针对数字视频IP核间高速流数据传输,设计并实现了一种基于AXI4-Stream总线的数字视频接口IP核,对外部输入ITU601格式的数字视频信号,将其格式转化为符合AXI4-Stream总线协议的信号,并通过IP核的主端口输出到下一级IP核的从端口。采用Xil...针对数字视频IP核间高速流数据传输,设计并实现了一种基于AXI4-Stream总线的数字视频接口IP核,对外部输入ITU601格式的数字视频信号,将其格式转化为符合AXI4-Stream总线协议的信号,并通过IP核的主端口输出到下一级IP核的从端口。采用Xilinx ISE Design Suite 14.6软件综合设计实现,结合ISE自带ISim软件完成功能仿真,通过实际硬件电路验证了设计的正确性及可行性。展开更多
Esculetin,a natural dihydroxy coumarin derived from the Chinese herbal medicine Cortex Fraxini,has demonstrated significant pharmacological activities,including anticancer properties.Ferroptosis,an iron-dependent form...Esculetin,a natural dihydroxy coumarin derived from the Chinese herbal medicine Cortex Fraxini,has demonstrated significant pharmacological activities,including anticancer properties.Ferroptosis,an iron-dependent form of regulated cell death,has garnered considerable attention due to its lethal effect on tumor cells.However,the exact role of ferroptosis in esculetin-mediated anti-hepatocellular carcinoma(HCC)effects remains poorly understood.This study investigated the impact of esculetin on HCC cells both in vitro and in vivo.The findings indicate that esculetin effectively inhibited the growth of HCC cells.Importantly,esculetin promoted the accumulation of intracellular Fe^(2+),leading to an increase in ROS production through the Fenton reaction.This event subsequently induced lipid peroxidation(LPO)and triggered ferroptosis within the HCC cells.The occurrence of ferroptosis was confirmed by the elevation of malondialdehyde(MDA)levels,the depletion of glutathione peroxidase(GSH-Px)activity,and the disruption of mitochondrial morphology.Notably,the inhibitor of ferroptosis,ferrostatin-1(Fer-1),attenuated the anti-tumor effect of esculetin in HCC cells.Furthermore,the findings revealed that esculetin inhibited the Nrf2-xCT/GPx4 axis signaling in HCC cells.Overexpression of Nrf2 upregulated the expression of downstream SLC7A11 and GPX4,consequently alleviating esculetin-induced ferroptosis.In conclusion,this study suggests that esculetin exerts an anti-HCC effect by inhibiting the activity of the Nrf2-xCT/GPx4 axis,thereby triggering ferroptosis in HCC cells.These findings may contribute to the potential clinical use of esculetin as a candidate for HCC treatment.展开更多
BACKGROUND Ferroptosis is an iron-dependent programmed non-apoptotic cell death characterized by the accumulation of free iron ions and lipid peroxidation.It is associated with the inactivation of glutathione peroxida...BACKGROUND Ferroptosis is an iron-dependent programmed non-apoptotic cell death characterized by the accumulation of free iron ions and lipid peroxidation.It is associated with the inactivation of glutathione peroxidase(GPX)and the accumulation of lipid peroxides within cells.Ferroptosis is closely related to the occurrence and development of hepatocellular carcinoma(HCC).Chlorogenic acid(CGA),an important bioactive component found in 61 traditional Chinese medicines such as Eucommia ulmoides,has been extensively studied for its effects on various malignant tumors.However,the specific role and potential mechanism of CGA in HCC remain unclear.AIM To elucidate the anti-tumor characteristics and potential mechanisms of CGA in inducing ferroptosis in HCC cells.METHODS The effects of CGA on the proliferation,migration,and invasion of HCC cells were evaluated through in vitro experiments.Bioinformatics analysis combined with network pharmacology was used to study the potential targets and molecular mechanisms of CGA intervention in HCC ferroptosis.In vitro experiments were conducted to verify and explore the anti-HCC effects and mechanisms of CGA through the ferroptosis pathway.RESULTS In vitro experiments showed that CGA dose-dependently inhibited the proliferation,invasion,and migration of HCC cells.Bioinformatics analysis combined with network pharmacology revealed that the pathway of CGA intervention in HCC cell ferroptosis was mainly enriched in the prostaglandin endoperoxide synthase 2(PTGS2)/aldoketo reductase family 1 member C3(AKR1C3)/GPX4 signaling pathway,which was associated with arachidonic acid.In vitro experiments further confirmed that CGA-induced ferroptosis in HCC cells was related to mitochondrial damage through the reprogramming of arachidonic acid metabolism by regulating the PTGS2/AKR1C3/GPX4 signaling pathway.CONCLUSION This study demonstrates that CGA inhibits HCC cell proliferation,migration,and invasion by inducing ferroptosis through the PTGS2/AKR1C3/GPX4 axis,suggesting its potential as a novel ferroptosis inducer or anti-HCC drug.展开更多
