Hepatocellular carcinoma (HCC) development is closely related to overexpression of tumor promoters or down-regulation of tumor suppressors.The mammalian sirtuin family was found to be a nicotinamide adenosine dinucleotide (NAD/NADH)-dependent histone deacetylase (HDAC),which implicated in the regulation of critical biological processes through deacetylation modifying on histone and nonhistone.SIRT1 can regulate metabolism,aging,inflammation and cancer progression.In particular,more and more evidence proves that SIRT1 can act as a tumor promot er in hepatocellular carcinoma through deacetylation on tumor suppressors.On the other hand,SIRT1 can strongly suppress metabolic syndrome-associated liver cancer in the mouse model.This review will discuss the expression of sirtuin family member in liver cancer and its clinical significance.

Critical Care ; Critical Illness ; Emergencies ; Female ; Humans ; Infant ; Infant, Newborn ; Intensive Care Units, Pediatric ; Male ; Retrospective Studies ; Transportation of Patients

The chemical constituents were isolated and purified by various chromatographic techniques indluding silica gel, reverse phase silica gel, sephadex LH-20 and pre-HPLC and identified by their physicochemical properties and spectral data. Sixteen phenolic compounds had been isolated and n-butanol extracts which were fractionated from the ethanol extract of Oplopanax horridus roots bark. Their structures were identified as below, including 7 phenylpropanoid compounds, ferulic acid (1), 3-acetylcaffeic acid (2), caffeic acid (3), homovanillyl alcohol 4-O-beta-D-glucopyranoside (4), 3-hydroxyphenethyl alcohol 4-O-beta-D-glucopyranoside (5), 3, 5-dimethoxycinnamyl alcohol 4-O-beta-D-glucopyranoside (6), and 3-dimethoxycinnamyl alcohol 4-O-beta-D-glucopyranoside (7). Three coumarins, scopoletin (8), esculetin (9) and 3'-angeloyl-4'-acetyl-cis-knellactone (10). And 6 lignan compounds, (+)-isolaricires-inol-9'-O-beta-D-glucopyranoside (11), 3, 3'-dimethoxy-4, 9, 9'-trihydroxy-4', 7-epoxy-5', 8-lignan-4, 9-bis-O-beta-D-glucopyranoside (12), (+)-5, 5'-dimethoxylariciresinol 4'-O-beta-D-glucopyranoside (13), (-)-5,5'-dimethoxylariciresinol 4'-O-beta-D-glucopyranoside (14), (-)-pinoresinol 4'-O-beta-D-glucopyranoside (15), and (+)-5, 5'-dimethoxylariciresinol 9'-O-beta-D-glucopyranoside (16). All compounds were isolated and identified for the first time from this plant All the constituents except compounds 4, 6, 12 and 13 were obtained for the first time from the genus Oplopanax.
Drugs, Chinese Herbal ; chemistry ; isolation & purification ; Magnetic Resonance Spectroscopy ; Molecular Structure ; Oplopanax ; chemistry ; Phenols ; chemistry ; isolation & purification ; Spectrometry, Mass, Electrospray Ionization

Objective:To stimulate innovation vitality, the government promulgated the Pilot Implementation Plan for Granting Scientific and Technological Achievements Ownership or Long- term Use Right to Scientific Research Investigators. As one of the 40 pilot institutions, Beijing JiShuiTan Hospital attached great attention to it and, through the exploration and practice of pilot work, combined with the transformation of medical institutions' achievements Status quo, summarized the experiences of job scientific and technological achievements empowerment. Methods:Explored the mechanism and mode to empower researchers with the ownership or long-term right of service invention according to the policy review and case studies.Results:Developed hospital-level empowerment reform program and related supporting documents, Beijing JiShuiTan Hospital has completed the first empowerment work in Beijing.Conclusions:The reform of empowering scientific and technological achievements gives a new pathway to transform scientific and technological achievements in medical institutions, which will promote the transformation process of service invention-creation.

