[目的]探讨母体运动能否降低肥胖小鼠成年子代对脑缺血再灌注损伤的敏感性。[方法]雌性C57BL/6J小鼠从5周龄开始喂食正常饮食(NCD,10%脂肪含量饲料)或高脂饮食(HFD,60%脂肪含量饲料)。8周后,雌鼠随机分为正常饮食安静组(NCD-SED)、正常...[目的]探讨母体运动能否降低肥胖小鼠成年子代对脑缺血再灌注损伤的敏感性。[方法]雌性C57BL/6J小鼠从5周龄开始喂食正常饮食(NCD,10%脂肪含量饲料)或高脂饮食(HFD,60%脂肪含量饲料)。8周后,雌鼠随机分为正常饮食安静组(NCD-SED)、正常饮食运动组(NCD-EX)、高脂饮食安静组(HFD-SED)和高脂饮食运动组(HFD-EX)。运动组进行无负重游泳训练,水温32~34°C,水深20 cm, 60 min/天,6天/周。经过4周的运动干预后,将雌鼠与正常饮食雄鼠按2∶1比例进行合笼交配。以见阴道栓且阴道涂片见精子确定为妊娠第1天(GD1)。进入妊娠期后,运动组母鼠继续接受运动干预,方案调整为45 min/天,5天/周。监测并评估母鼠孕前体重、体脂、葡萄糖耐量和胎鼠体重、体长、胎盘效率等生理指标;同时选取子代3月龄小鼠为研究对象,建立小鼠大脑中动脉短暂性缺血再灌注(tMCAO/R)损伤模型,观察脑梗死面积。[结果](1)HFD-SED组母鼠孕前体重、体脂和葡萄糖耐量曲线下面积显著高于NCD-SED组母鼠(P<0.01),而HFD-EX组母鼠显著低于HFD-SED组(P<0.05)。(2)HFD-SED组孕期体重始终高于NCD-SED组(P<0.05);GD15~GD18期间HFD-EX组的体重显著低于HFD-SED组(P<0.05);各组孕鼠产仔数差异无显著性。(3)各组胎鼠体长差异无显著性(P>0.05)。HFD-SED组胎鼠体重与胎盘重量显著高于NCD-SED组(P<0.01),且胎盘效率显著低于NCD-SED组(P<0.01);而HFD-EX组胎鼠体重和胎盘重量较HFD-SED组显著降低,胎盘效率显著升高(P<0.01)。(4)HFD-SED组3月龄雌、雄子代体重和体脂均显著高于NCD-SED组,而HFD-EX组体重和体脂较HFD-SED组显著下降(P<0.05)。(5)与NCD-SED组相比,HFD-SED组子代因tMCAO/R损伤引起的脑梗死面积显著增加(P<0.05),而母体运动使HFD-EX组子代的脑梗死面积显著减少(P<0.05)。[结论]母体有氧运动能够改善高脂饮食母鼠所致的胎鼠过度生长、成年子代体重和体脂增加等不良影响,并降低成年子代对脑缺血再灌注损伤的易感性。展开更多
背景:氧化应激与多种口腔疾病的发病有关,抗氧化纳米材料具有增强的活性氧清除特性,可以改善氧化应激,在口腔疾病中具有广阔的应用前景。目的:总结近年来抗氧化纳米材料的研究进展以及在口腔疾病中的应用、不足和未来研究方向。方法:以...背景:氧化应激与多种口腔疾病的发病有关,抗氧化纳米材料具有增强的活性氧清除特性,可以改善氧化应激,在口腔疾病中具有广阔的应用前景。目的:总结近年来抗氧化纳米材料的研究进展以及在口腔疾病中的应用、不足和未来研究方向。方法:以“reactive oxygen,antioxidant,nano,oxidative stress,oral”为关键词在PubMed和Web of Science数据库中检索文献,以“活性氧,抗氧化,纳米,氧化应激,口腔”为关键词在中国知网中检索文献,排除与研究主题关联性不强的文章,最终纳入103篇文献进行综述。结果与结论:氧化应激是口腔多种疾病发病的机制之一,清除过量产生的活性氧并纠正氧化与抗氧化失调,是治疗口腔相关疾病的重要措施。抗氧化纳米材料因纳米结构特性具有高效的活性氧清除能力,能够改善机体氧化应激,促进相关疾病的恢复,在口腔相关疾病的研究应用中具有显著效果。抗氧化纳米材料合成原料昂贵、工艺复杂且在体内应用的长期安全性不明确,还需要进一步研究改进和验证。未来抗氧化纳米材料在口腔疾病中的研究应用需多学科交叉,同时结合大数据和人工智能等领域,在材料的设计、实验、应用和验证等方面进行优化,以实现安全、有效且舒适的个性化口腔疾病治疗。展开更多
Stress granules are membraneless organelles that serve as a protective cellular response to external stressors by sequestering non-translating messenger RNAs(mRNAs)and regulating protein synthesis.Stress granules form...Stress granules are membraneless organelles that serve as a protective cellular response to external stressors by sequestering non-translating messenger RNAs(mRNAs)and regulating protein synthesis.Stress granules formation mechanism is conserved across species,from yeast to mammals,and they play a critical role in minimizing cellular damage during stress.Composed of heterogeneous ribonucleoprotein complexes,stress granules are enriched not only in mRNAs but also in noncoding RNAs and various proteins,including translation initiation factors and RNA-binding proteins.Genetic mutations affecting stress granule assembly and disassembly can lead to abnormal stress granule accumulation,contributing to the progression of several diseases.Recent research indicates that stress granule dynamics are pivotal in determining their physiological and pathological functions,with acute stress granule formation offering protection and chronic stress granule accumulation being detrimental.This review focuses on the multifaceted roles of stress granules under diverse physiological conditions,such as regulation of mRNA transport,mRNA translation,apoptosis,germ cell development,phase separation processes that govern stress granule formation,and their emerging implications in pathophysiological scenarios,such as viral infections,cancer,neurodevelopmental disorders,neurodegeneration,and neuronal trauma.展开更多
