Oxidative stress is caused by an imbalance of the antioxidant defense system and excessive production of free radicals,which can damage biological macromolecules such as proteins,lipids and nucleic acids,and can cause...Oxidative stress is caused by an imbalance of the antioxidant defense system and excessive production of free radicals,which can damage biological macromolecules such as proteins,lipids and nucleic acids,and can cause aging,ischemia-reperfusion injury,inflammatory injury,liver and kidney injury and other diseases.The nuclear factor erytheroid-2-related factor 2(Nrf2)is a major regulator of redox balance.The Nrf2 pathway also exerts a central function in cell apoptosis,oxidative stress damage and metabolic diseases.Bioactive peptides are small molecular peptides composed of amino acid residues.They have many biological activities and play important physiological roles in human body.Antioxidant peptide is a kind of peptide which can reduce oxidative stress damage.They are safe,non-toxic and easily absorbed.In this review,we summarized the mechanism of bioactive peptides in regulating oxidative stress,especially antioxidant peptides,through regulating the Nrf2 signaling pathway and the expressions of oxidative stress-related genes,to alleviate oxidative stress-induced damage.The paper will provide valuable reference to investigators in the antioxidant peptide field and also promote the applications of antioxidant peptides in the oxidative stress-associated diseases.展开更多
Acute myocardial infarction(MI)remains one of the leading causes of mortality and morbidity in the global communities.A prevailing topic that has attracted increasing attentions over the past few decades is the so-cal...Acute myocardial infarction(MI)remains one of the leading causes of mortality and morbidity in the global communities.A prevailing topic that has attracted increasing attentions over the past few decades is the so-called heart-brain interaction,in particular following a major traumatic event such as MI.Increased prevalence of depression and other mental disorders has been recognized in cardiac patients after MI,coronary catheterization,or cardiothoracic surgeries.In this review,we focus on the potential pathogenic mechanisms and pre-clinical transcriptomic evidence for identifying potential mediators of post-MI depression.We first summarize the conventional mechanistic understanding that leads to the current clinical management of post-MI depression with the use of selective serotonin reuptake inhibitors(SSRIs)and cognitive behavior and exercise therapies.We further envisage a possible role played by certain chemokines,e.g.,Chemokine(C-X-C motif)ligand 12(CXCL12)and Chemokine(C-C motif)ligand 2(CCL22),in serving as signaling molecules to connect the MI-induced heart damage to the pro-depressive changes in brain during the post-MI period.Future in-depth investigations into this chemokine hypothesis will be instrumental in developing new chemokine-targeted therapies for better management of the cardiac patients suffering from post-MI depression.展开更多
Suppression of stimulated Raman scattering(SRS)by means of chirped and tilted fiber Bragg gratings(CTFBGs)has become a key topic.However,research on high-power systems is still lacking due to two problems.Firstly,afte...Suppression of stimulated Raman scattering(SRS)by means of chirped and tilted fiber Bragg gratings(CTFBGs)has become a key topic.However,research on high-power systems is still lacking due to two problems.Firstly,after the inscription,there are a large number of hydroxyl compounds and hydrogen molecules in CTFBGs that cause significant heating due to their strong infrared absorption.Secondly,CTFBGs can couple Stokes light from the core to the cladding and the coating,which causes serious heating in the coating of the CTFBG.Aimed at overcoming these bottlenecks,a process that combines constant-low-temperature and variable-high-temperature annealing is used to reduce the thermal slope of the CTFBG.Also,a segmented-corrosion cladding power stripping technology is used on the CTFBG to remove the Stokes light which is coupled to the cladding,which solves the problem of overheating in the coating of the CTFBG.Thereby,a CTFBG with both a kilowatt-level power-carrying load and the ability to suppress SRS in a fiber laser has been developed.Further,we establish a kW-level CW oscillator to test the CTFBG.Experimental results demonstrate that the power-carrying load of the CTFBG is close to 1 kW,the thermal slope is lower than 0.015 ℃/W,and the SRS suppression ratio is nearly 23 dB.展开更多
