated the ubiquitylation and degradation of sirtuin 2 inβ-cells.α-ENaC also modulatedβ-cell function in correlation with the inositol-requiring enzyme 1 alpha/X-box binding protein 1(IRE1α/XBP1)and protein kinase RNA-like endoplasmic reticulum kinase/C/EBP homologous protein(PERK/CHOP)endoplasmic reticulum stress pathways.These results suggest thatα-ENaC may play a novel role in insulin synthesis and secretion in theβ-cells,and the upregulation ofα-ENaC promotes isletβ-cell dysfunction.In conclusion,α-ENaC may be a key regulator involved in isletβ-cell damage and a potential therapeutic target for type 2 diabetes mellitus.

Involvement of the ABA-and H_(2)O_(2)-Mediated Ascorbate-Glutathione Cycle in the Drought Stress Responses of Wheat Roots

Abscisic acid(ABA),hydrogen peroxide(H_(2)O_(2)) and ascorbate(AsA)–glutathione(GSH)cycle are widely known for their participation in various stresses.However,the relationship between ABA and H_(2)O_(2) levels and the AsA–GSH cycle under drought stress in wheat has not been studied.In this study,a hydroponic experiment was conducted in wheat seedlings subjected to 15%polyethylene glycol(PEG)6000–induced dehydration.Drought stress caused the rapid accumulation of endogenous ABA and H_(2)O_(2) and significantly decreased the number of root tips compared with the control.The application of ABA significantly increased the number of root tips,whereas the application of H_(2)O_(2) markedly reduced the number of root tips,compared with that under 15%PEG-6000.In addition,drought stress markedly increased the DHA,GSH and GSSG levels,but decreased the AsA levels,AsA/DHA and GSH/GSSG ratios compared with those in the control.The activities of the four enzymes in the AsA–GSH cycle were also markedly increased under drought stress,including glutathione reductase(GR),ascorbate peroxidase(APX),monodehydroascorbate reductase(MDHAR)and dehydroascorbate reductase(DHAR),compared with those in the control.However,the application of an ABA inhibitor significantly inhibited GR,DHAR and APX activities,whereas the application of an H_(2)O_(2) inhibitor significantly inhibited DHAR and MDHAR activities.Furthermore,the application of ABA inhibitor significantly promoted the increases of H_(2)O_(2) and the application of H_(2)O_(2) inhibitor significantly blocked the increases of ABA,compared with those under 15% PEG-6000.Taken together,the results indicated that ABA and H_(2)O_(2) probably interact under drought stress in wheat;and both of them can mediate drought stress by modulating the enzymes in AsA–GSH cycle,where ABA acts as the main regulator of GR,DHAR,and APX activities,and H_(2)O_(2) acts as the main regulator of DHAR and MDHAR activities.

Fe^(2+)螯合剂对羟脯氨酸发酵的影响

为解决反式-4-羟基脯氨酸发酵过程中Fe^(2+)供应不足、产酸效率低等问题。该研究以大肠杆菌HYP-08为供试菌株,首先通过单因素实验探究Fe^(2+)螯合剂种类及添加量对羟脯氨酸发酵生产的影响,并通过5 L发酵放大验证,以羟脯氨酸产量、生物量,糖酸转化率为指标,进一步探究其在放大过程中的影响,结果表明葡萄糖酸亚铁对羟脯氨酸发酵效果最好,流加发酵生产中,最终确定了10 h开始持连续流加的补料方式,反式-4-羟基脯氨酸生物量及产量达到最高,分别为146.2、118.6 g/L,较优化前提高了12.1%和4.2%,副产物乙酸减少到1.05 g/L,葡萄糖酸亚铁的添加有效增强了菌体活力,提高了羟脯氨酸的产量和糖酸转化率,为微生物发酵生产羟脯氨酸提供了依据。

Duodenal-jejunal bypass improves hypothalamic oxidative stress and inflammation in diabetic rats via glucagon-like peptide 1-mediated Nrf2/HO-1 signaling

