浓差流动电池依靠法拉第电极和存在浓度差的两股盐溶液之间可逆的反应,可将盐差能转化为电能;其与传统膜基盐差能提取技术相比具有成本低、寿命长和体积小等优点。然而已报道的浓差流动电池用电极需要预充电处理而且可能产生有毒离子。...浓差流动电池依靠法拉第电极和存在浓度差的两股盐溶液之间可逆的反应,可将盐差能转化为电能;其与传统膜基盐差能提取技术相比具有成本低、寿命长和体积小等优点。然而已报道的浓差流动电池用电极需要预充电处理而且可能产生有毒离子。铵钒青铜是一种对环境友好的法拉第电极材料。它作为电极与普通滤膜组成浓差流动电池,在不需要预充电处理的前提下,平均输出功率密度高达194.3 mW·m^(−2)(20和500 m mol·L^(−1)的NaCl溶液),相比于石墨烯水凝胶基盐差发电器件(141.4 mW·m^(−2))提升了37%。此外,盐离子价态和尺寸对盐差发电性能存在一定的影响。铵钒青铜的引入,为设计浓差流动电池中的电极材料提供了新思路。展开更多
Liver fibrosis is a dynamic wound-healing response characterized by the agglutination of the extracellular matrix(ECM).Si-Wu-Tang(SWT),a traditional Chinese medicine(TCM)formula,is known for treating gynecological dis...Liver fibrosis is a dynamic wound-healing response characterized by the agglutination of the extracellular matrix(ECM).Si-Wu-Tang(SWT),a traditional Chinese medicine(TCM)formula,is known for treating gynecological diseases and liver fibrosis.Our previous studies demonstrated that long non-coding RNA H19(H19)was markedly upregulated in fibrotic livers while its deficiency markedly reversed fibrogenesis.However,the mechanisms by which SWT influences H19 remain unclear.Thus,we established a bile duct ligation(BDL)-induced liver fibrosis model to evaluate the hepatoprotective effects of SWT on various cells in the liver.Our results showed that SWT markedly improved ECM deposition and bile duct reactions in the liver.Notably,SWT relieved liver fibrosis by regulating the transcription of genes involved in the cytoskeleton remodeling,primarily in hepatic stellate cells(HSCs),and influencing cytoskeleton-related angiogenesis and hepatocellular injury.This modulation collectively led to reduced ECM deposition.Through extensive bioinformatics analyses,we determined that H19 acted as a miRNA sponge and mainly inhibited miR-200,miR-211,and let7b,thereby regulating the above cellular regulatory pathways.Meanwhile,SWT reversed H19-related miRNAs and signaling pathways,diminishing ECM deposition and liver fibrosis.However,these protective effects of SWT were diminished with the overexpression of H19 in vivo.In conclusion,our study elucidates the underlying mechanisms of SWT from the perspective of H19-related signal networks and proposes a potential SWT-based therapeutic strategy for the treatment of liver fibrosis.展开更多
Liver fibrosis is characterized by chronic inflammatory responses and progressive fibrous scar formation.Macrophages play a central role in the pathogenesis of hepatic fibrosis by reconstructing the immune microenviro...Liver fibrosis is characterized by chronic inflammatory responses and progressive fibrous scar formation.Macrophages play a central role in the pathogenesis of hepatic fibrosis by reconstructing the immune microenvironment.Picroside Ⅱ(PIC Ⅱ),extracted from Picrorhizae Rhizoma,has demonstrated therapeutic potential for various liver damage.However,the mechanisms by which macrophage polarization initiates immune cascades and contributes to the development of liver fibrosis,and whether this process can be influenced by PIC Ⅱ,remain unclear.In the current study,RNA sequencing and multiple molecular approaches were utilized to explore the underlying mechanisms of PIC Ⅱ against liver fibrosis in multidrug-resistance protein 2 knockout(Mdr2^(−/−))mice.Our findings indicate that PIC Ⅱ activates M1-polarized macrophages to recruit natural killer cells(NK cells),potentially via the CXCL16-CXCR6 axis.Additionally,PIC Ⅱ promotes the apoptosis of activated hepatic stellate cells(aHSCs)and enhances the cytotoxic effects of NK cells,while also reducing the formation of neutrophil extracellular traps(NETs).Notably,the anti-hepatic fibrosis effects associated with PIC Ⅱ were largely reversed by macrophage depletion in Mdr2^(−/−)mice.Collectively,our research suggests that PIC Ⅱ is a potential candidate for halting the progression of liver fibrosis.展开更多
