This study aimed to verify the effects of berberine(BBR)on the fat metabolism proteins involved in the sirtuin 3(SIRT3)/adenosine 5'-monophosphate(AMP)-activated protein kinase(AMPK)/acetyl-CoA carboxylase(ACC)pat...This study aimed to verify the effects of berberine(BBR)on the fat metabolism proteins involved in the sirtuin 3(SIRT3)/adenosine 5'-monophosphate(AMP)-activated protein kinase(AMPK)/acetyl-CoA carboxylase(ACC)pathway in the liver tissues of rats with high-fat diet(HFD)-induced non-alcoholic fatty liver disease(NAFLD).Forty-eight rats were randomly divided into the normal control(NC)group,HFD group or BBR group,with 16 rats in each group.After 8 and 16 weeks of treatment,serum and liver samples were collected.Subsequently,body parameters,biochemical parameters and liver pathology were examined.The expression levels of proteins involved in the SIRT3/AMPK/ACC pathway in the liver were detected by Western blotting.After 8 and 16 weeks of a HFD,the successful establishment of rat models with different degrees of NAFLD was confirmed by hematoxylin and eosin(H&E)and Oil Red O staining.NAFLD rat models exhibited obesity and hyperlipidemia,and the protein expression levels of SIRT3,p-AMPK.p-ACC,and CPT-1A in the liver were significantly decreased compared to those in the NC group.The concurrent administration of BBR with the HFD effectively improved serum and liver lipid profiles and ameliorated liver injury.Furthermore,the protein expression levels of SIRT3,p-AMPK,p-ACC,and CPT-1 A in the liver were significantly increased in the BBR group as compared with those in the HFD group.In conclusion,our data suggest that the mechanism by which BBR ameliorates HFD-induced hepatic steatosis may be related to the activation of the SIRT3/AMPK/ACC pathway in the liver.展开更多
The performance degradation of gate-recessed metal–oxide–semiconductor high electron mobility transistor(MOSHEMT)is compared with that of conventional high electron mobility transistor(HEMT)under direct current(DC)s...The performance degradation of gate-recessed metal–oxide–semiconductor high electron mobility transistor(MOSHEMT)is compared with that of conventional high electron mobility transistor(HEMT)under direct current(DC)stress,and the degradation mechanism is studied.Under the channel hot electron injection stress,the degradation of gate-recessed MOS-HEMT is more serious than that of conventional HEMT devices due to the combined effect of traps in the barrier layer,and that under the gate dielectric of the device.The threshold voltage of conventional HEMT shows a reduction under the gate electron injection stress,which is caused by the barrier layer traps trapping the injected electrons and releasing them into the channel.However,because of defects under gate dielectrics which can trap the electrons injected from gate and deplete part of the channel,the threshold voltage of gate-recessed MOS-HEMT first increases and then decreases as the conventional HEMT.The saturation phenomenon of threshold voltage degradation under high field stress verifies the existence of threshold voltage reduction effect caused by gate electron injection.展开更多
基金This work was supported by the National Natural Science Foundation of China(Nos.51971040,52171101,52001036,51971044)the Natural Science Foundation of Chongqing,China(No.cstc2021jcyj-msxmX0613)the Independent Research Project of State Key Laboratory of Mechanical Transmissions,China(No.SKLMT-ZZKT-2022M12).
基金supported by the Chongqing Municipal Human Resources and Social Security Bureau,China(No.cx2022098)the National Natural Science Foundation of China(No.52001036)China Postdoctoral Science Foundation(Nos.2022T150767,2021M693708).
基金grants from the National Natural Science Foundation of China(No.81573844 and No.81774165)Medical Research Fund of Guangdong Province(No.A2017363).
文摘This study aimed to verify the effects of berberine(BBR)on the fat metabolism proteins involved in the sirtuin 3(SIRT3)/adenosine 5'-monophosphate(AMP)-activated protein kinase(AMPK)/acetyl-CoA carboxylase(ACC)pathway in the liver tissues of rats with high-fat diet(HFD)-induced non-alcoholic fatty liver disease(NAFLD).Forty-eight rats were randomly divided into the normal control(NC)group,HFD group or BBR group,with 16 rats in each group.After 8 and 16 weeks of treatment,serum and liver samples were collected.Subsequently,body parameters,biochemical parameters and liver pathology were examined.The expression levels of proteins involved in the SIRT3/AMPK/ACC pathway in the liver were detected by Western blotting.After 8 and 16 weeks of a HFD,the successful establishment of rat models with different degrees of NAFLD was confirmed by hematoxylin and eosin(H&E)and Oil Red O staining.NAFLD rat models exhibited obesity and hyperlipidemia,and the protein expression levels of SIRT3,p-AMPK.p-ACC,and CPT-1A in the liver were significantly decreased compared to those in the NC group.The concurrent administration of BBR with the HFD effectively improved serum and liver lipid profiles and ameliorated liver injury.Furthermore,the protein expression levels of SIRT3,p-AMPK,p-ACC,and CPT-1 A in the liver were significantly increased in the BBR group as compared with those in the HFD group.In conclusion,our data suggest that the mechanism by which BBR ameliorates HFD-induced hepatic steatosis may be related to the activation of the SIRT3/AMPK/ACC pathway in the liver.
基金the Laboratory Open Fund of Beijing Smart-chip Microelectronics Technology Co.Ltd and the National Natural Science Foundation of China(Grant No.11690042)+1 种基金the Science Challenge Project,China(Grant Nos.TZ2018004 and 12035019)the National Major Scientific Research Instrument Projects,China(Grant No.61727804)。
文摘The performance degradation of gate-recessed metal–oxide–semiconductor high electron mobility transistor(MOSHEMT)is compared with that of conventional high electron mobility transistor(HEMT)under direct current(DC)stress,and the degradation mechanism is studied.Under the channel hot electron injection stress,the degradation of gate-recessed MOS-HEMT is more serious than that of conventional HEMT devices due to the combined effect of traps in the barrier layer,and that under the gate dielectric of the device.The threshold voltage of conventional HEMT shows a reduction under the gate electron injection stress,which is caused by the barrier layer traps trapping the injected electrons and releasing them into the channel.However,because of defects under gate dielectrics which can trap the electrons injected from gate and deplete part of the channel,the threshold voltage of gate-recessed MOS-HEMT first increases and then decreases as the conventional HEMT.The saturation phenomenon of threshold voltage degradation under high field stress verifies the existence of threshold voltage reduction effect caused by gate electron injection.