Suppressing nonlinear effects in high-power fiber lasers based on fiber gratings has become a hotspot.At present,research is mainly focused on suppressing stimulated Raman scattering in a high-power fiber laser.Howeve...Suppressing nonlinear effects in high-power fiber lasers based on fiber gratings has become a hotspot.At present,research is mainly focused on suppressing stimulated Raman scattering in a high-power fiber laser.However,the suppression of spectral broadening,caused by self-phase modulation or four-wave mixing,is still a challenging attribute to the close distance between the broadened laser and signal laser.If using a traditional fiber grating with only one stopband to suppress the spectral broadening,the signal power will be stripped simultaneously.Confronting this challenge,we propose a novel method based on phase-shifted long-period fiber grating(PS-LPFG)to suppress spectral broadening in a high-power fiber master oscillator power amplifier(MOPA)laser system in this paper.A PS-LPFG is designed and fabricated on 10/130 passive fiber utilizing a point-by-point scanning technique.The resonant wavelength of the fabricated PS-LPFG is 1080 nm,the full width at half maximum of the passband is 5.48 nm,and stopband extinction exceeds 90%.To evaluate the performance of the PS-LPFG,the grating is inserted into the seed of a kilowattlevel continuous-wave MOPA system.Experiment results show that the 30 dB linewidth of the output spectrum is narrowed by approximately 37.97%,providing an effective and flexible way for optimizing the output linewidth of highpower fiber MOPA laser systems.展开更多
Chronic kidney disease is a prevalent and severe significant complication of hypoxia.This study found that peptide LVYPFPGPIPN could protect hypoxia-induced renal injury in the animal model.Network pharmacology and mo...Chronic kidney disease is a prevalent and severe significant complication of hypoxia.This study found that peptide LVYPFPGPIPN could protect hypoxia-induced renal injury in the animal model.Network pharmacology and molecular docking analysis indicated that cathepsin B(CTSB)and interleukin-1β(IL-1β)represent potential targets for the prevention/treatment of hypoxic-induced renal injury.GO analysis revealed the involvement of these genes in various biological processes,including apoptosis regulation,oxidative stress response,and adaptive immune modulation.Experimental results in vitro and in vivo demonstrated that peptide LVYPFPGPIPN could effectively inhibit apoptosis and stress responses of kidney cells by regulating the NRF2/IL-1β/mitochondrial apoptosis pathway,thereby protecting hypoxic human embryonic kidney cells from damage.The anti-hypoxic effect of the LVYPFPGPIPN offers a novel therapeutic clue for the treatment/prevention of hypoxic-induced kidney injury and inflammation-associated chronic kidney disease.展开更多
Myocardial ischemia-reperfusion(MI/R)not only causes cardiac damage,but also causes severe renal damage.T8 is the 8th peptide identified by peptiomics in digested yak milk dregs and our previous studies showed that T8...Myocardial ischemia-reperfusion(MI/R)not only causes cardiac damage,but also causes severe renal damage.T8 is the 8th peptide identified by peptiomics in digested yak milk dregs and our previous studies showed that T8 had strong antioxidant activity.This study evaluated the protective effects and molecular mechanisms of MI/R-induced kidney injury in rats.Our results indicated that peptide T8 could increase ejection fraction(EF)and shortened fraction(FS),and degraded ST segment elevation,which ameliorated cardiac function in the MI/R rats.Peptide T8 could increase activities of superoxide dismutase(SOD)and glutathione peroxidase(GSH-PX),and decreased the contents of malondialdehyde(MDA),serum creatinine(Scr)and blood urea nitrogen(BUN),which could ameliorate renal insufficiency.Peptide T8 and kidney injury-related targets in the MI/R-damaged rats were obtained from network pharmacology analysis.KEGG analysis revealed that T8 might affect 54 signaling pathways and 13 key targets were obtained by PPI network analysis.The binding affinity of peptide T8 to Keap1 was found to be the strongest by molecular docking analysis.In the H2O2-induced HEK293 cell model,peptide T8 decreased reactive oxygen species(ROS)content and changed the expression ratio of Bcl-2 and Bax,thereby inhibiting mitochondria-dependent apoptosis.Further studies indicated that T8 could regulate Nrf2 pathway and downstream target genes such as NQO1,which could reduce oxidative stress-induced damage.These results suggest that peptide T 8 can exert renal protection via regulating Nrf2 pathway and apoptosis-related genes.展开更多
Hyperlipidemia is closely related to multiple diseases and is characterized by abnormal serum lipid profiles.The biological function of lentinan in mice and rats was studied,but the mechanism of its lipid-lowering eff...Hyperlipidemia is closely related to multiple diseases and is characterized by abnormal serum lipid profiles.The biological function of lentinan in mice and rats was studied,but the mechanism of its lipid-lowering effect was not completely clear.In this study,network pharmacological analysis,molecular docking,and molecular dynamics simulation were used to explore the potential mechanism of its lipid-lowering effect and high-fat diet(HFD)mice was used to confirm the predicted mechanism.Our results indicated that lentinan could ameliorate hyperlipidemia by regulating peroxisome proliferator-activated receptors(PPARs),sterol response element-binding