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Hepatic ischemia/reperfusion injury (HIRI) is a serious complication that occurs following shock and/or liver surgery. Gut microbiota and their metabolites are key upstream modulators of development of liver injury. Herein, we investigated the potential contribution of gut microbes to HIRI. Ischemia/reperfusion surgery was performed to establish a murine model of HIRI. 16S rRNA gene sequencing and metabolomics were used for microbial analysis. Transcriptomics and proteomics analysis were employed to study the host cell responses. Our results establish HIRI was significantly increased when surgery occurred in the evening (ZT12, 20:00) when compared with the morning (ZT0, 08:00); however, antibiotic pretreatment reduced this diurnal variation. The abundance of a microbial metabolite 3,4-dihydroxyphenylpropionic acid was significantly higher in ZT0 when compared with ZT12 in the gut and this compound significantly protected mice against HIRI. Furthermore, 3,4-dihydroxyphenylpropionic acid suppressed the macrophage pro-inflammatory response in vivo and in vitro. This metabolite inhibits histone deacetylase activity by reducing its phosphorylation. Histone deacetylase inhibition suppressed macrophage pro-inflammatory activation and diminished the diurnal variation of HIRI. Our findings revealed a novel protective microbial metabolite against HIRI in mice. The potential underlying mechanism was at least in part, via 3,4-dihydroxyphenylpropionic acid-dependent immune regulation and histone deacetylase (HDAC) inhibition in macrophages.
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Objective To investigate the expression and clinical significance of Bcl-2,NF-κB and C-myc in diffuse large B cell lymphoma (DLBCL) tissue.Methods Sixty-seven cases of DLBCL tissue were selected as the observation group,and contemporaneous 21 cases of lymphoid reactive hyperplasia(RH) tissues as the control group.The levels of Bcl-2,NF-κB,C-myc protein expression in tissues were detected by the S-P method.Then their relationship with the clinicopathological features of DLBCL was analyzed.Results Th epositive expression rates of Bcl-2,NF-κB and C-myc protein in DLBCL tissues were 58.21%,62.69% and 77.61% respectively,which in RH tissue were 0.00%,19.05% and 23.81% respectively,the difference was statistically significant(P0.05),was significantly correlated with clinical stage and IPI grade (P0.05),was significantly correlated with clinical stage,location,IPI grade and serum LDH level (P0.05),was significantly correlated with clinical stage and IPI grade (P0.05),NF-κB and C-myc expression in DLBCL tissues showed weak positive correlation (r=0.293,P<0.05).Conclusion Bcl-2,NF-κB,C-myc expressions are closely correlated with the clinical stage and IPI grade of DLBCL and can serve as the reference indicators for evaluating DLBCL prognosis.
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Objective To investigate the clinical effect of mild hypothermia on neonatal bilirubin encephalopathy, and the value of 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET)/CT and amplitude integrated electroencephalogram (aEEG) for diagnosis and evaluation of curative effect. Methods From May, 2013 to December, 2014, 29 newborns with bilirubin encephalopathy were divided into conventional group (n=15) and mild hypothermia group (n=14). The conventional group received conventional therapy, and the other group received mild hypothermia in addition. The aEEG and neuron-specific enolase (NSE) were measured before and after treatment, as well as the glucose metabolism rate with 18F-FDG PET/CT after treatment. Results The NSE was lower after treatment in both groups (t>9.670, P2.943, P0.640, P<0.05). Conclusion Mild hypothermia therapy could further promote the energy metabolism of brain cells in neonatal bilirubin encephalopathy. 18F-FDG PET/CT and aEEG can be used for early diagnosis and therapeutic evaluation.