Hepatic ischemia/reperfusion injury(HIRI)is a common pathophysiological condition occurring during or after liver resection and transplantation,leading to hepatic viability impairment and functional deterioration.Rece...Hepatic ischemia/reperfusion injury(HIRI)is a common pathophysiological condition occurring during or after liver resection and transplantation,leading to hepatic viability impairment and functional deterioration.Recently,ferroptosis,a newly recognized form of programmed cell death,has been implicated in IRI.Rehmanniae Radix Praeparata(RRP),extensively used in Chinese herbal medicine for its hepatoprotective,anti-inflammatory,and antioxidant properties,presents a potential therapeutic approach.However,the mechanisms by which RRP mitigates HIRI,particularly through the regulation of ferroptosis,remain unclear.In this study,we developed a HIRI mouse model and monocrotaline(MCT)-and erastin-induced in vitro hepatocyte injury models.We conducted whole-genome transcriptome analysis to elucidate the protective effects and mechanisms of RRP on HIRI.The RRP aqueous extract was characterized by the presence of acteoside,rehmannioside D,and 5-hydroxymethylfurfural.Our results demonstrate that the RRP aqueous extract ameliorated oxidative stress,reduced intracellular iron accumulation,and attenuated HIRI-induced liver damage.Additionally,RRP significantly inhibited hepatocyte death by restoring intracellular iron homeostasis both in vivo and in vitro.Mechanistically,the RRP aqueous extract reduced intrahepatocellular iron accumulation by inhibiting ZIP14-mediated iron uptake,promoting hepcidin-and ferroportin-mediated iron efflux,and ameliorating mitochondrial iron aggregation through upregulation of Cisd1 expression.Moreover,siRNA-mediated inhibition of hamp synergistically enhanced the RRP aqueous extract's inhibitory effect on ferroptosis.In conclusion,our study elucidates the mechanisms by which RRP aqueous extracts alleviate HIRI,highlighting the restoration of iron metabolic balance.These findings position RRP as a promising candidate for clinical intervention in HIRI treatment.展开更多
文摘浓差流动电池依靠法拉第电极和存在浓度差的两股盐溶液之间可逆的反应,可将盐差能转化为电能;其与传统膜基盐差能提取技术相比具有成本低、寿命长和体积小等优点。然而已报道的浓差流动电池用电极需要预充电处理而且可能产生有毒离子。铵钒青铜是一种对环境友好的法拉第电极材料。它作为电极与普通滤膜组成浓差流动电池,在不需要预充电处理的前提下,平均输出功率密度高达194.3 mW·m^(−2)(20和500 m mol·L^(−1)的NaCl溶液),相比于石墨烯水凝胶基盐差发电器件(141.4 mW·m^(−2))提升了37%。此外,盐离子价态和尺寸对盐差发电性能存在一定的影响。铵钒青铜的引入,为设计浓差流动电池中的电极材料提供了新思路。
基金This work was supported by the National Natural Science Foundation of China(No.82004045)the National High-Level Talents Special Support Program,the Fundamental Research Funds for the Central Universities(No.2023-JYB-XJSJJ009)+1 种基金the Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medicine(No.ZYYCXTD-C-202006)the Young Talents Promotion Project of China Association of Traditional Chinese Medicine(No.2020-QNRC2-01).
文摘Liver fibrosis is a dynamic wound-healing response characterized by the agglutination of the extracellular matrix(ECM).Si-Wu-Tang(SWT),a traditional Chinese medicine(TCM)formula,is known for treating gynecological diseases and liver fibrosis.Our previous studies demonstrated that long non-coding RNA H19(H19)was markedly upregulated in fibrotic livers while its deficiency markedly reversed fibrogenesis.However,the mechanisms by which SWT influences H19 remain unclear.Thus,we established a bile duct ligation(BDL)-induced liver fibrosis model to evaluate the hepatoprotective effects of SWT on various cells in the liver.Our results showed that SWT markedly improved ECM deposition and bile duct reactions in the liver.Notably,SWT relieved liver fibrosis by regulating the transcription of genes involved in the cytoskeleton remodeling,primarily in hepatic stellate cells(HSCs),and influencing cytoskeleton-related angiogenesis and hepatocellular injury.This modulation collectively led to reduced ECM deposition.Through extensive bioinformatics analyses,we determined that H19 acted as a miRNA sponge and mainly inhibited miR-200,miR-211,and let7b,thereby regulating the above cellular regulatory pathways.Meanwhile,SWT reversed H19-related miRNAs and signaling pathways,diminishing ECM deposition and liver fibrosis.However,these protective effects of SWT were diminished with the overexpression of H19 in vivo.In conclusion,our study elucidates the underlying mechanisms of SWT from the perspective of H19-related signal networks and proposes a potential SWT-based therapeutic strategy for the treatment of liver fibrosis.