Gastric cancer(GC)is characterized by high morbidity and mortality rates.Chinese agarwood comprises the resin-containing wood of Aquilaria sinensis(Lour.)Gilg.,traditionally utilized for treating asthma,cardiac ischem...Gastric cancer(GC)is characterized by high morbidity and mortality rates.Chinese agarwood comprises the resin-containing wood of Aquilaria sinensis(Lour.)Gilg.,traditionally utilized for treating asthma,cardiac ischemia,and tumors.However,comprehensive research regarding its anti-GC effects and underlying mechanisms remains limited.In this study,Chinese agarwood petroleum ether extract(CAPEE)demonstrated potent cytotoxicity against human GC cells,with half maximal inhibitory concentration(IC_(50))values for AGS,HGC27,and MGC803 cells of 2.89,2.46,and 2.37μg·mL^(−1),respectively,at 48 h.CAPEE significantly induced apoptosis in these GC cells,with B-cell lymphoma-2(BCL-2)associated X protein(BAX)/BCL-2 antagonist killer 1(BAK)likely mediating CAPEE-induced apoptosis.Furthermore,CAPEE induced G_(0)/G_(1)phase cell cycle arrest in human GC cells via activation of the deoxyribonucleic acid(DNA)damage-p21-cyclin D1/cyclin-dependent kinase 4(CDK4)signaling axis,and increased Fe^(2+),lipid peroxides and reactive oxygen species(ROS)levels,thereby inducing ferroptosis.Ribonucleic acid(RNA)sequencing,real-time quantitative polymerase chain reaction(RT-qPCR),and Western blotting analyses revealed CAPEE-mediated upregulation of heme oxygenase-1(HO-1)in human GC cells.RNA interference studies demonstrated that HO-1 knockdown reduced CAPEE sensitivity and inhibited CAPEE-induced ferroptosis in human GC cells.Additionally,CAPEE administration exhibited robust in vivo anti-GC activity without significant toxicity in nude mice while inhibiting tumor cell growth and promoting apoptosis in tumor tissues.These findings indicate that CAPEE suppresses human GC cell growth through upregulation of the DNA damage-p21-cyclin D1/CDK4 signaling axis and HO-1-mediated ferroptosis,suggesting its potential as a candidate drug for GC treatment.展开更多
文摘针对数字视频IP核间高速流数据传输,设计并实现了一种基于AXI4-Stream总线的数字视频接口IP核,对外部输入ITU601格式的数字视频信号,将其格式转化为符合AXI4-Stream总线协议的信号,并通过IP核的主端口输出到下一级IP核的从端口。采用Xilinx ISE Design Suite 14.6软件综合设计实现,结合ISE自带ISim软件完成功能仿真,通过实际硬件电路验证了设计的正确性及可行性。
基金supported by the Natural Science Foundations of Fujian Province(Nos.2021J05063 and 2023J01541)a startup grant for High-level Talents of Fujian Medical University(No.XRCZX2021014)。
文摘Esculetin,a natural dihydroxy coumarin derived from the Chinese herbal medicine Cortex Fraxini,has demonstrated significant pharmacological activities,including anticancer properties.Ferroptosis,an iron-dependent form of regulated cell death,has garnered considerable attention due to its lethal effect on tumor cells.However,the exact role of ferroptosis in esculetin-mediated anti-hepatocellular carcinoma(HCC)effects remains poorly understood.This study investigated the impact of esculetin on HCC cells both in vitro and in vivo.The findings indicate that esculetin effectively inhibited the growth of HCC cells.Importantly,esculetin promoted the accumulation of intracellular Fe^(2+),leading to an increase in ROS production through the Fenton reaction.This event subsequently induced lipid peroxidation(LPO)and triggered ferroptosis within the HCC cells.The occurrence of ferroptosis was confirmed by the elevation of malondialdehyde(MDA)levels,the depletion of glutathione peroxidase(GSH-Px)activity,and the disruption of mitochondrial morphology.Notably,the inhibitor of ferroptosis,ferrostatin-1(Fer-1),attenuated the anti-tumor effect of esculetin in HCC cells.Furthermore,the findings revealed that esculetin inhibited the Nrf2-xCT/GPx4 axis signaling in HCC cells.Overexpression of Nrf2 upregulated the expression of downstream SLC7A11 and GPX4,consequently alleviating esculetin-induced ferroptosis.In conclusion,this study suggests that esculetin exerts an anti-HCC effect by inhibiting the activity of the Nrf2-xCT/GPx4 axis,thereby triggering ferroptosis in HCC cells.These findings may contribute to the potential clinical use of esculetin as a candidate for HCC treatment.