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Objective]To investigate the effect of acupuncture-assisted anesthesia on cerebral state index(CSI) under the steady-state anesthesia of sevoflurane. [Methods] Fifty patients scheduled for elective knee arthroscopy operation were randomly divided into two groups with 25 in each. All patients were induced with sevoflurane, the end-tidal concentrations of sevoflurane in two groups were adjusted to 1.0 MAC and maintained for 15 min after tracheal intubation, acupuncture-assisted anesthesia was used on the affected side in group A, Yanglingquan(GB34) and Zusanli(ST36) were selected as the acupoints. The positive and negative electrodes of the electropuncture apparatus(G8650) were respectively connected with Yanglingquan(GB34) and Zusanli(ST36). People reccived transcutaneous electrical acupoint stimulation with condensation-rarefaction wave(2/15 Hz, 8~12mA) untill the end of operation, patiant's body types SBP, SDP, MAP, HR and CSI were recorded at lying still for 5 min(T1), steady state of sevoflurane(T2), acupuncture-assisted anesthesia after 20 and 30 min(T3, T4). [Results] SBP, DBP, MBP, HR and CSI at T3~T4 were significantly lower in group A than those in group B and T2(P<0.05). [Conclusion]Acupuncture-assisted anesthesia can reduce the CSI under the steady-state anesthesia of sevoflurane and lower blood pressure and heart rate at the same time.
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Objective To evaluate the effect of Budesonide combined with Poractant Alfa(pulmonary surfactants,PS) on preventing the bronchopulmonary dysplasia (BPD) in preterm infants.Methods One hundred and twenty preterm infants 6 hours after birth(gestational ages≤32 weeks and birth weights ≤1500 g)admitted to the Department of Newborn Medicine,the Affiliated Hospital of Southeast Medical University from October 2013 to February 2015 were randomly divided into 4 group(30 cases in each group).Group A was a control group,group B was neonatal respiratory distress syndrome(NRDS) group,group C was NRDS with PS group,and group D was NRDS with PS and Budesonide group.Thirty-two-week preterms without other diseases and without uptaking oxygen within 48 h were assigned as group A.Group B were treated by continuous uptaking oxygen with continuous positive airway pressure(CPAP) (oxygen uptaken lasting more than 48 h and oxygen concentrations more than 40％).Group C were treated with 100 mg/kg PS within 48 h on the basis of group B.Group D were treated with 0.25 mg/kg Budesonide suspension for inhalation on the basis of group C.The pH value,partial pressure of oxygen [pa(O2)],partial pressure of carbon dioxide [pa(CO2)] in the blood gas analysis were all detected in all groups before treatment,1,6,12,24 and 48 hours after using drug,respectively.All groups were also observed for whether to use respirator assisted ventilation,the duration of high oxygen use,the total time of uptaking oxygen,the rate of using PS again,the rate of BPD,the total hospitalization days and the adverse effects.The adverse effects included high blood pressure,high blood sugar,necrotizing enterocolitis and the incidence of nosocomial infection.Results Compared with group B,the pH value at 1 and 6 hours after using drugs,the pa(O2) and pa(CO2) at 1,6 and 12 hours after using drugs were improved obviously in the group C,and the differences were statistically significant (all P＜0.01).Compared with group B,the above indicators were improved more obvious in group D,and the differences were statistically significant (all P＜0.01).Moreover,compared with the group B,the oxygen inhalation duration,the rate of having a respirator assisted ventilation and using PS again,and the incidence of BPD were obviously decreased in other groups,the differences were statistically significant (all P＜0.05).The incidence of BPD in group D was less than that of group C,and the differences were statistically significant (3.33％ vs 10.00％,x2=4.00,P=0.046).The total oxygen time and the rate of adverse effects of each group were similar.The differences were not statistically significant (all P＞0.05).Conclusions Budesonide combined with Poractant Alfa can prevent BPD in preterm infants.Its effect is better than the simple use of Poractant Alfa,and the rate of adverse effects are not increased significantly.