protein-1(SREBP1),and nuclear factor kappa-B(NF-κB)in the hepatic tissues of mices.Further animal experiment showed that lentinan could regulate the mRNA expressions of lipid metabolism-related genes,such as PPARα,PPARδ,PPARγ,cluster of differentiation 36(CD36)and SREBP-1c.Moreover,lentinan supplementation could reduce the expressions of inflammatory cytokines such as tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and inducible nitric oxide sythase(iNOS).In cell model,lentinan also could inhibit oleic acid-induced lipid droplet formation and the expressions of lipid metabolism-related genes and reduced inflammatory factor expressions in HepG2 cells,which further approved the results of animal experiment.Taken together,our results suggest that lentinan can ameliorate hyperlipidemia via regulating lipid metabolism-related gene expressions and reduce obesity-induced inflammatory response.展开更多
Sinensetin is a polymethoxylated flavone,which is considered to be an important functional composition in citrus peels.In this study,the anti-inflammatory effect and potential mechanism of sinensetin were evaluated by...Sinensetin is a polymethoxylated flavone,which is considered to be an important functional composition in citrus peels.In this study,the anti-inflammatory effect and potential mechanism of sinensetin were evaluated by multi-omics analysis in the dextran sulfate sodium(DSS)-induced colitis model.The results showed that sinensetin significantly inhibited inflammation and alleviated gut microbiota imbalance in the DSS-induced mice.Sinensetin supplementation increased the abundance of Faecalibaculum,Colidextribacter,Lachnospiraceae_NK4A136_group,norank_f_norank_Clostridia_UCG-014 and Christensenella,reduced abundance of Bacteroides,Escherichia-Shigella,Parasutterella and Clostridium_sensu_stricto_1.The metabolome of serum samples showed 117 differential metabolites were significantly altered by sinensetin supplementation in colitis mice,and 24 of these metabolites were involved in the Kyoto Encyclopedia of Genes and Genomes(KEGG)signaling pathway.KEGG predictions based on both gut microbiota and serum metabolites suggested that cysteine and methionine metabolism are mainly affected by sinensetin supplementation.These results indicate that sinensetin inhibit DSSinduced colitis by modulating gut microbiota and ameliorating serum metabolism.展开更多
基金the funds from the National Key R&D Program of China(2022YFF1100200).
文摘Oxidative stress is caused by an imbalance of the antioxidant defense system and excessive production of free radicals,which can damage biological macromolecules such as proteins,lipids and nucleic acids,and can cause aging,ischemia-reperfusion injury,inflammatory injury,liver and kidney injury and other diseases.The nuclear factor erytheroid-2-related factor 2(Nrf2)is a major regulator of redox balance.The Nrf2 pathway also exerts a central function in cell apoptosis,oxidative stress damage and metabolic diseases.Bioactive peptides are small molecular peptides composed of amino acid residues.They have many biological activities and play important physiological roles in human body.Antioxidant peptide is a kind of peptide which can reduce oxidative stress damage.They are safe,non-toxic and easily absorbed.In this review,we summarized the mechanism of bioactive peptides in regulating oxidative stress,especially antioxidant peptides,through regulating the Nrf2 signaling pathway and the expressions of oxidative stress-related genes,to alleviate oxidative stress-induced damage.The paper will provide valuable reference to investigators in the antioxidant peptide field and also promote the applications of antioxidant peptides in the oxidative stress-associated diseases.
文摘Acute myocardial infarction(MI)remains one of the leading causes of mortality and morbidity in the global communities.A prevailing topic that has attracted increasing attentions over the past few decades is the so-called heart-brain interaction,in particular following a major traumatic event such as MI.Increased prevalence of depression and other mental disorders has been recognized in cardiac patients after MI,coronary catheterization,or cardiothoracic surgeries.In this review,we focus on the potential pathogenic mechanisms and pre-clinical transcriptomic evidence for identifying potential mediators of post-MI depression.We first summarize the conventional mechanistic understanding that leads to the current clinical management of post-MI depression with the use of selective serotonin reuptake inhibitors(SSRIs)and cognitive behavior and exercise therapies.We further envisage a possible role played by certain chemokines,e.g.,Chemokine(C-X-C motif)ligand 12(CXCL12)and Chemokine(C-C motif)ligand 2(CCL22),in serving as signaling molecules to connect the MI-induced heart damage to the pro-depressive changes in brain during the post-MI period.Future in-depth investigations into this chemokine hypothesis will be instrumental in developing new chemokine-targeted therapies for better management of the cardiac patients suffering from post-MI depression.
