Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer

As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities have emerged in the study of liver cancer,providing a new perspective for understanding the development of liver cancer.Ferroptosis regulation,lipid peroxidation and metabolic abnormalities play important roles in the occurrence and development of liver cancer.The regulation of ferroptosis is involved in apoptosis and necrosis,affecting cell survival and death.Lipid peroxidation promotes oxidative damage and promotes the invasion of liver cancer cells.Metabolic abnormalities,especially the disorders of glucose and lipid metabolism,directly affect the proliferation and growth of liver cancer cells.Studies of ferroptosis regulation and lipid peroxidation may help to discover new therapeutic targets and improve therapeutic outcomes.The understanding of metabolic abnormalities can provide new ideas for the prevention of liver cancer,and reduce the risk of disease by adjusting the metabolic process.This review focuses on the key roles of ferroptosis regulation,lipid peroxidation and metabolic abnormalities in this process.

Mechanisms and active substances of targeting lipid peroxidation in ferroptosis regulation

Ferroptosis is a novel form of cell death driven by iron-dependent lipid peroxidation and it is implicated in various diseases,such as liver disease,acute kidney injury,cardiovascular disease,neurodegenerative disease and cancer.Lipid-based reactive oxygen species(ROS),particularly lipid hydroperoxides in the cellular membrane can lead to membrane disruption and cell death mediated by ferroptosis.There are three necessary stages involving in the process of lipid peroxidation regulation in ferroptosis,including the synthesis of membrane phospholipids,initiation of lipid peroxidation and clearance of lipid peroxides.In this review,we summarized the molecular modulation mechanisms of lipid peroxidation in ferroptosis from the above three stages,as well as various ferroptosis modulators targeting lipid peroxidation,including commonly used products,natural bioactive compounds and selenocompounds.Collectively,these findings suggest the vital role of lipid peroxidation in ferroptosis,and targeting lipid peroxidation in ferroptosis is potential to treat ferroptosis-associated diseases.

Correction to“Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence of primary liver cancer”

Correction to“Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer”in World J Gastrointest Oncol 2024;16:2335-2349,published by Shu YJ,Lao B,and Qiu YY.In this article,we added the correct citations of images.

Ferroptosis regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer

BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attention in recent years.However,the regulatory mechanism of iron death in gastric cancer and its effect on lipid peroxidation metabolism remain unclear.AIM To explore the role of iron death in the development of gastric cancer,reveal its relationship with lipid peroxidation,and provide a new theoretical basis for revealing the molecular mechanism of the occurrence and development of gastric cancer.METHODS The process of iron death in gastric cancer cells was simulated by cell culture model,and the occurrence of iron death was detected by fluorescence microscopy and flow cytometry.The changes of gene expression related to iron death and lipid peroxidation metabolism were analyzed by high-throughput sequencing technology.In addition,a mouse model of gastric cancer was established,and the role of iron death in vivo was studied by histology and immunohistochemistry,and the level of lipid peroxidation was detected.These methods comprehensively and deeply reveal the regulatory mechanism of iron death on lipid peroxidation metabolism in the occurrence and development of gastric cancer.RESULTS Iron death was significantly activated in gastric cancer cells,and at the same time,associated lipid peroxidation levels increased significantly.Through high-throughput sequencing analysis,it was found that iron death regulated the expression of several genes related to lipid metabolism.In vivo experiments demonstrated that increased iron death in gastric cancer mice was accompanied by a significant increase in lipid peroxidation.CONCLUSION This study confirmed the important role of iron death in regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.The activation of iron death significantly increased lipid peroxidation levels,revealing its regulatory mechanism inside the cell.

Changes in erythrocyte membrane ATPases and plasma lipid peroxides in upper abdominal surgery under intravenous procaine-balanced anesthesia