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Objective To explore the mechanism for the increase in reactive oxygen species regulated by p47phox of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit in peripheral blood mononuclear cells (PBMCs) after oxygen therapy in premature infants.Methods According to different volume fractions of oxygen,premature infants less than 32 weeks were divided into 3 groups:fractional concentration of inspired oxygen (FiO2) ＜ 30％ was low concentration oxygen group,FiO2 between 30％ and 40％ as middle concentration oxygen group,and FiO2 ＞ 40％ as high concentration oxygen group.Premature infants less than 32 weeks without oxygen was control group.After 48 h,3 mL blood was collected via radial artery from each group,PBMCs and serum were separated.Then intracellular reactive oxygen species (ROS) by confocal laser scanning microscopy,malondialdehyde (MDA) within serum by thiobarbituric acid colorimetric,and the location and activation rate of p47phox through immunofluorescence.Results After premature infants were exposed to oxygen,as the oxygen volume fraction was increasing,ROS and MDA gradually rised.More PBMCs with p47phox translocated to membrane,then the translocation rate of p47phox also increased.Compared with the control group,ROS were significantly higher(q =4.48,6.5,16.22,all P ＜ 0.05) among the other 3 groups ; MDA significantly increased as well(q =5.08,8.22,12.76,all P ＜ 0.05) ; the activation rate of p47phox also had significant differences (x2 =134.008,P ＜ 0.05);compared with the middle concentration oxygen group,the high concentration oxygen group had higher ROS and MDA(q =15.03,4.53,all P ＜ 0.05) ; the activation rate of p47phox increased significantly(x2 =19.26,P ＜ 0.05).Conclusions After oxygen exposure,p47phox translocated to membrane may regulate the NADPH oxidase-derived ROS increase in extremely premature infants.
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Objective The renin-angiotensin system ( RAS) is involved in myocardial anoxic injury .This study aimed to in-vestigate the expressions of AT 1-R, AT2-R, and angiotensin-converting enzyme ( ACE ) in bone marrow mesenchymal stem cells (MSCs) under hypoxia. Methods Rat MSCs were isolated, cultured, and identified with CD29 and CD11b/c antibodies.The is-chemic injury model was established by exposing the MSCs to hypoxia and serum deprivation ( Hypoxia/SD) for 24 hours, while the control cells were cultured in L-DMEM with 10%FBS.The vitality and apoptosis of the cells were detected by trypan blue staining , CCK8 assay, and Annexin V-FITC staining.The mRNA and protein expressions of AT 1-R, AT2-R, and ACE were determined by real-time quantitative PCR and Western blot , respectively. Results The positive rate of CD29 was >97%and that of CD11b/c was <1% in the MSCs.Compared with the control group, Hypoxia/SD significantly increased the rate of cell apoptosis ([6.73 ±0.78]%vs [19.93 ±4.92]%, P<0.01), decreased the rate of cell viability ([78.49 ±4.94]%vs [37.33 ±2.91]%, P<0.01), and up-regulated the mRNA and protein expressions of AT 1-R, AT2-R, and ACE. Conclusion Hypoxia/SD activates the RAS in MSCs and improves the protective function of the cells against myocardial anoxic injury .
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Objective To analyze if the increasing the dose and time of vancomycin will increase the renal toxicity risk in patients with resistance to toluene penicillin Staphylococcus aureus (methicillin-resistant Staphylococcus aureus, MRSA) and blood drug concentration significance in the course of treatment.Methods We enrolled 105 patients, mean age (58.0 ±5.8) years;59 males (61.9%) treated in our hospital with MRSA.Patients’ age, sex, serum creatinine (SCr), creatinine clearance rate (CrCl), serum vancomycin concentrations, duration of treatment, acute physiology and chronic health evaluation II score were analysed.The definition of renal toxicity is that SCr is higher than the baseline 0.5 mg/dL, or according to the measurement results of a series SCr:SCr elevation≥50%.The relevant data in patients with renal toxicity and non toxicity were compared.Results 45 (42.9%) had renal toxicity.Vancomycin concentration was significantly higher in renal toxicity patients than non toxicity [(20.9 ±9.8)μg/mL vs. (14.2 ±6.6)μg/mL, P<0.001), serum drug concentration≥15μg/mL (67.8% vs 40.3%; P =0.01) and vancomycin treatment duration (14 days) ( 46.0% vs 21.4%; P =0.011 ) has obvious different scale between two groups. Regression analysis showed that: vancomycin serum concentration≥15μg/mL and prolonged treatment were independent predictors of renal toxicity ( adjusted likelihood ratio =2.83; 95%CI, 1.03 ~7.72, P=0.045).Conclusion The increase of vancomycin dosage and treatment time was the risk of nephrotoxicity.
