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
OBJECTIVE: To investigate the effects of electroacupuncture(EA) at the Guanyuan(CV 4) or Sanyinjiao(SP 6) acupoints on the hypothalamus-pituitary-ovary(HPO) axis and spatial learning and memory in female mice.METHODS:...OBJECTIVE: To investigate the effects of electroacupuncture(EA) at the Guanyuan(CV 4) or Sanyinjiao(SP 6) acupoints on the hypothalamus-pituitary-ovary(HPO) axis and spatial learning and memory in female mice.METHODS: Nine-month-old female mice with senescence-accelerated mouse prone 8(SAMP8)were divided into three groups: the disease model,EA-Guanyuan and EA-Sanyinjiao groups. Concurrently, 9-month old female mice with senescence-accelerated mouse resistance 1(SAMR1)were set as the control model group. The two treatment groups were given the same pattern of EA stimulation. Gonadotropin-releasing hormone, luteinizing hormone, follicle-stimulating hormone(FSH) and Serum estradiol levels in the Hypothalamus-pituitary-ovary axis were assessed by enzyme-linked immunosorbent assay to determinethe HPO axis function level. Spatial learning and memory were assessed by the Morris Water Maze(MWM) test.RESULTS:(a) HPO axis: compared with the control model group, the disease model group displayed a decrease in E2 levels(P < 0.01), and an increase in Gn RH, LH and FSH levels(P < 0.01). E2 levels were increased in EA treatment groups compared with the disease model group(P < 0.05). In contrast,Gn RH and LH and FSH levels were reduced(P <0.05). EA-Sanyinjiao group was superior than EA-Guanyuan group on increasing E2 and declining Gn RH levels(P < 0.01).(b) The MWM test demonstrated that the response latency in the EA-Sanyinjiao treatment group declined from day 2 to day5 compared with the disease model group(P <0.05), whereas the EA-Guanyuan treatment group showed no significant difference.CONCLUSION: EA can regulate hormone(E2, FSH,LH, Gn RH) levels in the HPO axis and the spatial learning and memory ability in female SAMP8 mice. Moreover, this effect may have been more pronounced in the EA-Sanyinjiao group than the EA-Guanyuan group. The underlying mechanism of the EA-induced changes may be related to gonadal hormone shifts in the HPO axis, followed by an improvement in spatial learning and memory.展开更多
BACKGROUND Esophageal cancer is one of the most common cancers around the world, and it has high incidence and mortality rates. The conventional therapy for esophageal cancer is radiotherapy, although its effect is hi...BACKGROUND Esophageal cancer is one of the most common cancers around the world, and it has high incidence and mortality rates. The conventional therapy for esophageal cancer is radiotherapy, although its effect is highly limited by the resistance of esophageal cancer cells. Thus, strong radiosensitizers can be very crucial during radiotherapy against esophageal cancer. Brucea javanica oil emulsion (BJOE) is a widely used drug against various cancers, such as liver, colon, and ovarian cancer. However, its anti-cancer effect and mechanism and the use of BJOE as a radiosensitizer have not been explored in esophageal cancer. AIM To evaluate the anti-cancer effect and mechanism of BJOE and explore the potential use of BJOE as a radiosensitizer during radiotherapy. METHODS The inhibitory effect of BJOE and its enhancement function with radiation on cell viability were examined with the calculated half-maximal effective concentration and half-maximal lethal concentration. The influence of BJOE on cell migration and invasion were measured with EC109 and JAR cells by wound-healing and transwell assay. Clonogenesis and apoptotic rate, which was measured by Hoechst staining, were investigated to confirm its enhancement function with radiation. To investigate the molecular pathway underlying the effect of BJOE, the expressions of several apoptosis- and cycle-related proteins was detected by western blotting.cell lines more than normal cell lines, and it markedly reduced migration and invasion in esophageal cancer cells (EC109 and JAR). Moreover, it promoted cell apoptosis and enhanced the effect of radiotherapy against esophageal cancerous cells. In the viability test, the values of half-maximal effective concentration and half-maximal lethal concentration were reduced. Compared to the control, only around 1/5 colonies formed when using BJOE and radiation together in the clonogenic assay. The apoptotic rate in EC109 was obviously promoted when BJOE was added during radiotherapy. Our study suggests that the expression of the apoptosis-proteins Bax and p21 were increased, while the expression of Bcl-2 was stable. Further detection of downstream proteins revealed that the expression of cyclin D1 and cyclin-dependent kinase 4/6 were significantly decreased. CONCLUSION BJOE has a strong anti-cancer effect on esophageal cancer and can be used as a radiosensitizer to promote apoptosis in cancerous esophageal cells via the cyclin D1-cyclin-dependent kinase 4/6 axis.展开更多