Ferroptosis is an iron-dependent,excessive lipid peroxidation-driven form of regulated cell death.The core mechanisms of ferroptosis include lipid peroxidation cascade,System X_(c)^(−)-glutathioneglutathione peroxidas...Ferroptosis is an iron-dependent,excessive lipid peroxidation-driven form of regulated cell death.The core mechanisms of ferroptosis include lipid peroxidation cascade,System X_(c)^(−)-glutathioneglutathione peroxidase 4 axis,iron and lipid metabolism chaos,the NAD(P)Hferroptosis suppressor protein 1—ubiquinone axis,and GTP cyclohydrolase 1 tetrahydrobiopterin-dihydrofolate reductase axis.Cuproptosis is triggered by copper ions and involves ferredoxin 1-mediated aggregation of lipoylated proteins,differing fundamentally from ferroptosis.Both ferroptosis and cuproptosis exhibit dual roles(promote or inhibit)in cancers.And the sensitivity of different cancer types to ferroptosis varies,which may depend on special metabolic signatures(e.g.,E-cadherin loss causes epithelial–mesenchymal transition,making tumors gain resistance to ferroptosis)and expression of antioxidant defense regulators(e.g.,high expression of Acyl-CoA synthetase long-chain family member 4 and lncFASA make tumors easily sensitive).At present,traditional Chinese herbal medicine,combination therapy,and nano-delivery technology correlated with ferroptosis are being hotly studied by researchers in order to realize clinical translation of ferroptosis.In this review,we have summarized the core mechanisms of ferroptosis,ferroptosis differences from cuproptosis,its impact on cancers,and its translational implications in cancer therapy,helping readers quickly get the new information and horizons on them.展开更多
文摘[目的]探讨母体运动能否降低肥胖小鼠成年子代对脑缺血再灌注损伤的敏感性。[方法]雌性C57BL/6J小鼠从5周龄开始喂食正常饮食(NCD,10%脂肪含量饲料)或高脂饮食(HFD,60%脂肪含量饲料)。8周后,雌鼠随机分为正常饮食安静组(NCD-SED)、正常饮食运动组(NCD-EX)、高脂饮食安静组(HFD-SED)和高脂饮食运动组(HFD-EX)。运动组进行无负重游泳训练,水温32~34°C,水深20 cm, 60 min/天,6天/周。经过4周的运动干预后,将雌鼠与正常饮食雄鼠按2∶1比例进行合笼交配。以见阴道栓且阴道涂片见精子确定为妊娠第1天(GD1)。进入妊娠期后,运动组母鼠继续接受运动干预,方案调整为45 min/天,5天/周。监测并评估母鼠孕前体重、体脂、葡萄糖耐量和胎鼠体重、体长、胎盘效率等生理指标;同时选取子代3月龄小鼠为研究对象,建立小鼠大脑中动脉短暂性缺血再灌注(tMCAO/R)损伤模型,观察脑梗死面积。[结果](1)HFD-SED组母鼠孕前体重、体脂和葡萄糖耐量曲线下面积显著高于NCD-SED组母鼠(P<0.01),而HFD-EX组母鼠显著低于HFD-SED组(P<0.05)。(2)HFD-SED组孕期体重始终高于NCD-SED组(P<0.05);GD15~GD18期间HFD-EX组的体重显著低于HFD-SED组(P<0.05);各组孕鼠产仔数差异无显著性。(3)各组胎鼠体长差异无显著性(P>0.05)。HFD-SED组胎鼠体重与胎盘重量显著高于NCD-SED组(P<0.01),且胎盘效率显著低于NCD-SED组(P<0.01);而HFD-EX组胎鼠体重和胎盘重量较HFD-SED组显著降低,胎盘效率显著升高(P<0.01)。(4)HFD-SED组3月龄雌、雄子代体重和体脂均显著高于NCD-SED组,而HFD-EX组体重和体脂较HFD-SED组显著下降(P<0.05)。(5)与NCD-SED组相比,HFD-SED组子代因tMCAO/R损伤引起的脑梗死面积显著增加(P<0.05),而母体运动使HFD-EX组子代的脑梗死面积显著减少(P<0.05)。[结论]母体有氧运动能够改善高脂饮食母鼠所致的胎鼠过度生长、成年子代体重和体脂增加等不良影响,并降低成年子代对脑缺血再灌注损伤的易感性。
文摘背景:氧化应激与多种口腔疾病的发病有关,抗氧化纳米材料具有增强的活性氧清除特性,可以改善氧化应激,在口腔疾病中具有广阔的应用前景。目的:总结近年来抗氧化纳米材料的研究进展以及在口腔疾病中的应用、不足和未来研究方向。方法:以“reactive oxygen,antioxidant,nano,oxidative stress,oral”为关键词在PubMed和Web of Science数据库中检索文献,以“活性氧,抗氧化,纳米,氧化应激,口腔”为关键词在中国知网中检索文献,排除与研究主题关联性不强的文章,最终纳入103篇文献进行综述。结果与结论:氧化应激是口腔多种疾病发病的机制之一,清除过量产生的活性氧并纠正氧化与抗氧化失调,是治疗口腔相关疾病的重要措施。抗氧化纳米材料因纳米结构特性具有高效的活性氧清除能力,能够改善机体氧化应激,促进相关疾病的恢复,在口腔相关疾病的研究应用中具有显著效果。抗氧化纳米材料合成原料昂贵、工艺复杂且在体内应用的长期安全性不明确,还需要进一步研究改进和验证。未来抗氧化纳米材料在口腔疾病中的研究应用需多学科交叉,同时结合大数据和人工智能等领域,在材料的设计、实验、应用和验证等方面进行优化,以实现安全、有效且舒适的个性化口腔疾病治疗。