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Objective To construct p66shc gene interfering lentivirus vectors recombination and transfect it to 293T cells ,RNA interfering was carried out to induce p66shc gene silence ,so as to provide basis for further study of the p66shc function .Methods Screening of three RNA targets which were named after p66shc‐shc1 ,p66shc‐shc2 ,p66shc‐shc3 ,cloned into the pLenR‐GPH vec‐tor ,which contained green fluorescent protein(GFP) and transformed into DH5αcells .The positive clone were picked out for right sequencing and transfected to 293T cells with pRsv‐REV ,pMDlg‐pRRE ,pMD2G .The expression of GFP in inverted fluorescence microscope confirmed the virus packaging success .Fluorescence quantitative PCR and Western blot technology were used to investi‐gate the expression of p66shc at the molecular and protein levels ,p66shc‐shc1 target of effective silencing p66shc gene was selected to prepare for subsequent tests .Results The shRNA lentivirus vector was constructed which could express p66shc and was trans‐fected into 293T cells successfully .Fluorescence quantitative PCR and Western blot technology were used to investigate p66shc gene silence by RNA interference .Conclusion The lentivirus RNAi vector of targeted expression p66shc could induce p66shc gene si‐lence at the molecular and protein levels after transfected into 293T cells by RNA interference .
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Objective To explore the effects of endoplasmic reticulum (ER) stress in the hyperoxia-induced lung injury in premature rats. Methods Forty-eight premature Wistar rats were randomized into two groups 12 hours after birth:hyperoxia group (n=24) inhaled 95%oxygen and control group (n=24) inhaled air. Eight rats were sacriifced in each group on day 1, 3, 7 after the treatment and the left lungs were embedded. The pathological changes in the HE stained sections of lung tissues were observed. The expressions of ER related protein ERp57 and c/EBP homologous protein CHOP were detected by immuno histo-chemistry and the apoptosis of lung cells was detected by TUNEL analysis. Results The typical pathological characteristics of acute lung injury were observed in hyperoxia group. The expressions of ERp57 and CHOP were increased with the exposure time in hyperoxia group, and were signiifcantly higher than in control group (P<0.05). The apoptosis rate of lung cells in hyperoxia group was signiifcantly higher than in control group (P<0.01). There was signiifcant positive correlation between cell apoptosis index and expressions of Erp57 and c/EBP homogeneous protein. Conclusions ER stress initiated apoptosis participates and plays an important role in the process of hyperoxia-induced lung injury in premature rats.