基金supported by the National Key Research and Development Program on Modernization of Traditional Chinese Medicine(No.2022YFC3502100)the National Natural Science Foundation of China(No.82274186)+2 种基金the National High-Level Talents Special Support Programthe Young Talents Promotion Project of China Association of Traditional Chinese Medicine(No.2020-QNRC2-01)the Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medicine(No.ZYYCXTD-C-202006).
文摘Liver fibrosis is characterized by chronic inflammatory responses and progressive fibrous scar formation.Macrophages play a central role in the pathogenesis of hepatic fibrosis by reconstructing the immune microenvironment.Picroside Ⅱ(PIC Ⅱ),extracted from Picrorhizae Rhizoma,has demonstrated therapeutic potential for various liver damage.However,the mechanisms by which macrophage polarization initiates immune cascades and contributes to the development of liver fibrosis,and whether this process can be influenced by PIC Ⅱ,remain unclear.In the current study,RNA sequencing and multiple molecular approaches were utilized to explore the underlying mechanisms of PIC Ⅱ against liver fibrosis in multidrug-resistance protein 2 knockout(Mdr2^(−/−))mice.Our findings indicate that PIC Ⅱ activates M1-polarized macrophages to recruit natural killer cells(NK cells),potentially via the CXCL16-CXCR6 axis.Additionally,PIC Ⅱ promotes the apoptosis of activated hepatic stellate cells(aHSCs)and enhances the cytotoxic effects of NK cells,while also reducing the formation of neutrophil extracellular traps(NETs).Notably,the anti-hepatic fibrosis effects associated with PIC Ⅱ were largely reversed by macrophage depletion in Mdr2^(−/−)mice.Collectively,our research suggests that PIC Ⅱ is a potential candidate for halting the progression of liver fibrosis.
基金supported by Beijing Nova Program(No.Z201100006820025)the National Natural Science Foundation of China(No.82274186)+3 种基金the Fundamental Research Funds for the Central Universities(No.2023-JYB-JBZD-046)the National High-Level Talents Special Support Program to LI Xiaojiaoyanthe National Key Research and Development Program on Modernization of Traditional Chinese Medicine(No.2022YFC3502100)Beijing Municipal Science&Technology Commission(No.7212174)。
文摘Hepatic ischemia/reperfusion injury(HIRI)is a common pathophysiological condition occurring during or after liver resection and transplantation,leading to hepatic viability impairment and functional deterioration.Recently,ferroptosis,a newly recognized form of programmed cell death,has been implicated in IRI.Rehmanniae Radix Praeparata(RRP),extensively used in Chinese herbal medicine for its hepatoprotective,anti-inflammatory,and antioxidant properties,presents a potential therapeutic approach.However,the mechanisms by which RRP mitigates HIRI,particularly through the regulation of ferroptosis,remain unclear.In this study,we developed a HIRI mouse model and monocrotaline(MCT)-and erastin-induced in vitro hepatocyte injury models.We conducted whole-genome transcriptome analysis to elucidate the protective effects and mechanisms of RRP on HIRI.The RRP aqueous extract was characterized by the presence of acteoside,rehmannioside D,and 5-hydroxymethylfurfural.Our results demonstrate that the RRP aqueous extract ameliorated oxidative stress,reduced intracellular iron accumulation,and attenuated HIRI-induced liver damage.Additionally,RRP significantly inhibited hepatocyte death by restoring intracellular iron homeostasis both in vivo and in vitro.Mechanistically,the RRP aqueous extract reduced intrahepatocellular iron accumulation by inhibiting ZIP14-mediated iron uptake,promoting hepcidin-and ferroportin-mediated iron efflux,and ameliorating mitochondrial iron aggregation through upregulation of Cisd1 expression.Moreover,siRNA-mediated inhibition of hamp synergistically enhanced the RRP aqueous extract's inhibitory effect on ferroptosis.In conclusion,our study elucidates the mechanisms by which RRP aqueous extracts alleviate HIRI,highlighting the restoration of iron metabolic balance.These findings position RRP as a promising candidate for clinical intervention in HIRI treatment.