AIM To observe the changes in erythrocyte membrane ATPases and plasma lipid peroxides (LPO) patients with in abdominal surgery under intravenous procaine-balanced anesthesia.METHODS By determining the ATPase activities of erythrocyte membrane, effects of upper abdominal surgery under intravenous procaine-balanced anesthesia on the function of erythrocytes were observed in 15 patients undergoing cholecystectomy and gastrectomy (5 males and 10 females, aged 45.9±10.20 years and weighed 60.60kg±11.93kg). All patients were free from severe renal, hepatic, pulmonary, cardiac, metabolic and endocrinological diseases and acute infection for at least 2 weeks before surgery. Patients receiving any drug known to affect carbohydrate metabolism prior to anesthesia were excluded from the study.RESULTS Erythrocyte membrane Na+, K+-ATPase, Mg2+-ATPase, Ca2+, Mg2+-ATPase activities were not significantly changed 60min-90min after incision as compared with 30min before anesthesia, but were decreased markedly 10min and 24 hours after completion of operation (P＜0.01). Plasma lipid peroxides (LPO) were increased significantly 24 hours after surgery (P＜0.01) following an initially marked but transient reduction. Plasma LPO changes were not correlated with erythrocyte membrane ATPase activities, r=-0.0396, -0.0097 and 0.4383, respectively (P＞0.05).CONCLUSION Abdominal surgical trauma under intravenous procaine-balanced anesthesia may be associated with the decreased ATPase activities of erythrocyte membrane and increased LPO in plasma.

Vicious cycle of lipid peroxidation and iron accumulation in neurodegeneration

Lipid peroxidation and iron accumulation are closely associated with neurodegenerative diseases,such as Alzheimer’s,Parkinson’s,and Huntington’s diseases,or neurodegeneration with brain iron accumulation disorders.Mitochondrial dysfunction,lipofuscin accumulation,autophagy disruption,and ferroptosis have been implicated as the critical pathomechanisms of lipid peroxidation and iron accumulation in these disorders.Currently,the connection between lipid peroxidation and iron accumulation and the initial cause or consequence in neurodegeneration processes is unclear.In this review,we have compiled the known mechanisms by which lipid peroxidation triggers iron accumulation and lipofuscin formation,and the effect of iron overload on lipid peroxidation and cellular function.The vicious cycle established between both pathological alterations may lead to the development of neurodegeneration.Therefore,the investigation of these mechanisms is essential for exploring therapeutic strategies to restrict neurodegeneration.In addition,we discuss the interplay between lipid peroxidation and iron accumulation in neurodegeneration,particularly in PLA2G6-associated neurodegeneration,a rare neurodegenerative disease with autosomal recessive inheritance,which belongs to the group of neurodegeneration with brain iron accumulation disorders.

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.

Level of lipid peroxides and cuprozinc superoxide dismutase in gastric mucosa and serum of gastrectomized patients

The level of lipid peroxides (LPO) and copper-zinc containing superoxide dismutase (SOD-Ⅰ) in the gastric mucosa and serum was determined in 141 samples from 25 patients after con-ventional subtotal gastrectomy (11 cases of Billroth Ⅰ and 14 cases of Billroth Ⅱ) and 11 patientsafter pylorus and antroseromuscular flap preserving gastrectomy (PAFPG).Those of 11 normal subjects were examined likewise to serve as control.It was found that:(1) The average LPO levelwas much higher and the average SOD-Ⅰ level much lower in the gastric mucosa of the patientsafter conventional subtotal gastrectomy especially the Billroth Ⅱ type than in that of those afterPAFPG.(2) In 36 specimens of stump mucosa,the average LPO level was significantly higher inthe tissue around the anastomotic ring than in that of the body of the stump;no marked differ-ence of SOD-Ⅰ level between the 2 was revealed.(3) The LPO value in the stump mucosa waspositively correlated to and the SOD-Ⅰ value negatively correlated to the pH value of gastric juice.These rindings suggest that the reation of oxygen free radicals in the stump mucosa may be influ-enced by the intragastric pH or by the type of digestive continuity reconstruction,and that thereaction of oxygen free radicals especially the lipid peroxidation may play a role in the pathogenesisof the lesions in the anastomotic stoma.

Changes in erythrocyte membrane ATPase and plasma lipid peroxides during perioperative period

Changes in erythrocyte membrane ATPases and plasma lipid peroxides（LPO） were studiedperioperatively in 15 abdominal surgical patients under intravenous procaine-balanced anesthesia.The resultsrevealed that erythrocyte membrne Na+-K+ATPase,Mg2+ATPase and Ca2+-Mg2+ATPase activities werenot significantly changed at 60～90 min after incision as compared with 30 min before anesthesia,but weredecreased markedly at 10 rain and 24 hours after completion of operation（P【0.01）.Plasma LPO wereincreased significantly by 24 hours after surgery（P【0.01） following an initially marked but transientreduction.Plasma LPO changes were not correlated with erythrocyte membrane ATPase activities,r=-0.0396,-0.0097 and-0.4383 respeetively（P】0.05）.These correlations are suggested to be inducedby neuroendoerine responses after anesthesia and/or surgical trauma.