BACKGROUND Type 2 diabetes mellitus(T2DM)is often accompanied by impaired glucose utilization in the brain,leading to oxidative stress,neuronal cell injury and inflammation.Previous studies have shown that duodenal jejunal bypass(DJB)surgery significantly improves brain glucose metabolism in T2DM rats,the role and the metabolism of DJB in improving brain oxidative stress and inflammation condition in T2DM rats remain unclear.AIM To investigate the role and metabolism of DJB in improving hypothalamic oxidative stress and inflammation condition in T2DM rats.METHODS A T2DM rat model was induced via a high-glucose and high-fat diet,combined with a low-dose streptozotocin injection.T2DM rats were divided into DJB operation and Sham operation groups.DJB surgical intervention was carried out on T2DM rats.The differential expression of hypothalamic proteins was analyzed using quantitative proteomics analysis.Proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of T2DM rats were analyzed by flow cytometry,quantitative real-time PCR,Western blotting,and immunofluorescence.RESULTS Quantitative proteomics analysis showed significant differences in proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of rats with T2DM-DJB after DJB surgery,compared to the T2DM-Sham groups of rats.Oxidative stress-related proteins(glucagon-like peptide 1 receptor,Nrf2,and HO-1)were significantly increased(P<0.05)in the hypothalamus of rats with T2DM after DJB surgery.DJB surgery significantly reduced(P<0.05)hypothalamic inflammation in T2DM rats by inhibiting the activation of NF-κB and decreasing the expression of interleukin(IL)-1βand IL-6.DJB surgery significantly reduced(P<0.05)the expression of factors related to neuronal injury(glial fibrillary acidic protein and Caspase-3)in the hypothalamus of T2DM rats and upregulated(P<0.05)the expression of neuroprotective factors(C-fos,Ki67,Bcl-2,and BDNF),thereby reducing hypothalamic injury in T2DM rats.CONCLUSION DJB surgery improve oxidative stress and inflammation in the hypothalamus of T2DM rats and reduce neuronal cell injury by activating the glucagon-like peptide 1 receptor-mediated Nrf2/HO-1 signaling pathway.

以研促教:利用荧光探针检测Fe^(2+)的实验设计

本文以荧光探针的设计合成和监测亚铁离子(Fe^(2+))应用于分析化学拓展实验教学为主题,介绍了一种新型的荧光探针DCM-Fe,其通过引入N-氧化物基团有效抑制了分子内电荷转移的发生,实现了对Fe^(2+)荧光“turn on”型检测。本文还阐述了在实验教学中,通过本实验的设计和实施,学生可以深入理解荧光探针的设计合成原理和荧光检测技术的应用,在实践中掌握荧光探针的合成、分析和应用,并培养了学生的实验技能和创新意识。本实验教学可为分析化学实验教学的拓展提供一种新思路和方法。

营养液不同浓度Fe^(2+)对水培小白菜生长发育及品质的影响

为筛选适宜水培小白菜生长的Fe^(2+)浓度,该文以苏州青为试验材料,开展了不同浓度Fe^(2+)对小白菜生长发育及品质的影响试验。试验结果表明,水培营养液Fe^(2+)浓度为0.03 mmol/L处理,水培小白菜株高、茎粗均显著高于其他处理,地上部鲜质量、地上部干质量、地下部鲜质量、地下部干质量最大,较对照分别提高92.5%、266.7%、115.5%、357.9%,叶绿素含量(57.12 mg/g)、维生素C含量[92.15 mg/(100 g)]、可溶性糖含量(0.43%)最高,较对照分别提高77.67%、50.44%、30.30%,小白菜丙二醛含量最低(11.06 nmol/g),较对照降低39.33%。综上,营养液Fe2+浓度为0.03 mmol/L时,水培小白菜生长势最旺、品质最佳、抗逆性最强。

甲基磺酸盐电镀液中Fe^(2+)质量浓度对镀锡板的影响

采用扫描电镜(SEM)、X射线衍射(XRD)、塔费尔曲线及循环伏安曲线等测试方法,研究了在甲基磺酸盐体系镀锡工艺中,Fe^(2+)质量浓度对镀锡板的耐蚀性、电镀过程中Sn^(2+)扩散系数及电流效率的影响.结果表明:Fe^(2+)质量浓度增加会导致镀锡板表面孔隙数量增多,抑制镀层中的锡粒向(200)晶面生长,致使镀锡板耐蚀性下降,当Fe^(2+)质量浓度超过8.0 g/L时,镀锡板耐蚀性明显降低;同时,Fe^(2+)质量浓度增加会导致电镀锡过程中Sn^(2+)扩散系数减小、电流效率降低.