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Objective To determine the expression of adapter protein p66Shc in mediating alveolar epithelial cells induced by hyperoxia and to explore their relationship.Methods A549 cells were cultured in vitro and divided randomly into a control group and a hyperoxia group.The hyperoxia group was exposed to a mixture of oxygen(O2,900 mL/L) and carbon dioxide(CO2,50 mL/L) for 10 min,then cultured in a closed environment.The changes in morphology were observed under inverted microscope after exposure to oxygen or air for 24 hours.The cell apoptosis was detected by flow cytometry (FC) after 24 hours.And the expression of p66Shc was detected by immunohistochemical method after 24 hours.The correlation of the changes in mitochondrial membrane potential and p66Shc protein expression was analyzed by using Bivariate correlation analysis.Results 1.Under inverted microscopy,A549 cells from the air group significantly increased,stuck to each other tightly and grew very quickly.Their adhesion was better,multy-angle oblate and many cells were in division phase.Compared with the control group,the changes in morphology of A549 were remarked and obvious than those in the hyperoxia group.The cells grew slowly,their counts decreased and the cell morphology changed from typical multi-angle oblate to round or ellipse.2.Compared with the control group,after 24 h,in hyperoxia group of A549 cells,red fluorescence decreased,and green fluorescence enhanced.3.Compared with the controls (0.057 664 88 ± 0.006 517 84),the expression of p66Shc (0.123 600 50 ± 0.004 227 23) was significantly increased in the hyperoxia group(t =-24.006,P ＜ 0.001).4.The decline of membrane potential was negatively correlated with the increased expression of p66Shc protein (R =-0.988,P ＜ 0.001).Conclusions The hyperoxia induction could significantly increase in injured mediating alveolar epithelial cells induced by hyperoxia,the expression of p66Shc increases,the membrane potential declined,and they exhibit a negative correlation.So p66Shc may be involved in the process of high oxygen damage to human alveolar epithelial cells.
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Objectives To explore the role of PKCβ/p66Shc oxidative stress signaling pathway in hyperoxia-induced apoptosis of alveolar epithelial cells A549. Methods A549 cells were cultured in vitro and divided randomly into control (incubated with 5%CO2), hyperoxia group (exposed to a mixture of 900 ml/L O2 and 50 ml/L CO2 at speed of 3 L/min for 10 mins, then cultured in a closed environment) and LY333531 group (treated with 10μmol/L of PKCβinhibitor LY333531 for 24h then induced with hyperoxia for 10 mins). The cellular morphology was observed under inverted microscope at 12, 24 and 48 h of treatment. The cell apoptosis was detected by lfow cytometry. Expression of PKCβ/Pin1/p66Shc/p66Shc-Ser36 were detected by immunohistochemistry after 24 h of treatment. Results Comparing to the control group, the cellular morphology of A549 in the hyperoxia group changed to spherical shapes and space between cells increased, the living cell count decreased and suspension cell increased. The living cell count in LY333531 group increased and suspension cell decreased than those in hyperoxia group but not reach the levels of the control group. The apoptosis rate of A549 cells and the expression of PKCβ/Pin1/p66Shc/p66Shc-Ser36 at 24 h were signiifcantly increased in the hyperoxia group than those in the control group, while the apoptosis rate and the expression of PKCβ/Pin1/p66Shc/p66Shc-Ser36 were greatly decreased in the LY333531 group than those in the hyperoxia group (all P<0.01). Conclusions The expression of PKCβin A549 cells can be increased by the hyper-oxia induction but reduced by LY333531, and then the expressions of Pin1, p66Shc and p66Shc-Ser36 are reduced. Thus the re-duced apoptosis of A549 cells relieve the cell injury induced by hyperoxia.
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Objective To explore the potential mechanism of abnormal behavior resulted from maternal separation in neo-natal period in rat. Methods Neonatal rats were equally and randomly divided into maternal separation group and control group. The rats in maternal separation group were separated from the dam for 3h per day on postnatal days (PND) 2 to 21, nothing was done to the rats in the control group. The brain tissues were taken out after being killed on PND 7, 14, and 21. The expressions of Caveolin-l, BDNF and GFAP in hippocampal formation were detected by immunohistochemistry. Semiquantitative assessment of immunohistochemical images was performed by Image-Pro Plus software. Results Compared with control groups, the expres-sion of Caveolin-l on PND 7 had no signiifcant change, while BDNF and GFAP were signiifcantly increased in maternal separa-tion group (P<0.05). On PND 14 and 21, the expressions of Caveolin-l, BDNF and GFAP were signiifcantly decreased in maternal separation group (P<0.05). Conclusions Decreased expressions of Caveolin-l, BDNF and GFAP caused by maternal separation in neonatal period may be associated with abnormal behaviors in adulthood in rat.