Flavonoids Reduce Lipid Peroxides and Increase Glutathione Levels in Pooled Human Liver Microsomes (HLMs)

The effects of each of the flavonoids;genistein (G), quercetin (Q) and kaempferol (K) at several doses on lipid peroxides (LP) and reduced glutathione (GSH) in pooled human liver microsomes (HLMs) were investigated following the oxidative damage for 4, 6, 18 and 24 hr. HLMs (1 mg/ml) were exposed to each of the above flavonoids at 0, 5, 10, 15, 20 or 25 μM and incubated for the respective times as previously stated. Our hypothesis was that HLMs exposed to the flavonoids for the respective exposure times can decrease LP and increase GSH in HLMs to better cope with the oxidative stress. The results of our studies indicate that each of the flavonoids significantly (p < 0.01) decreased LP compared to their respective controls. The highest decrease in LP was observed for K followed by Q and G. Significant increases (p < 0.01) in GSH were observed for the flavonoid doses tested with the highest levels observed for Q for the 24-hr. incubation. The findings suggest that the flavonoids modulate oxidative stress in HLMs by decreasing LP and such decreases in LPs may be due to the increasing and or the replenished levels of GSH in the said cells to better cope with the oxidative stress.

Effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7S)and glycinin(11S)

This study aimed to analyze the effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7 S)and glycinin(11 S).Oxidation complexes were determined using the lipid peroxidation method.Functional properties were analyzed based on emulsifying and foaming properties.The potential allergenicity was evaluated by in vitro and in vivo methods.The results found that oxidation altered structures of the proteins and resulted in the formation of cross-linked protein polymers.The emulsion and foaming properties of the proteins were improved after oxidation.The IgE-binding capacity of 7 S and11 S reduced after oxidation.KU812 cell assays showed that both histamine and IL-4 release decreased after oxidation treatment.A mouse model showed that oxidation reduced the IgE,IgG,and IgG1 levels,as well as reduced histamine and mMCP-1 release in serum,which might suppress the allergic reaction.In conclusion,the lipid peroxidation treatment likely causes changes to the functional properties of soybean,decreasing the potential allergenicity of 7 S and 11 S.

Investigation of heavy metals and lipid peroxidation level in the muscles of Clarias gariepinus from IBI,Gindin-Dorowa and D onga community rivers in Taraba State,Nigeria

Heavy metals have harmful effects on human health,and exposure to these metals has been increased by industrial and anthropogenic activities and modern industrialization.Heavy metals content of the liver tissues was determine d using Atomic Absorption Spectrophotometer method,while lipid peroxidation was carried out.Heavy metals analyzed include;lead(Pb),cadmium(Cd),zinc(Zn),Arsenic(As),and Mercury(Hg).The findings revealed that the heavy metal Zinc(Zn)has high concentrations in the muscles of the fish species,the concentration of this heavy metal Zinc is high in River Gindin Dorowa th a n in River Ibi and River Donga shows less concentration of this heavy metal though it’s above WHO permissible limits.Results revealed that only Zn and Cd were present in the muscle from the three rivers.Pb was found only in the liver from Gindin-Dorowa at the concentration of 0.017 mg/kg,which is not significant(P<0.05)when compared with other locations,while Hg and As were absent in all the muscle samples.The highest concentration of Zn was found in the muscle sample from Gindin-Dorowa(7.450 mg/kg)followed by Ibi(6.16 mg/kg)and the least being Donga(4.365 mg/kg)which are significantly(P<0.05)different from one another.However,there was no significant(P<0.05)difference among the Cd composition of muscle from Gindin-Dorowa(0.025 mg/kg),Donga(0.024 mg/kg)and Ibi(0.015 mg/kg),respectively.The TBA was found in the hepatic tissue sample from Gidin-Dorowa,which has the highest Zn,Cd and no Pb content,followed by Ibi and then the Donga sample.This suggests that there is a positive relationship between heavy metals and the effect of TBA on the hepatic tissues,justifying the fact that heavy metals affect the hepatic tissues of fish,while on the cerebral tissue.In conclusion,it revealed that there is a negative relation between heavy metals and the effect of TBA on the cerebral tissues to protect or save aquatic habitat s of fish quality and aquatic life.