Interfacial stress engineering toward enhancement of ferroelectricity in Al doped HfO_(2) thin films

Ferroelectric HfO_(2)has attracted much attention owing to its superior ferroelectricity at an ultra-thin thickness and good compatibility with Si-based complementary metal-oxide-semiconductor(CMOS)technology.However,the crystallization of polar orthorhombic phase(o-phase)HfO_(2)is less competitive,which greatly limits the ferroelectricity of the as-obtained ferroelectric HfO_(2)thin films.Fortunately,the crystallization of o-phase HfO_(2)can be thermodynamically modulated via interfacial stress engineering.In this paper,the growth of improved ferroelectric Al doped HfO_(2)(HfO_(2):Al)thin films on(111)-oriented Si substrate has been reported.Structural analysis has suggested that nonpolar monoclinic HfO_(2):Al grown on(111)-oriented Si substrate suffered from a strong compressive strain,which promoted the crystallization of(111)-oriented o-phase HfO_(2)in the as-grown HfO_(2):Al thin films.In addition,the in-plane lattice of(111)-oriented Si substrate matches well with that of(111)-oriented o-phase HfO_(2),which further thermally stabilizes the o-phase HfO_(2).Accordingly,an improved ferroelectricity with a remnant polarization(2P_(r))of 26.7C/cm^(2) has been obtained.The results shown in this work provide a simple way toward the preparation of improved ferroelectric HfO_(2)thin films.

Baicalin reduces chronic stress-induced breast cancer metastasis via directly targeting b2-adrenergic receptor

Recent studies have shown that stress can substantially facilitate breast cancer metastasis,which can be reduced by nonselective β1/β2-adrenergic receptor(β1/β2-AR)blocker.However,several side effects were identified.Thus,it is extremely warranted to explore more effective and better-tolerated β2-AR blocker.Currently,we demonstrated that baicalin(BA),a major bioactive component of Scutellaria baicalensis Georgi,could significantly attenuate stress hormones especially epinephrine(Epi)-induced breast cancer cell migration and invasion in vitro.Mechanistically,we identified that β2-AR was a direct target of BA via the drug affinity responsive target stability(DARTS)combined with mass spectrum assay,and BA photoaffinity probe with pull-down assay,which was further confirmed by a couple of biophysical and biochemical assays.Furthermore,we demonstrated that BA could directly bind to the Phe193 and Phe-289 of β2-AR,subsequently inhibit cyclic adenosine monophosphate-protein kinase A-focal adhesion kinase(cAMP-PKA-FAK)pathway,and thus impede epithelial-mesenchymal transition(EMT),thereby hindering the metastatic progression of the chronic stress coupled with syngeneic and xenograft in vivo orthotopic and tail vein mouse model.These findings firstly identify BA as a potential b2-AR inhibitor in the treatment of stress-induced breast cancer metastasis.

Hesperidin ameliorates H_(2)O_(2)-induced bovine mammary epithelial cell oxidative stress via the Nrf2 signaling pathway

Background Hesperidin is a citrus flavonoid with anti-inflammatory and antioxidant potential. However, its protective effects on bovine mammary epithelial cells(b MECs) exposed to oxidative stress have not been elucidated.Results In this study, we investigated the effects of hesperidin on H_(2)O_(2)-induced oxidative stress in b MECs and the underlying molecular mechanism. We found that hesperidin attenuated H_(2)O_(2)-induced cell damage by reducing reactive oxygen species(ROS) and malondialdehyde(MDA) levels, increasing catalase(CAT) activity, and improving cell proliferation and mitochondrial membrane potential. Moreover, hesperidin activated the Keap1/Nrf2/ARE signaling pathway by inducing the nuclear translocation of Nrf2 and the expression of its downstream genes NQO1 and HO-1, which are antioxidant enzymes involved in ROS scavenging and cellular redox balance. The protective effects of hesperidin were blocked by the Nrf2 inhibitor ML385, indicating that they were Nrf2 dependent.Conclusions Our results suggest that hesperidin could protect b MECs from oxidative stress injury by activating the Nrf2 signaling pathway, suggesting that hesperidin as a natural antioxidant has positive potential as a feed additive or plant drug to promote the health benefits of bovine mammary.