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Objective To investigate the role of Astragahs in alleviating adhesion of neutrophils to HK-2 cells induced by postasphyxial-serum of neonate and its signal transduction mechanism. MethodsHK-2 cells were used as target cell. Control group, asphyxia group, Astragalus group were divided in the experiment. The 20％ (volume fraction) postasphyxial-serum was used as attacking factor. The following indicators were detected: cellular morphology and neutrophils adhesion were observed with inverted microscope. The activity of myeloperoxidase (MPO) in the cell suspension were determined by biochemistry assay as the indicator for adhesion of neutrophils to HK-2. Intercellular adhesion molecule-1(ICAM-1) were examined by flow eytometer. ResultsThe neutrophils numbers (MPO activity) and ICAM-1 expression in asphyxia group were higher than that of the control group, but dramatically decreased in Astragalus group (P < 0.05). ConclusionsThese data demonstrated that Astragalus could alleviate the adhesion of neutrophils from neonate with asphyxia to HK-2 and it' s intracellular signal transduction mechanism is presumably involved in the inhibition of ICAM-1 expression on HK-2 cellular membrane.
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AIM: To investigate whether the circadian mRNA expression of the renin-angiotensin system (RAS) components (ATNG、AT_1R、AT_2R) in myocardium is correlated with left ventricular hypertrophy in both spontaneously hypertensive rats (SHR) and renal hypertensive rats (RHR). METHODS: The model of RHR was established using 2K1C (two-kidney one clip). SHR, RHR, and normotensive control rats (CON) were housed in a separate environment-controlled room for two weeks, in which a strict 12-hour light/12-hour dark cycle regimen was enforced (lights on at 900, zeitgeber time [ZT0]). Rats were killed every 4 hours from 900 am (ZT0) to 500 pm (ZT20) on three separate days. We examined the circadian mRNA expression of ATNG、AT_1R、AT_2R in the hearts of SHR, RHR and CON rats by RT-PCR. RESULTS: Heart weight to body weight ratios and left ventricle weight to heart weight ratios indicated a significant increase in SHR and RHR compared with normotensive rats. The cardiac mRNA expression of the RAS components showed circadian oscillations in SHR, RHR and CON rats. The amplitudes of these circadian fluctuations were greater in the SHR and RHR than in the CON rats. The mRNA levels of the RAS components were increased in the SHR and RHR compared with the CON rats at many time points. CONCLUSION: The data indicate that overexpression and enhanced amplitudes of circadian fluctuations of RAS components in SHR and RHR may play a role in the development of left ventricular hypertrophy.
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AIM: To establish a PCR method for investigating the expression of clock genes in cultured rattus cardiac myocytes. METHODS: PCR was carried out using 3 primer pairs based on the published sequences of dbp, bmal1 and per2 genes of rattus. The conditions of PCR were optimized and the specificity of amplication was tested. RESULTS: In a volume of 20 ?l, the optimal PCR mixture of bmal1 gene contains 0.5 U Taq polymerase, 0.006 ?mol dNTP and 0.035 ?mol Mg 2+; the annealing temperature being 57 ℃; and circle times being 30. In a same volume, the optimal PCR mixture of dbp gene contains 0.5 U Taq polymerase, 0.006 ?mol dNTP and 0.03 ?mol Mg 2+; the annealing temperature being 58 ℃; and circle times being 32. The optimal PCR mixture of per2 gene contains 0.5 U Taq polymerase, 0.006 ?mol dNTP and 0.05 ?mol Mg 2+; the annealing temperature being 57 ℃; circle times being 30. The specificity of amplication was very high. CONCLUSION: The PCR method can successfully detect mRNA expression of clock genes in cultured rattus cardiac myocytes.