铁死亡在非酒精性脂肪性肝病发病中作用的研究进展

铁死亡是近年提出的一种新型细胞死亡方式,其主要特征为铁过载及脂质过氧化。铁死亡参与非酒精性脂肪性肝病的发生发展。铁过载可通过芬顿反应产生大量活性氧,在脂氧合酶的作用下,肝细胞膜上的不饱和脂肪酸发生脂质过氧化,从而诱导肝细胞死亡,导致非酒精性脂肪性肝病/非酒精性脂肪性肝炎的发生。阻断铁死亡可能成为保护肝细胞的治疗策略之一。

心力衰竭患者血清MMP-9、LPO、cathepsin S水平检测及其临床意义

目的研究心力衰竭患者血清基质金属蛋白酶9(MMP-9)、脂质过氧化物(LPO)、组织蛋白酶S(cathepsin S)水平变化及其临床意义。方法选取2021年3月至2022年3月期间同济大学附属杨浦医院收治的50例心衰患者作为研究组,根据NYHA心功能分级分为Ⅰ~Ⅳ级,其中Ⅰ级10例、Ⅱ级13例、Ⅲ级11例、Ⅳ级16例,另选取我院同期体检健康者50例作为对照组。比较两组受检者及不同NYHA分级患者的血清MMP-9、LPO、cathepsin S水平,采用受试者工作特征曲线(ROC)分析各指标对心衰的诊断价值。结果研究组患者的血清MMP-9、LPO、cathepsin S水平分别为(564.56±28.43)ng/mL、(13.38±0.23)μmol/L、(8.56±0.78)U/L,明显高于对照组的(108.56±27.54)ng/mL、(9.48±0.42)μmol/L、(4.75±0.46)U/L,差异均有统计学意义(P<0.05);不同NYHA分级患者的血清MMP-9、LPO、cathepsin S水平比较差异均有统计学意义(P<0.05),且NYHA分级越高患者的血清MMP-9、LPO、cathepsin S水平越高;MMP-9、LPO、cathepsin S各指标对心衰均具有一定的诊断价值,联合诊断的准确度最高,为93.48%,三个指标中MMP-9的特异性与灵敏度均最高,分别为81.62%、84.28%,但cathepsin S的准确度最高,为86.24%。结论心力衰竭患者血清MMP-9、LPO、cathepsin S水平均明显升高,且NYHA分级越高,三项指标水平也越高,在临床上可作为评估心衰严重程度的重要指标。

解毒固肾汤治疗血液透析患者对肾功能及血清LPO、PAI-1的影响

目的 探讨解毒固肾汤治疗血液透析患者对其肾功能及血清脂质过氧化物(LPO)、纤溶酶原激活物抑制物-1 (PAI-1)的影响。方法 选择2019年1月至2022年1月在安康市中医医院肾病—血液净化中心行血液透析治疗的80例患者为研究对象,按随机数表法分为观察组和对照组各40例。对照组患者接受常规药物干预,观察组患者在对照组治疗的基础上联合解毒固肾汤治疗,两组患者均治疗3个月。比较两组患者的治疗效果,以及治疗前后的肾功能[胱抑素C (Cys-C)、血肌酐(Scr)、血尿素氮(BUN)]和血清LPO、PAI-1水平,同时比较两组患者治疗期间的不良反应发生情况。结果 观察组患者的治疗总有效率为97.50%,明显高于对照组的80.00%,差异有统计学意义(P<0.05);治疗后,两组患者的Cys-C、Scr、BUN水平均降低,且观察组患者的Cys-C、Scr、BUN水平分别为(1.02±0.21) mg/L、(80.21±7.31)μmol/L、(6.21±1.12) mmol/L,明显低于对照组的(1.72±0.26) mg/L、(89.13±7.45)μmol/L、(8.91±1.32) mmol/L,差异均有统计学意义(P<0.05);治疗后,两组患者的血清LPO、PAI-1水平均明显降低,且观察组患者的血清LPO、PAI-1水平分别为(7.21±1.13) nmol/L、(21.19±3.28) mg/L,明显低于对照组的(10.37±1.21) nmol/L、(24.91±3.31) mg/L,差异均有统计学意义(P<0.05);观察组患者的不良反应发生率为5.00%,略低于对照组的10.00%,但差异无统计学意义(P>0.05)。结论 解毒固肾汤治疗血液透析患者可改善其肾功能,调节血清LPO、PAI-1水平,临床应用效果好且安全性高。