Objective: To discuss the application principle in tuina manipulation for lumbar intervertebral disc herniation (LIDH) in Chinese literatures published in recent 30 years. Methods: The three major Chinese databases, Wanfang Academic Journal Full-text Database (Wanfang), Chongqing VIP Database (CQVIP) and China National Knowledge Infrastructure (CNKI), were searched to collect the studies of tuina manipulations in treatment of LIDH published in recent 30 years. Clustering analysis was applied to analyze the top 20 tuina manipulations for LIDH. Results: The top 20 most frequently used manipulations for LIDH were Gun-rolling, Rou-kneading, Dian-digital pressing, oblique Ban-pulling, An-pressing, Tanbo-plucking, Bashen-pulling and extending, horizontal Tui-pushing, Na-grasping, Anrou-pressing and kneading, Dou-shaking, Yao-rocking, Ca-scrubbing, Pai-patting, post-extension Ban-pulling, Mo-rubbing, Zhen-vibrating, Nie-pinching, fist-back Ji-tapping, and dorsal Shen-extending methods. The involved manipulations can be divided into two categories by the treated body areas. One category is applied to the soft tissues, including Gun-rolling, Rou-kneading, Dian-digital pressing, An-pressing, Tanbo-plucking, horizontal Tui-pushing, Na-grasping, Anrou-pressing and kneading, Ca-scrubbing, Pai-patting, Mo-rubbing, Zhen-vibrating, Nie-pinching, and fist-back Ji-tapping methods. The other category is applied to bones and joints, including oblique Ban-pulling, Bashen-pulling and extending, Dou-shaking, Yao-rocking, post-extension Ban-pulling, and dorsal Shen-extending methods. Conclusion: Based on the treated body area, the tuina manipulations applied to treat LIDH are predominated by the ones performed on soft tissues, assisted by those on bones and joints. From the way of force exertion, the involved manipulations are majorly the swinging methods, followed by squeezing and pressing ones. The manipulations applied to bones and joints are predominated by the Ban-pulling ones, followed by the Bashen-pulling and extending ones.

Objective To establish a HPLC method for the determination of paraquat in human plasma which can be used in clinical practice.Methods The plasma samples were processed with WCX solid phase extraction column and were determinated by RP-HPLC.The HPLC determination was conducted on a Diamonsil C18 column (250 mm × 4.6 mm,5 μm)with the mobile phase consisted of 0.1 mol · L-1 phosphate buffer (containing 80 mmol · L-1 sodium heptanesulfonate,pH 3.0)-acetonitrile (80:20),and the flow rate was 1.0 mL · min-1.The detection wavelength was set at 258 nm,and the column temperature was 25 ℃.Results The plasma concentration of paraquat had good linearity over the range of 20-5000 ng· mL-1 (r =0.999 9).The limit of detection for the paraquat was 20 ng· mL-1.The relative recovery rates of paraquat were 90.06％-104.50％.The absolute recovery rates were 97.66％-99.11％,respectively.The intra-day and inter-day precision (RSD) were all less than 4.00％.The paraquat plasma sample was all stable at the conditions of maintaining at 4 ℃ for 8 h,after freeze thaw cycle and keeping at-40 ℃ for 21 days.The method was applied to the clinical determination of paraquat and the calculation of severityindex of paraquatpoison (SIPP),which was helpful in the clinical treatment of patients with paraquat poison and to predict the prognosis.Conclusion A rapid,sensitive and accurate RP-HPLC method was established,which can be used in the determination of paraquat in human plasma and predict the effect of clinical treatment of patients with paraquat poison.