基金the National Natural Science Foundation of China,No.82074425Natural Foundation of Hunan Province,No.2023JJ30364 and No.2023JJ30361+1 种基金Hunan Provincial Key R&D Program,No.2023SK2057Key Project of Hunan Provincial Administration of Traditional Chinese Medicine,No.A2023042.
文摘BACKGROUND Ferroptosis is an iron-dependent programmed non-apoptotic cell death characterized by the accumulation of free iron ions and lipid peroxidation.It is associated with the inactivation of glutathione peroxidase(GPX)and the accumulation of lipid peroxides within cells.Ferroptosis is closely related to the occurrence and development of hepatocellular carcinoma(HCC).Chlorogenic acid(CGA),an important bioactive component found in 61 traditional Chinese medicines such as Eucommia ulmoides,has been extensively studied for its effects on various malignant tumors.However,the specific role and potential mechanism of CGA in HCC remain unclear.AIM To elucidate the anti-tumor characteristics and potential mechanisms of CGA in inducing ferroptosis in HCC cells.METHODS The effects of CGA on the proliferation,migration,and invasion of HCC cells were evaluated through in vitro experiments.Bioinformatics analysis combined with network pharmacology was used to study the potential targets and molecular mechanisms of CGA intervention in HCC ferroptosis.In vitro experiments were conducted to verify and explore the anti-HCC effects and mechanisms of CGA through the ferroptosis pathway.RESULTS In vitro experiments showed that CGA dose-dependently inhibited the proliferation,invasion,and migration of HCC cells.Bioinformatics analysis combined with network pharmacology revealed that the pathway of CGA intervention in HCC cell ferroptosis was mainly enriched in the prostaglandin endoperoxide synthase 2(PTGS2)/aldoketo reductase family 1 member C3(AKR1C3)/GPX4 signaling pathway,which was associated with arachidonic acid.In vitro experiments further confirmed that CGA-induced ferroptosis in HCC cells was related to mitochondrial damage through the reprogramming of arachidonic acid metabolism by regulating the PTGS2/AKR1C3/GPX4 signaling pathway.CONCLUSION This study demonstrates that CGA inhibits HCC cell proliferation,migration,and invasion by inducing ferroptosis through the PTGS2/AKR1C3/GPX4 axis,suggesting its potential as a novel ferroptosis inducer or anti-HCC drug.
基金supported by the Natural Science Foundation of Beijing City(No.J230034)the Fundamental Research Funds for the Central Universities(No.2023-JYB-JBQN-051)the Talent Cultivation Project of Beijing University of Chinese Medicine(No.JZPY202206).
文摘Gastric cancer(GC)is characterized by high morbidity and mortality rates.Chinese agarwood comprises the resin-containing wood of Aquilaria sinensis(Lour.)Gilg.,traditionally utilized for treating asthma,cardiac ischemia,and tumors.However,comprehensive research regarding its anti-GC effects and underlying mechanisms remains limited.In this study,Chinese agarwood petroleum ether extract(CAPEE)demonstrated potent cytotoxicity against human GC cells,with half maximal inhibitory concentration(IC_(50))values for AGS,HGC27,and MGC803 cells of 2.89,2.46,and 2.37μg·mL^(−1),respectively,at 48 h.CAPEE significantly induced apoptosis in these GC cells,with B-cell lymphoma-2(BCL-2)associated X protein(BAX)/BCL-2 antagonist killer 1(BAK)likely mediating CAPEE-induced apoptosis.Furthermore,CAPEE induced G_(0)/G_(1)phase cell cycle arrest in human GC cells via activation of the deoxyribonucleic acid(DNA)damage-p21-cyclin D1/cyclin-dependent kinase 4(CDK4)signaling axis,and increased Fe^(2+),lipid peroxides and reactive oxygen species(ROS)levels,thereby inducing ferroptosis.Ribonucleic acid(RNA)sequencing,real-time quantitative polymerase chain reaction(RT-qPCR),and Western blotting analyses revealed CAPEE-mediated upregulation of heme oxygenase-1(HO-1)in human GC cells.RNA interference studies demonstrated that HO-1 knockdown reduced CAPEE sensitivity and inhibited CAPEE-induced ferroptosis in human GC cells.Additionally,CAPEE administration exhibited robust in vivo anti-GC activity without significant toxicity in nude mice while inhibiting tumor cell growth and promoting apoptosis in tumor tissues.These findings indicate that CAPEE suppresses human GC cell growth through upregulation of the DNA damage-p21-cyclin D1/CDK4 signaling axis and HO-1-mediated ferroptosis,suggesting its potential as a candidate drug for GC treatment.