Background:A considerable number of muscle development-related genes were differentially expressed in the early stage of avian adipocyte differentiation.However,the functions of them in adipocyte differentiation remai...Background:A considerable number of muscle development-related genes were differentially expressed in the early stage of avian adipocyte differentiation.However,the functions of them in adipocyte differentiation remain largely known.In this study,the myoblast determination protein 1(MYOD1)was selected as a representative of muscle development.We investigated its expression,function,and regulation in avian adipocyte differentiation.Results:The expression of MYOD1 decreased significantly in the early stage of avian adipocyte differentiation.CRIS PR/Cas9-mediated deletion of MYOD1 induced adipocyte differentiation,whereas over-expression of MYOD1 inhibited adipogenesis.The mRNA-seq data showed that MYOD1 could perturb the lipid biosynthetic process during differentiation.Our results showed that MYOD1 directly up-regulates the miR-206 expression by binding the upstream 1200 bp region of miR-206.Then,over-expression of miR-206 can inhibit the adipogenesis.Furthermore,MYOD1 affected the expression of endogenous miR-206 and its target gene Kruppel-like factor 4(KLF4),which is an important activator of adipogenesis.Accordingly,the inhibition of miR-206 or over-expression of KLF4 could counteract the inhibitory effect of MYOD1 on adipocyte differentiation.Conclusions:Our results establish that MYOD1 inhibits adipocyte differentiation by up-regulating miR-206 to suppress the KLF4 expression.These findings identify a novel function of MYOD1 in adipocyte differentiation,suggesting a potential role in body-fat distribution regulation.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the National Science Foundation of China(the Experimental Research on Acupuncture for Prevention and Treatment Alzheimer's Disease Based on the Adjustment Imbalances of NIM,No.81072768)
文摘OBJECTIVE: To investigate the effects of electroacupuncture(EA) at the Guanyuan(CV 4) or Sanyinjiao(SP 6) acupoints on the hypothalamus-pituitary-ovary(HPO) axis and spatial learning and memory in female mice.METHODS: Nine-month-old female mice with senescence-accelerated mouse prone 8(SAMP8)were divided into three groups: the disease model,EA-Guanyuan and EA-Sanyinjiao groups. Concurrently, 9-month old female mice with senescence-accelerated mouse resistance 1(SAMR1)were set as the control model group. The two treatment groups were given the same pattern of EA stimulation. Gonadotropin-releasing hormone, luteinizing hormone, follicle-stimulating hormone(FSH) and Serum estradiol levels in the Hypothalamus-pituitary-ovary axis were assessed by enzyme-linked immunosorbent assay to determinethe HPO axis function level. Spatial learning and memory were assessed by the Morris Water Maze(MWM) test.RESULTS:(a) HPO axis: compared with the control model group, the disease model group displayed a decrease in E2 levels(P < 0.01), and an increase in Gn RH, LH and FSH levels(P < 0.01). E2 levels were increased in EA treatment groups compared with the disease model group(P < 0.05). In contrast,Gn RH and LH and FSH levels were reduced(P <0.05). EA-Sanyinjiao group was superior than EA-Guanyuan group on increasing E2 and declining Gn RH levels(P < 0.01).(b) The MWM test demonstrated that the response latency in the EA-Sanyinjiao treatment group declined from day 2 to day5 compared with the disease model group(P <0.05), whereas the EA-Guanyuan treatment group showed no significant difference.CONCLUSION: EA can regulate hormone(E2, FSH,LH, Gn RH) levels in the HPO axis and the spatial learning and memory ability in female SAMP8 mice. Moreover, this effect may have been more pronounced in the EA-Sanyinjiao group than the EA-Guanyuan group. The underlying mechanism of the EA-induced changes may be related to gonadal hormone shifts in the HPO axis, followed by an improvement in spatial learning and memory.