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To study the effects of tetrandrine (Tet) on hypertrophied myocardial hydroxyproline content and myosin ATPase activity, left ventricular hypertrophy(LVH) was induced by renovascular hypertension (two-kidney, one-clip) in rats. Eight weeks after operation Tet 50 mg*kg-1*d-1 and enalapril(Ena) 6 mg*kg-1*d-1 were given by gavage for 8 weeks. The results showed that hydroxyproline content in LVH group was much higher than that of sham-operated one 〔(5.9±0.3) vs (3.6±0.4) mg*g-1 dry weight〕, and was decreased by 28.2% and 39.0% in Tet and Ena groups, respectively. Myosin ATPase activity in LVH group was much lower than that of sham-operated group 〔(0.43±0.09) vs (0.97±0.06) mmol Pi*min-1*g-1 protein, P<0.01〕. In Tet and Ena groups they were 60.5% and 118.6% higher than that of LVH group, respectively. The results suggest that Tet or Ena partially reduce the hydroxyproline content and elevate myosin ATPase activity of hypertrophied myocardium in renovascular hypertensive rats.
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To analyse the effect of tetrandrine(Tet) on proliferation of aortic vascular smooth muscle cells ( AVSMC), AVSMC were isolated and cultured from sham-operated rats(Sham), renovascular hypertensive rats〔RHR, 18 weeks after two kidney one clip(2K1C) operation〕, and Tet (50 mg*kg-1*d-1 po for 9 weeks from week 9 after 2K1C operation)treated RHR. The proliferation of AVSMC was detected by MTT method, and the DNA synthesis was evaluated by ［3H］-thymidine incorporation. The results showed that ①The ultrastructure of aorta suggested that AVSMC in RHR had transferred from contractile phenotype to synthetic phenotype; ②Compared to Sham, AVSMC from RHR showed a higher proliferative property with a higher cell number and an increased growth rate stimulated by norepinephrine(NE) or angiotensinⅡ(AngⅡ); ③Compared to untreated RHR, AVSMC from Tet treated RHR showed a reduced reactivity to NE- or AngⅡ-stimulated proliferation and growth rate; ④Tet(0.1－10 μmol*L-1) treated in vitro induced a concentration-dependent depression in ［3H］ thymidine-incorporation stimulated by NE or AngⅡ in AVSMC from either RHR or Sham. This study provides an evidence of increased reactivity to NE or AngⅡ in AVSMC of RHR. Tet inhibits the proliferation and DNA synthesis in AVSMC, depresses the susceptibility of AVSMC to AngⅡ and NE, both contribute to the regression effect on hypertensive vascular remodeling.
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AIM: To study the effect of curcumin on the extracellular matrix of aorta in cardiac overloaded rats. METHODS: Cardiac overloaded model was made by partial click of the abdominal aorta in Sprague Dawley rats. Curcmin, 100 mg?kg -1 ?d -1 for 3 weeks, was given by po 1 week after the click operation. The ratio of aorta wet weight to body weight was calculated; the collagen content was measured with Woessner's method and the activity of matrix metallproteinase 2 was analyzed with zymography. RESULTS: In cardiac overloaded rats, the wet weight and collagen content of aorta was increased, and the activity of matrix metallproteinse 2 of aorta was decreased. Compared with the cardiac overloaded rats without any drugs, the increased weight and collagen content of aorta was reversed, but the activity of matrix metallproteinse 2 of aorta was seldom changed in curcumin treated rats. CONCLUSION: Curcumin can reverse the hypertrophy of aorta of cardiac overloaded rats mainly by means of inhibiting the synthesis of collagen.
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AIM:To investigate the expression of estrogen receptors in myocardium of ovariectomized female rats.METHODS:One week after bilateral ovariectomy,the female SD rats were divided into 3 groups randomly:OVX +estrogen(0.15 mg/kg,s.c.),OVX + normal sodium and control.After 4 weeks of treatment,the expression of estrogen receptors in the myocardium were evaluated by Western blotting.RESULTS:After ovariectomy,serum estrogen decreased significantly,compared with control[(88?22 vs 403?59)pmol/L,P