基金supported by the National Key Research and Development Program of China(No.2017YFB1104400)
文摘Suppression of stimulated Raman scattering(SRS)by means of chirped and tilted fiber Bragg gratings(CTFBGs)has become a key topic.However,research on high-power systems is still lacking due to two problems.Firstly,after the inscription,there are a large number of hydroxyl compounds and hydrogen molecules in CTFBGs that cause significant heating due to their strong infrared absorption.Secondly,CTFBGs can couple Stokes light from the core to the cladding and the coating,which causes serious heating in the coating of the CTFBG.Aimed at overcoming these bottlenecks,a process that combines constant-low-temperature and variable-high-temperature annealing is used to reduce the thermal slope of the CTFBG.Also,a segmented-corrosion cladding power stripping technology is used on the CTFBG to remove the Stokes light which is coupled to the cladding,which solves the problem of overheating in the coating of the CTFBG.Thereby,a CTFBG with both a kilowatt-level power-carrying load and the ability to suppress SRS in a fiber laser has been developed.Further,we establish a kW-level CW oscillator to test the CTFBG.Experimental results demonstrate that the power-carrying load of the CTFBG is close to 1 kW,the thermal slope is lower than 0.015 ℃/W,and the SRS suppression ratio is nearly 23 dB.
基金supported by the National Key Research and Development Program of China(No.2017YFB1104402)the Pre-research Foundation of Equipment Development Department(No.61404140105)+3 种基金the Key Laboratory of Optical System Advanced Manufacturing Technology of the Chinese Academy of Sciences(No.KLOMT190101)the Jiangsu Provincial Key Research and Development Program(No.BE2019114)the Basic Research Program of Jiangsu Province(No.BK20190456)the National Natural Science Foundation of China(No.62005120)。
文摘Suppressing nonlinear effects in high-power fiber lasers based on fiber gratings has become a hotspot.At present,research is mainly focused on suppressing stimulated Raman scattering in a high-power fiber laser.However,the suppression of spectral broadening,caused by self-phase modulation or four-wave mixing,is still a challenging attribute to the close distance between the broadened laser and signal laser.If using a traditional fiber grating with only one stopband to suppress the spectral broadening,the signal power will be stripped simultaneously.Confronting this challenge,we propose a novel method based on phase-shifted long-period fiber grating(PS-LPFG)to suppress spectral broadening in a high-power fiber master oscillator power amplifier(MOPA)laser system in this paper.A PS-LPFG is designed and fabricated on 10/130 passive fiber utilizing a point-by-point scanning technique.The resonant wavelength of the fabricated PS-LPFG is 1080 nm,the full width at half maximum of the passband is 5.48 nm,and stopband extinction exceeds 90%.To evaluate the performance of the PS-LPFG,the grating is inserted into the seed of a kilowattlevel continuous-wave MOPA system.Experiment results show that the 30 dB linewidth of the output spectrum is narrowed by approximately 37.97%,providing an effective and flexible way for optimizing the output linewidth of highpower fiber MOPA laser systems.
基金funds from the Key Project of State Key R&D Program,China(No.2022YFF1100200)Central Committee of Xizang Autonomous Region guides the Special Project of Local Science and Technology Development(XZ202202YD0004C)+3 种基金the Program for Science&Technology Innovation Platform of Hunan Province(2019TP1029)Hunan Provincial Innovation Foundation for Postgraduate(No.CX20220750)Major Project of Changsha Science and Technology Program(kh2301028)Scientific Innovation Fund for Post-graduates of Central South University of Forestry and Technology(No.CX 202201028).
文摘Chronic kidney disease is a prevalent and severe significant complication of hypoxia.This study found that peptide LVYPFPGPIPN could protect hypoxia-induced renal injury in the animal model.Network pharmacology and molecular docking analysis indicated that cathepsin B(CTSB)and interleukin-1β(IL-1β)represent potential targets for the prevention/treatment of hypoxic-induced renal injury.GO analysis revealed the involvement of these genes in various biological processes,including apoptosis regulation,oxidative stress response,and adaptive immune modulation.Experimental results in vitro and in vivo demonstrated that peptide LVYPFPGPIPN could effectively inhibit apoptosis and stress responses of kidney cells by regulating the NRF2/IL-1β/mitochondrial apoptosis pathway,thereby protecting hypoxic human embryonic kidney cells from damage.The anti-hypoxic effect of the LVYPFPGPIPN offers a novel therapeutic clue for the treatment/prevention of hypoxic-induced kidney injury and inflammation-associated chronic kidney disease.
基金acknowledge the funds from the National Key R&D Program of China(2022YFF1100200).
