This study aimed to explore the effect of Bifidobacterium animalis F1-7 on the improvement of atherosclerotic inflammation.Arteriosclerosis model ApoE^(-/-)mice were orally administered with B.animalis F1-7 for 12 wee...This study aimed to explore the effect of Bifidobacterium animalis F1-7 on the improvement of atherosclerotic inflammation.Arteriosclerosis model ApoE^(-/-)mice were orally administered with B.animalis F1-7 for 12 weeks.The probiotic intervention reduced the plaque areas in aorta and the accumulation of macrophages,and downregulated the expression of toll-like receptor 4(TLR4)/nuclear factorκB(NF-κB)pathway to reduce the levels of inflammatory factors.The widely-targeted metabolomics analysis showed that acetyl-L-carnitine(ALC)in the intestine of atherosclerotic mice was significantly increased after B.animalis F1-7 intervention.Correlation analysis proved that ALC was associated with atherosclerotic inflammatory response.By using oxidized low density lipoprotein induced macrophage foam cells,we further verified that ALC could reduce lipid accumulation and inflammatory response in foam cells by downregulating the TLR4/NF-κB pathway.Finally,our results revealed that B.animalis F1-7 upregulated the metabolite ALC to downregulate the inflammatory responses,leading to the reduction of plaque accumulation of atherosclerosis.展开更多
An important factor in the emergence and progre sion of osteosarcoma(OS)is the dysregulated expression of microRNAs(miRNAs).Transcription factor 7-like 1(TCF7LI),a member of the T cell factor/lymphoid enhancer factor(...An important factor in the emergence and progre sion of osteosarcoma(OS)is the dysregulated expression of microRNAs(miRNAs).Transcription factor 7-like 1(TCF7LI),a member of the T cell factor/lymphoid enhancer factor(TCF/LEF)transcription factor family,interacts with the Wnt signaling pathway regulator β-catenin and acts as a DNA-specific binding protein.This study sought to elucidate the impact of the interaction between miR 3293p and TCF7L1 on.the growth and apoptosis of OS and analyze the regulatory expression relationship between miRNA and mRNA in osteosarcoma cells using a variety of approaches.MiR329-3p was significantly downregulated,while TCF7L1 was considerably up-regulated in all examined OS cell lines.Additionally,a clinical comparison study was performed using the TCGA database.Subsequently,the regulatory relationship between miR-329-3p and TCF7L1 on the proliferation and apoptosis of OS cells was verified through in vitro and in vivo experiments.When miR 329-3p was transfected into the OS cell line,the expression of TCF7L1 decreased,the proliferation of OS cells was inhibited,the cytoskeleton disintegrated,and the nucleus condensed to fom apoptotic bodies.The expression of proteins that indicate apoptosis increased simultaneously.The cell cycle was arrested in the G0/G1 phase,and the G1/S transition was blocked.The introduction of miR 3293p also inhibited downstream Cyclin D1 of the Wnt pathway.Xenograf experiments indicated that the overexpression of miR-329-3p signi ficanly inhibited the growth of OS xenografts in nude mice,and the expression of TCF7L1 and C-Myc in tumor tssues decreased.MiR 329-3p was significantly reduced in OS cells and played a suppressive role in tumorigenesis and proliferation by targeting TCF7L1 both in vitro and in vivo.Osteosarcoma cell cycle arrest and pathway inhibition were observed upon the regulation of TCF7LI by miR 3293p.Summarizing these results,it can be inferred that miR.3293p exerts anticancer efects in osteosarcoma by inhibiting TCF7L1.展开更多
目的:探讨子痫前期(PE)患者血清和胎盘中的肿瘤坏死因子-α(TNF-α)、基质金属蛋白酶-1(MMP-1)、基质金属蛋白酶-7(MMP-7)的表达水平。方法:选取2021年11月—2023年8月扬州大学临床医学院妇产科收治的86例PE患者,分为早发型PE(n=33)和...目的:探讨子痫前期(PE)患者血清和胎盘中的肿瘤坏死因子-α(TNF-α)、基质金属蛋白酶-1(MMP-1)、基质金属蛋白酶-7(MMP-7)的表达水平。方法:选取2021年11月—2023年8月扬州大学临床医学院妇产科收治的86例PE患者,分为早发型PE(n=33)和晚发型PE(n=53),另外选取健康孕妇(n=45)作为对照。检测所有纳入患者血清及胎盘组织中的TNF-α、MMP-1和MMP-7水平。结果:早发型PE患者(34.71±1.35周vs 40.43±0.70周)及晚发型PE患者(38.43±0.60周vs 40.43±0.70周)的孕周明显小于对照组(均P<0.05);早发型PE患者血清中TNF-α(507.92±28.99 ng/L vs 478.50±41.15 ng/L)、MMP-1(1156.67±158.07μg/L vs 1037.59±163.10μg/L)和MMP-7(211.00±18.64μg/L vs 196.32±19.87μg/L)的表达较晚发型PE患者显著增加(均P<0.05),晚发型PE患者血清中TNF-α(478.50±41.15 ng/L vs 446.90±41.52 ng/L)、MMP-1(1037.59±163.10μg/L vs 840.78±174.43μg/L)和MMP-7(196.32±19.87μg/L vs 166.01±15.09μg/L)的表达较对照组显著增加(均P<0.05);免疫组化结果显示,早发型PE患者胎盘组织中TNF-α、MMP-1和MMP-7表达水平较晚发型PE及对照组明显升高(均P<0.05)。结论:早发型PE患者及晚发型PE患者的TNF-α、MMP-1和MMP-7表达明显增加,这可能在PE的发生发展中起到重要作用。展开更多
基金This work was supported by National Natural Science Foundation of China （NSFC） （No. 81400265 and No. 81270274）, and Peking University People＇s Hospital Research and Development funds （RDB2014-16）.