BACKGROUND:There are currently no effective drugs to mitigate the ischemia/reperfusion injury caused by fluid resuscitation after hemorrhagic shock(HS).The aim of this study was to explore the potential of the histone deacetylase 6(HDAC6)-specific inhibitor tubastatin A(TubA)to suppress nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome activation in macrophages under hypoxia/reoxygenation(H/R)conditions. METHODS:The viability of RAW264.7 cells subjected to H/R after treatment with different concentrations of TubA was assessed using a cell-counting kit-8(CCK8)assay.Briefly,2.5 μmol/L TubA was used with RAW264.7 cells under H/R condition.RAW264.7 cells were divided into three groups,namely the control,H/R,and TubA groups.The levels of reactive oxygen species(ROS)in the cells were detected using fluorescence microscopy.The protein expression of HDAC6,heat shock protein 90(Hsp90),inducible nitric oxide synthase(iNOS),NLRP3,gasdermin-D(GSDMD),Caspase-1,GSDMD-N,and Caspase-1 p20 was detected by western blotting.The levels of interleukin-1β(IL-1β)and IL-18 in the supernatants were detected using enzyme-linked immunosorbent assay(ELISA). RESULTS:HDAC6,Hsp90,and iNOS expression levels were significantly higher(P<0.01)in the H/R group than in the control group,but lower in the TubA group than in the H/R group(P<0.05).When comparing the H/R group to the control group,ROS levels were significantly higher(P<0.01),but significantly reduced in the TubA group(P<0.05).The H/R group had higher NLRP3,GSDMD,Caspase-1,GSDMD-N,and Caspase-1 p20 expression levels than the control group(P<0.05),however,the TubA group had significantly lower expression levels than the H/R group(P<0.05).IL-1β and IL-18 levels in the supernatants were significantly higher in the H/R group compared to the control group(P<0.01),but significantly lower in the TubA group compared to the H/R group(P<0.01). CONCLUSION:TubA inhibited the expression of HDAC6,Hsp90,and iNOS in macrophages subjected to H/R.This inhibition led to a decrease in the content of ROS in cells,which subsequently inhibited the activation of the NLRP3 inflammasome and the secretion of IL-1β and IL-18.

BACKGROUND:There are currently no effective drugs to mitigate the ischemia/reperfusion injury caused by fluid resuscitation after hemorrhagic shock(HS).The aim of this study was to explore the potential of the histone deacetylase 6(HDAC6)-specific inhibitor tubastatin A(TubA)to suppress nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome activation in macrophages under hypoxia/reoxygenation(H/R)conditions. METHODS:The viability of RAW264.7 cells subjected to H/R after treatment with different concentrations of TubA was assessed using a cell-counting kit-8(CCK8)assay.Briefly,2.5 μmol/L TubA was used with RAW264.7 cells under H/R condition.RAW264.7 cells were divided into three groups,namely the control,H/R,and TubA groups.The levels of reactive oxygen species(ROS)in the cells were detected using fluorescence microscopy.The protein expression of HDAC6,heat shock protein 90(Hsp90),inducible nitric oxide synthase(iNOS),NLRP3,gasdermin-D(GSDMD),Caspase-1,GSDMD-N,and Caspase-1 p20 was detected by western blotting.The levels of interleukin-1β(IL-1β)and IL-18 in the supernatants were detected using enzyme-linked immunosorbent assay(ELISA). RESULTS:HDAC6,Hsp90,and iNOS expression levels were significantly higher(P<0.01)in the H/R group than in the control group,but lower in the TubA group than in the H/R group(P<0.05).When comparing the H/R group to the control group,ROS levels were significantly higher(P<0.01),but significantly reduced in the TubA group(P<0.05).The H/R group had higher NLRP3,GSDMD,Caspase-1,GSDMD-N,and Caspase-1 p20 expression levels than the control group(P<0.05),however,the TubA group had significantly lower expression levels than the H/R group(P<0.05).IL-1β and IL-18 levels in the supernatants were significantly higher in the H/R group compared to the control group(P<0.01),but significantly lower in the TubA group compared to the H/R group(P<0.01). CONCLUSION:TubA inhibited the expression of HDAC6,Hsp90,and iNOS in macrophages subjected to H/R.This inhibition led to a decrease in the content of ROS in cells,which subsequently inhibited the activation of the NLRP3 inflammasome and the secretion of IL-1β and IL-18.