血清LPO、APN和TGF-β1水平检测对酒精性肝硬化患者病情严重程度和预后评估的价值

目的 探讨过氧化脂质(LPO)、脂联素(APN)和转化生长因子-β1(TGF-β1)水平联合检测对酒精性肝硬化(ALC)病情严重程度和预后评估的价值。方法 选择2019年1月—2021年6月南通大学附属海安医院收治的152例酒精性肝病(ALD)患者,按疾病类型分为酒精性脂肪肝(AFL)组、酒精性肝炎(AH)组和ALC组;将ALC组按照改良Child-Pugh分级标准分为A级、B级和C级亚组,按照终末期肝病模型(MELD)评分标准分为轻度、中度和重度亚组。比较AFL、AH和ALC三组的血清LPO、APN和TGF-β1水平,比较ALC组中改良Child-Pugh分级标准A级、B级和C级亚组以及MELD评分轻度、中度和重度亚组的血清LPO、APN和TGF-β1水平,Pearson分析ALC组LPO、APN和TGF-β1水平与总胆红素(TBil)、白蛋白(Alb)和肝脏硬度值(LSM)水平的相关性,绘制ROC曲线,分析LPO、APN和TGF-β1水平对ALC的诊断效能。结果 ALC组的LPO和TGF-β1水平分别为(7.56±1.68)μmol/L和(287.63±59.52)μg/L,高于AH组和AFL组的(4.92±1.03)μmol/L、(3.46±0.85)μmol/L和(215.19±43.87)μg/L、(168.53±32.48)μg/L;APN水平为(4.29±1.03) mg/L,低于AH组和AFL组的(7.46±1.82) mg/L和(12.57±3.46) mg/L(F=16.736、13.275、19.418,P<0.05)。ALC组中,Child-Pugh C级亚组的LPO和TGF-β1水平为(9.04±1.85)μmol/L和(341.67±70.25)μg/L,高于B级和A级亚组的(7.38±1.52)μmol/L、(6.13±1.27)μmol/L和(279.83±57.46)μg/L、(234.51±48.38)μg/L;APN水平为(3.37±0.85) mg/L,低于B级和A级亚组的(4.42±1.16) mg/L和(5.76±1.34) mg/L(F=13.259、11.762、15.386,P<0.05)。重度亚组的LPO和TGF-β1水平为(9.83±1.96)μmol/L和(364.78±76.91)μg/L,高于中度和轻度亚组的(7.54±1.61)μmol/L、(5.83±1.14)μmol/L和(290.62±59.73)μg/L、(225.76±45.82)μg/L;APN水平为(3.08±0.74) mg/L,低于中度和轻度亚组的(4.26±1.09) mg/L和(5.93±1.42) mg/L(F=15.461、13.628、17.853,P<0.05)。Pearson分析显示,ALC的LPO和TGF-β1水平与TBil和LSM水平呈正相关,与Alb水平呈负相关;APN水平与Alb水平呈正相关,与TBil和LSM水平呈负相关(P<0.05)。ROC曲线显示,LPO、APN和TGF-β1水平以及三者联合诊断ALC的AUC分别为0.806、0.784、0.835和0.928,联合检测的效能高于任一单项检测(P<0.05)。结论 LPO、APN和TGF-β1水平检测对ALC患者病情严重程度和预后评估的价值较高,联合检测的效能更佳。