文摘BACKGROUND Esophageal cancer is one of the most common cancers around the world, and it has high incidence and mortality rates. The conventional therapy for esophageal cancer is radiotherapy, although its effect is highly limited by the resistance of esophageal cancer cells. Thus, strong radiosensitizers can be very crucial during radiotherapy against esophageal cancer. Brucea javanica oil emulsion (BJOE) is a widely used drug against various cancers, such as liver, colon, and ovarian cancer. However, its anti-cancer effect and mechanism and the use of BJOE as a radiosensitizer have not been explored in esophageal cancer. AIM To evaluate the anti-cancer effect and mechanism of BJOE and explore the potential use of BJOE as a radiosensitizer during radiotherapy. METHODS The inhibitory effect of BJOE and its enhancement function with radiation on cell viability were examined with the calculated half-maximal effective concentration and half-maximal lethal concentration. The influence of BJOE on cell migration and invasion were measured with EC109 and JAR cells by wound-healing and transwell assay. Clonogenesis and apoptotic rate, which was measured by Hoechst staining, were investigated to confirm its enhancement function with radiation. To investigate the molecular pathway underlying the effect of BJOE, the expressions of several apoptosis- and cycle-related proteins was detected by western blotting.cell lines more than normal cell lines, and it markedly reduced migration and invasion in esophageal cancer cells (EC109 and JAR). Moreover, it promoted cell apoptosis and enhanced the effect of radiotherapy against esophageal cancerous cells. In the viability test, the values of half-maximal effective concentration and half-maximal lethal concentration were reduced. Compared to the control, only around 1/5 colonies formed when using BJOE and radiation together in the clonogenic assay. The apoptotic rate in EC109 was obviously promoted when BJOE was added during radiotherapy. Our study suggests that the expression of the apoptosis-proteins Bax and p21 were increased, while the expression of Bcl-2 was stable. Further detection of downstream proteins revealed that the expression of cyclin D1 and cyclin-dependent kinase 4/6 were significantly decreased. CONCLUSION BJOE has a strong anti-cancer effect on esophageal cancer and can be used as a radiosensitizer to promote apoptosis in cancerous esophageal cells via the cyclin D1-cyclin-dependent kinase 4/6 axis.
基金supported by the National Waterfowl-Industry Technology Research System(CARS-42)National Nature Science Foundation of China(31972525,31572388)+1 种基金Beijing Municipal Science&Technology Commission(Z181100002418008)Key-Area Research and Development Program of Guangdong Province(2020B020222003).
文摘Background:A considerable number of muscle development-related genes were differentially expressed in the early stage of avian adipocyte differentiation.However,the functions of them in adipocyte differentiation remain largely known.In this study,the myoblast determination protein 1(MYOD1)was selected as a representative of muscle development.We investigated its expression,function,and regulation in avian adipocyte differentiation.Results:The expression of MYOD1 decreased significantly in the early stage of avian adipocyte differentiation.CRIS PR/Cas9-mediated deletion of MYOD1 induced adipocyte differentiation,whereas over-expression of MYOD1 inhibited adipogenesis.The mRNA-seq data showed that MYOD1 could perturb the lipid biosynthetic process during differentiation.Our results showed that MYOD1 directly up-regulates the miR-206 expression by binding the upstream 1200 bp region of miR-206.Then,over-expression of miR-206 can inhibit the adipogenesis.Furthermore,MYOD1 affected the expression of endogenous miR-206 and its target gene Kruppel-like factor 4(KLF4),which is an important activator of adipogenesis.Accordingly,the inhibition of miR-206 or over-expression of KLF4 could counteract the inhibitory effect of MYOD1 on adipocyte differentiation.Conclusions:Our results establish that MYOD1 inhibits adipocyte differentiation by up-regulating miR-206 to suppress the KLF4 expression.These findings identify a novel function of MYOD1 in adipocyte differentiation,suggesting a potential role in body-fat distribution regulation.