文摘Myocardial ischemia-reperfusion(MI/R)not only causes cardiac damage,but also causes severe renal damage.T8 is the 8th peptide identified by peptiomics in digested yak milk dregs and our previous studies showed that T8 had strong antioxidant activity.This study evaluated the protective effects and molecular mechanisms of MI/R-induced kidney injury in rats.Our results indicated that peptide T8 could increase ejection fraction(EF)and shortened fraction(FS),and degraded ST segment elevation,which ameliorated cardiac function in the MI/R rats.Peptide T8 could increase activities of superoxide dismutase(SOD)and glutathione peroxidase(GSH-PX),and decreased the contents of malondialdehyde(MDA),serum creatinine(Scr)and blood urea nitrogen(BUN),which could ameliorate renal insufficiency.Peptide T8 and kidney injury-related targets in the MI/R-damaged rats were obtained from network pharmacology analysis.KEGG analysis revealed that T8 might affect 54 signaling pathways and 13 key targets were obtained by PPI network analysis.The binding affinity of peptide T8 to Keap1 was found to be the strongest by molecular docking analysis.In the H2O2-induced HEK293 cell model,peptide T8 decreased reactive oxygen species(ROS)content and changed the expression ratio of Bcl-2 and Bax,thereby inhibiting mitochondria-dependent apoptosis.Further studies indicated that T8 could regulate Nrf2 pathway and downstream target genes such as NQO1,which could reduce oxidative stress-induced damage.These results suggest that peptide T 8 can exert renal protection via regulating Nrf2 pathway and apoptosis-related genes.
基金supported by the Key Project of State Key R&D Program,China(No.2022YFF1100200).
文摘Hyperlipidemia is closely related to multiple diseases and is characterized by abnormal serum lipid profiles.The biological function of lentinan in mice and rats was studied,but the mechanism of its lipid-lowering effect was not completely clear.In this study,network pharmacological analysis,molecular docking,and molecular dynamics simulation were used to explore the potential mechanism of its lipid-lowering effect and high-fat diet(HFD)mice was used to confirm the predicted mechanism.Our results indicated that lentinan could ameliorate hyperlipidemia by regulating peroxisome proliferator-activated receptors(PPARs),sterol response element-binding protein-1(SREBP1),and nuclear factor kappa-B(NF-κB)in the hepatic tissues of mices.Further animal experiment showed that lentinan could regulate the mRNA expressions of lipid metabolism-related genes,such as PPARα,PPARδ,PPARγ,cluster of differentiation 36(CD36)and SREBP-1c.Moreover,lentinan supplementation could reduce the expressions of inflammatory cytokines such as tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and inducible nitric oxide sythase(iNOS).In cell model,lentinan also could inhibit oleic acid-induced lipid droplet formation and the expressions of lipid metabolism-related genes and reduced inflammatory factor expressions in HepG2 cells,which further approved the results of animal experiment.Taken together,our results suggest that lentinan can ameliorate hyperlipidemia via regulating lipid metabolism-related gene expressions and reduce obesity-induced inflammatory response.
基金the Key Projects of State Key R&D Program,China(No.2022YFF1100200)the Natural Science Foundation of Hunan Province,China(Grant No.2021JJ31075)+2 种基金the Program for Science&Technology Innovation Platform of Hunan Province(2019TP1029)the Postgraduate Scientific Research Innovation Project of Hunan Province(CX20240070)the Scientific Innovation Fund for Post-graduates of Central South University of Forestry and Technology(2024CX02089).
文摘Sinensetin is a polymethoxylated flavone,which is considered to be an important functional composition in citrus peels.In this study,the anti-inflammatory effect and potential mechanism of sinensetin were evaluated by multi-omics analysis in the dextran sulfate sodium(DSS)-induced colitis model.The results showed that sinensetin significantly inhibited inflammation and alleviated gut microbiota imbalance in the DSS-induced mice.Sinensetin supplementation increased the abundance of Faecalibaculum,Colidextribacter,Lachnospiraceae_NK4A136_group,norank_f_norank_Clostridia_UCG-014 and Christensenella,reduced abundance of Bacteroides,Escherichia-Shigella,Parasutterella and Clostridium_sensu_stricto_1.The metabolome of serum samples showed 117 differential metabolites were significantly altered by sinensetin supplementation in colitis mice,and 24 of these metabolites were involved in the Kyoto Encyclopedia of Genes and Genomes(KEGG)signaling pathway.KEGG predictions based on both gut microbiota and serum metabolites suggested that cysteine and methionine metabolism are mainly affected by sinensetin supplementation.These results indicate that sinensetin inhibit DSSinduced colitis by modulating gut microbiota and ameliorating serum metabolism.