基金supported by a grant from the Merkin Peripheral Neuropathy and Nerve Regeneration Center(to PKS)the Rutgers University Startup Fund(to PKS).
文摘Stress granules are membraneless organelles that serve as a protective cellular response to external stressors by sequestering non-translating messenger RNAs(mRNAs)and regulating protein synthesis.Stress granules formation mechanism is conserved across species,from yeast to mammals,and they play a critical role in minimizing cellular damage during stress.Composed of heterogeneous ribonucleoprotein complexes,stress granules are enriched not only in mRNAs but also in noncoding RNAs and various proteins,including translation initiation factors and RNA-binding proteins.Genetic mutations affecting stress granule assembly and disassembly can lead to abnormal stress granule accumulation,contributing to the progression of several diseases.Recent research indicates that stress granule dynamics are pivotal in determining their physiological and pathological functions,with acute stress granule formation offering protection and chronic stress granule accumulation being detrimental.This review focuses on the multifaceted roles of stress granules under diverse physiological conditions,such as regulation of mRNA transport,mRNA translation,apoptosis,germ cell development,phase separation processes that govern stress granule formation,and their emerging implications in pathophysiological scenarios,such as viral infections,cancer,neurodevelopmental disorders,neurodegeneration,and neuronal trauma.
基金supported by National Natural Science Foundation(82272695)the Key Program of Natural Science Foundation of Zhejiang Province(LZ23H160004)National Undergraduate Training Program for Innovation and Entrepreneurship,Zhejiang Xinmiao Talents Program,China.
文摘Ferroptosis is an iron-dependent,excessive lipid peroxidation-driven form of regulated cell death.The core mechanisms of ferroptosis include lipid peroxidation cascade,System X_(c)^(−)-glutathioneglutathione peroxidase 4 axis,iron and lipid metabolism chaos,the NAD(P)Hferroptosis suppressor protein 1—ubiquinone axis,and GTP cyclohydrolase 1 tetrahydrobiopterin-dihydrofolate reductase axis.Cuproptosis is triggered by copper ions and involves ferredoxin 1-mediated aggregation of lipoylated proteins,differing fundamentally from ferroptosis.Both ferroptosis and cuproptosis exhibit dual roles(promote or inhibit)in cancers.And the sensitivity of different cancer types to ferroptosis varies,which may depend on special metabolic signatures(e.g.,E-cadherin loss causes epithelial–mesenchymal transition,making tumors gain resistance to ferroptosis)and expression of antioxidant defense regulators(e.g.,high expression of Acyl-CoA synthetase long-chain family member 4 and lncFASA make tumors easily sensitive).At present,traditional Chinese herbal medicine,combination therapy,and nano-delivery technology correlated with ferroptosis are being hotly studied by researchers in order to realize clinical translation of ferroptosis.In this review,we have summarized the core mechanisms of ferroptosis,ferroptosis differences from cuproptosis,its impact on cancers,and its translational implications in cancer therapy,helping readers quickly get the new information and horizons on them.