鹿茸多肽对顺铂所致卵巢早衰大鼠卵巢功能的保护作用及其机制

目的:探讨鹿茸多肽(VAP)对顺铂(DDP)致卵巢早衰模型大鼠的影响及机制。方法:取动情周期正常的雌性大鼠并将其随机分为对照组、模型组、VAP干预组,每组各10只。模型组和VAP干预组通过连续20 d腹腔注射DDP(4 mg·kg^(−1)·d^(−1))建立卵巢早衰大鼠模型,干预组同时连续20 d灌胃VAP(400 mg·kg^(−1)·d^(−1))。HE染色观察卵巢形态学表现,并对各级发育卵泡计数。ELISA检测血清雌二醇(E2)、促卵泡生成素(FSH)、抗穆勒管激素(AMH)水平。生化法检测卵巢组织中谷胱甘肽(GSH)和丙二醛(MDA)水平。探针标记法检测卵巢组织中活性氧(ROS)水平。普鲁士蓝染色观察卵巢组织中铁蓄积情况并检测亚铁离子(Fe^(2+))水平。免疫组化和Western blot检验卵巢组织中溶质载体家族7成员11(SCL7A11)、谷胱甘肽过氧化酶4(GPX4)和酰基辅酶A合成酶长链家族成员4(ACSL4)的表达。通过生育力监测观察各组大鼠生育能力。结果:与对照组相比,模型组卵巢萎缩,铁蓄积(P<0.01),各级发育卵泡和总卵泡减少(P<0.05),闭锁卵泡增多(P<0.01),产仔数减少(P<0.01),血清E2、AMH水平降低(P<0.01),FSH水平提高(P<0.01),卵巢组织中GSH水平、SCL7A11和GPX4蛋白表达均降低(P<0.05),Fe^(2+)、MDA和ROS水平及ACSL4蛋白表达均升高(P<0.01)。与模型组相比,VAP能改善DDP导致的上述指标改变(P<0.01)。结论:鹿茸多肽可改善顺铂致卵巢早衰大鼠的卵巢功能、维持正常的卵泡发育并提高其生育能力,机制可能与脂质过氧化反应和铁死亡有关。

中药靶向铁死亡干预糖尿病肾病基础研究进展

糖尿病肾病是糖尿病最严重的微血管病变之一,也是导致终末期肾病患者死亡的主要原因。铁死亡作为一种细胞程序性死亡模式,主要表现为细胞内脂质过氧化物及铁的过度累积。铁死亡参与糖尿病肾病肾足细胞、系膜细胞及肾小管上皮细胞损伤等一系列病理过程。中药治疗具有疗效显著、不良反应小等特点,已广泛用于糖尿病肾病防治。本文总结调节糖尿病肾病铁死亡的关键因子,以及靶向抑制铁死亡防治糖尿病肾病的中药活性成分及中药复方,为糖尿病肾病靶向药物研发提供参考。

亚精胺对渗透胁迫下甜瓜幼苗膜脂过氧化和抗氧化系统的影响

为探讨多胺提高作物抗渗透胁迫的生理机制,以甜瓜品种‘齐甜2号’为材料,采用营养液法培养甜瓜幼苗,以15%PEG-6000模拟渗透胁迫,研究1 mmol·L^(-1)亚精胺(Spd)对不同渗透胁迫时间下甜瓜幼苗的生长、活性氧代谢、抗氧化酶活性、渗透调节物质和非酶抗氧化剂的影响。结果表明:渗透胁迫后4 d,与胁迫处理相比,1mmol·L^(-1)Spd处理使甜瓜幼苗生物量提高11.34%,根系活力提高24.20%;叶片和根系H_(2)O_(2)含量、■产生速率、MDA含量和相对电解质渗透率降低,叶片中分别降低30.72%、29.99%、29.34%和14.62%,根中分别降低29.33%、25.31%、28.23%和20.34%。Spd诱导甜瓜叶片和根系中抗氧化酶活性增加,与胁迫处理相比,叶中SOD、POD、CAT和APX抗氧化酶活性分别提高25.54%、28.70%、27.72%和28.41%,根中分别提高23.35%、27.38%、25.06%和20.34%。与渗透胁迫处理相比,Spd处理在渗透胁迫后16 d甜瓜幼苗叶片脯氨酸、可溶性糖和可溶性蛋白的含量分别增加46.51%、49.72%和40.25%;渗透胁迫后16 d幼苗叶片ASA含量增加62.50%,渗透胁迫后12 d幼苗叶片GSH含量增加37.17%,ASA/DHA和GSH/GSSG分别提高74.46%、60.95%。说明在渗透胁迫下1 mmol·L^(-1)浓度Spd能够促进甜瓜幼苗生长,稳定生物膜系统,增强甜瓜幼苗抗氧化能力,有效缓解渗透胁迫对甜瓜幼苗伤害的作用。

铁死亡对心血管疾病影响的研究进展

铁死亡(ferroptosis)与体内氧化与抗氧化系统失衡相关,是一种铁依赖性的调节性细胞死亡,参与各类肿瘤、神经系统病变、心血管疾病等多种疾病的发生进展。因其与多种疾病相关,近年来,铁死亡在医学界备受关注,但其对疾病的作用机制尚未完全明晰,有待更深入探索。现基于已有研究成果,就铁死亡在心血管疾病中的研究进展展开综述,以期发现治疗新靶点,为临床疾病治疗提供新思路。