BTG2 interference ameliorates high glucose-caused oxidative stress, cell apoptosis, and lipid deposition in HK-2 cells

Objective:Diabetic nephropathy(DN)is a deleterious microangiopathy of diabetes,constituting a critical determinant of fatality in diabetic patients.This work is purposed to disclose the effects and modulatory mechanism of BTG anti-proliferation factor 2(BTG2)during the pathological process of DN.Methods:BTG2 expression in kidney tissues of diabetic mice and high glucose(HG)-exposed human proximal tubular cell line HK-2 was assessed with Western blot and RT-qPCR.The diabetic mice model was constructed by streptozotocin injection and confirmed by the blood glucose level beyond 16.7 mmol/L.Hematoxylin and eosin(H&E)staining and measurement of kidney function hallmarks were conducted to assess kidney injury.Cell counting kit(CCK)-8 method and TUNEL assay appraised cell activity and apoptosis.Oil red O staining assayed lipid accumulation.Relevant commercial kits were used to estimate oxidative stress-related factors.Co-immunoprecipitation(Co-IP)assay testified the binding relationship of BTG2 with protein arginine methyltransferase 1(PRMT1).Results:BTG2 expression was significantly raised in renal tissues of diabetic mice and HK-2 cells exposed to HG.BTG2 deficiency improved viability and extenuated the apoptosis,lipid deposition as well as oxidative stress in HK-2 cells following HG exposure.In addition,PRMT1 was also overexpressed in HK-2 cells exposed to HG.BTG2 interacted with PRMT1 and positively modulated PRMT1 expression.The effects of BTG2 interference on viability,apoptosis,lipid deposition,and oxidative stress in HG-challenged HK-2 cells were partially abrogated by PRMT1 overexpression.Conclusion:Altogether,BTG2 might aggravate HK-2 cell injury in response to HG by binding with PRMT1,providing a novel target for the therapeutic strategy of DN.

8-Hydroxy-2'-Deoxyguanosine (8-OH-2dG) as a Biomarker of Oxidative Stress (OS) in the Acute Exacerbation of Spontaneous Preterm Birth (SPTB)

Spontaneous preterm birth (SPTB) is characterized by the delivery of a baby before 37 completed weeks of gestation, and this condition is associated with significant health challenges for the newborn. Emerging evidence highlights the importance of biomarkers for understanding the mechanisms underlying SPTB. One such biomarker, 8-OH-2dG, plays a critical role in evaluating oxidative stress and its impact on pregnancy outcomes. It has been demonstrated that 8-OH-2dG is a product of oxidative DNA damage and is widely recognized as a key indicator of cellular oxidative stress. Elevated reactive oxygen species in SPTB result in higher levels of the DNA degradation product 8-OH-2dG in amniotic fluid, causing damage to maternal and fetal tissues that could lead to premature rupture of fetal membranes. Therefore, evaluating the role of 8-OH-2dG in SPTB is of great interest. This review provides an overview of the current knowledge on 8-OH-2dG as a biomarker for SPTB and aims to elucidate its mechanism in this condition.

不同因素对Fe^(3+)-TiO_(2)/ACF降解NH_(3)的影响

为了探究不同因素对Fe^(3+)-TiO_(2)/活性炭纤维(ACF)降解氨气(NH_(3))的影响规律,采用Fe^(3+)-TiO_(2)/ACF复合材料,以NH_(3)为目标降解物,研究初始浓度、流速、光催化剂负载量以及光照强度对Fe^(3+)-TiO_(2)/ACF降解NH_(3)的影响,并进行了相应的反应动力学分析。结果表明:随着初始浓度的增加,NH_(3)降解率呈现略微降低的趋势,光催化过程基本符合L-H一级反应动力学模型;随着流速的增加,NH_(3)降解率表现为先升高后降低,其光催化过程也基本符合L-H一级反应动力学模型;随着光催化剂负载量以及光照强度的增加,NH_(3)降解率表现为略微增加的趋势。

Oxidative stress mediates glycidol-induced endothelial injury and its protection by 6-C-(E-2-fluorostyryl)naringenin

Glycidol is a common lipid-derived foodborne toxicant mainly presents in refined oils and related foodstuffs.Vascular endothelial cells may be potential targets of the deleterious effects associated with glycidol exposure.In human umbilical vein endothelial cells(HUVECs),we found that glycidol treatment promoted endothelialto-mesenchymal transition(EndMT)at a lower concentration(0.5 mmol/L),while induced apoptosis and inflammation at a higher concentration(1 mmol/L).These harmful effects were achieved by the activation of NF-κB/MAPK signaling pathway and were mediated by reactive oxygen species(ROS).In addition,the protective potential of 6-C-(E-2-fluorostyryl)naringenin(6-CEFN)against glycidol was evaluated and compared with naringenin.HUVECs pre-treated with 6-CEFN,but not naringenin,displayed resistance to endothelial dysfunction caused by glycidol.