BACKGROUND:There are currently no effective drugs to mitigate the ischemia/reperfusion injury caused by fluid resuscitation after hemorrhagic shock(HS).The aim of this study was to explore the potential of the histone deacetylase 6(HDAC6)-specific inhibitor tubastatin A(TubA)to suppress nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome activation in macrophages under hypoxia/reoxygenation(H/R)conditions. METHODS:The viability of RAW264.7 cells subjected to H/R after treatment with different concentrations of TubA was assessed using a cell-counting kit-8(CCK8)assay.Briefly,2.5 μmol/L TubA was used with RAW264.7 cells under H/R condition.RAW264.7 cells were divided into three groups,namely the control,H/R,and TubA groups.The levels of reactive oxygen species(ROS)in the cells were detected using fluorescence microscopy.The protein expression of HDAC6,heat shock protein 90(Hsp90),inducible nitric oxide synthase(iNOS),NLRP3,gasdermin-D(GSDMD),Caspase-1,GSDMD-N,and Caspase-1 p20 was detected by western blotting.The levels of interleukin-1β(IL-1β)and IL-18 in the supernatants were detected using enzyme-linked immunosorbent assay(ELISA). RESULTS:HDAC6,Hsp90,and iNOS expression levels were significantly higher(P<0.01)in the H/R group than in the control group,but lower in the TubA group than in the H/R group(P<0.05).When comparing the H/R group to the control group,ROS levels were significantly higher(P<0.01),but significantly reduced in the TubA group(P<0.05).The H/R group had higher NLRP3,GSDMD,Caspase-1,GSDMD-N,and Caspase-1 p20 expression levels than the control group(P<0.05),however,the TubA group had significantly lower expression levels than the H/R group(P<0.05).IL-1β and IL-18 levels in the supernatants were significantly higher in the H/R group compared to the control group(P<0.01),but significantly lower in the TubA group compared to the H/R group(P<0.01). CONCLUSION:TubA inhibited the expression of HDAC6,Hsp90,and iNOS in macrophages subjected to H/R.This inhibition led to a decrease in the content of ROS in cells,which subsequently inhibited the activation of the NLRP3 inflammasome and the secretion of IL-1β and IL-18.

BACKGROUND:There are currently no effective drugs to mitigate the ischemia/reperfusion injury caused by fluid resuscitation after hemorrhagic shock(HS).The aim of this study was to explore the potential of the histone deacetylase 6(HDAC6)-specific inhibitor tubastatin A(TubA)to suppress nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome activation in macrophages under hypoxia/reoxygenation(H/R)conditions. METHODS:The viability of RAW264.7 cells subjected to H/R after treatment with different concentrations of TubA was assessed using a cell-counting kit-8(CCK8)assay.Briefly,2.5 μmol/L TubA was used with RAW264.7 cells under H/R condition.RAW264.7 cells were divided into three groups,namely the control,H/R,and TubA groups.The levels of reactive oxygen species(ROS)in the cells were detected using fluorescence microscopy.The protein expression of HDAC6,heat shock protein 90(Hsp90),inducible nitric oxide synthase(iNOS),NLRP3,gasdermin-D(GSDMD),Caspase-1,GSDMD-N,and Caspase-1 p20 was detected by western blotting.The levels of interleukin-1β(IL-1β)and IL-18 in the supernatants were detected using enzyme-linked immunosorbent assay(ELISA). RESULTS:HDAC6,Hsp90,and iNOS expression levels were significantly higher(P<0.01)in the H/R group than in the control group,but lower in the TubA group than in the H/R group(P<0.05).When comparing the H/R group to the control group,ROS levels were significantly higher(P<0.01),but significantly reduced in the TubA group(P<0.05).The H/R group had higher NLRP3,GSDMD,Caspase-1,GSDMD-N,and Caspase-1 p20 expression levels than the control group(P<0.05),however,the TubA group had significantly lower expression levels than the H/R group(P<0.05).IL-1β and IL-18 levels in the supernatants were significantly higher in the H/R group compared to the control group(P<0.01),but significantly lower in the TubA group compared to the H/R group(P<0.01). CONCLUSION:TubA inhibited the expression of HDAC6,Hsp90,and iNOS in macrophages subjected to H/R.This inhibition led to a decrease in the content of ROS in cells,which subsequently inhibited the activation of the NLRP3 inflammasome and the secretion of IL-1β and IL-18.