基金supported by Shandong Taishan industry leading talent project(LJNY202101)the National Key R&D of China(2018YFC0311201)。
文摘This study aimed to explore the effect of Bifidobacterium animalis F1-7 on the improvement of atherosclerotic inflammation.Arteriosclerosis model ApoE^(-/-)mice were orally administered with B.animalis F1-7 for 12 weeks.The probiotic intervention reduced the plaque areas in aorta and the accumulation of macrophages,and downregulated the expression of toll-like receptor 4(TLR4)/nuclear factorκB(NF-κB)pathway to reduce the levels of inflammatory factors.The widely-targeted metabolomics analysis showed that acetyl-L-carnitine(ALC)in the intestine of atherosclerotic mice was significantly increased after B.animalis F1-7 intervention.Correlation analysis proved that ALC was associated with atherosclerotic inflammatory response.By using oxidized low density lipoprotein induced macrophage foam cells,we further verified that ALC could reduce lipid accumulation and inflammatory response in foam cells by downregulating the TLR4/NF-κB pathway.Finally,our results revealed that B.animalis F1-7 upregulated the metabolite ALC to downregulate the inflammatory responses,leading to the reduction of plaque accumulation of atherosclerosis.
基金The Fund of National Cancer Center Research and Development(26-A-4),The Grants-in-Aid for Scientific Research(Grant Nos.15K10451,16K10866 and 16K20063)from Japan Society for the Promotion of Science.
文摘An important factor in the emergence and progre sion of osteosarcoma(OS)is the dysregulated expression of microRNAs(miRNAs).Transcription factor 7-like 1(TCF7LI),a member of the T cell factor/lymphoid enhancer factor(TCF/LEF)transcription factor family,interacts with the Wnt signaling pathway regulator β-catenin and acts as a DNA-specific binding protein.This study sought to elucidate the impact of the interaction between miR 3293p and TCF7L1 on.the growth and apoptosis of OS and analyze the regulatory expression relationship between miRNA and mRNA in osteosarcoma cells using a variety of approaches.MiR329-3p was significantly downregulated,while TCF7L1 was considerably up-regulated in all examined OS cell lines.Additionally,a clinical comparison study was performed using the TCGA database.Subsequently,the regulatory relationship between miR-329-3p and TCF7L1 on the proliferation and apoptosis of OS cells was verified through in vitro and in vivo experiments.When miR 329-3p was transfected into the OS cell line,the expression of TCF7L1 decreased,the proliferation of OS cells was inhibited,the cytoskeleton disintegrated,and the nucleus condensed to fom apoptotic bodies.The expression of proteins that indicate apoptosis increased simultaneously.The cell cycle was arrested in the G0/G1 phase,and the G1/S transition was blocked.The introduction of miR 3293p also inhibited downstream Cyclin D1 of the Wnt pathway.Xenograf experiments indicated that the overexpression of miR-329-3p signi ficanly inhibited the growth of OS xenografts in nude mice,and the expression of TCF7L1 and C-Myc in tumor tssues decreased.MiR 329-3p was significantly reduced in OS cells and played a suppressive role in tumorigenesis and proliferation by targeting TCF7L1 both in vitro and in vivo.Osteosarcoma cell cycle arrest and pathway inhibition were observed upon the regulation of TCF7LI by miR 3293p.Summarizing these results,it can be inferred that miR.3293p exerts anticancer efects in osteosarcoma by inhibiting TCF7L1.
文摘目的:探讨子痫前期(PE)患者血清和胎盘中的肿瘤坏死因子-α(TNF-α)、基质金属蛋白酶-1(MMP-1)、基质金属蛋白酶-7(MMP-7)的表达水平。方法:选取2021年11月—2023年8月扬州大学临床医学院妇产科收治的86例PE患者,分为早发型PE(n=33)和晚发型PE(n=53),另外选取健康孕妇(n=45)作为对照。检测所有纳入患者血清及胎盘组织中的TNF-α、MMP-1和MMP-7水平。结果:早发型PE患者(34.71±1.35周vs 40.43±0.70周)及晚发型PE患者(38.43±0.60周vs 40.43±0.70周)的孕周明显小于对照组(均P<0.05);早发型PE患者血清中TNF-α(507.92±28.99 ng/L vs 478.50±41.15 ng/L)、MMP-1(1156.67±158.07μg/L vs 1037.59±163.10μg/L)和MMP-7(211.00±18.64μg/L vs 196.32±19.87μg/L)的表达较晚发型PE患者显著增加(均P<0.05),晚发型PE患者血清中TNF-α(478.50±41.15 ng/L vs 446.90±41.52 ng/L)、MMP-1(1037.59±163.10μg/L vs 840.78±174.43μg/L)和MMP-7(196.32±19.87μg/L vs 166.01±15.09μg/L)的表达较对照组显著增加(均P<0.05);免疫组化结果显示,早发型PE患者胎盘组织中TNF-α、MMP-1和MMP-7表达水平较晚发型PE及对照组明显升高(均P<0.05)。结论:早发型PE患者及晚发型PE患者的TNF-α、MMP-1和MMP-7表达明显增加,这可能在PE的发生发展中起到重要作用。
