ABSTRACT
Objective@#To investigate the effects of curcumin on pneumococcal pneumonia-induced pneumonia, apoptosis and p38 MAPK expression in infant mice.@*Methods@#A total of 60 male infant C57BL/6 mice at three weeks of age were randomly divided into 6 groups: control group, model group, high-dose curcumin treatment group, middle-dose curcumin treatment group, low-dose curcumin treatment group and SB203580 treatment group. The Curcumin and SB203580 were intraperitoneally applied at doses of 200, 60, and 20 mg/kg (for curcumin) and 100 mg/kg (for SB203580) from two days before bacterial infection to three days post-infection. The control group and model group were intraperitoneally injected with an equal volume of saline. The model group, curcumin treatment groups and SB203580 treatment group were transnasally inoculated with approximately 106 CFU/ml of pneumococcal pneumonia in 50 μl of PBS applied to the tip of the nose to establish the experimental pneumococcal pneumonia. Subsequently, all the mice were killed and lung tissues were harvested for hematoxylin-eosin staining, calculation of lung score indexes, measurement of IL-1β and TNF-α contents by ELISA, and measurement of Bax, Bcl-2and p38 MAPK expression by Western blot.@*Results@#Compared to the model group, the edema score (0.50 ± 0.10, 1.51 ± 0.16, 1.38±0.11, vs. 2.50 ± 0.20), hemorrhage score (0.32 ± 0.09, 1.01 ± 0.11, 0.85±0.09 vs. 1.80 ± 0.20), inflammatory cell infiltrate score (0.35 ± 0.09, 1.61 ± 0.16, 1.52±0.10 vs. 3.21 ± 0.22), small airway damage score (0.12 ± 0.03, 0.53 ± 0.14, 0.50±0.04 vs. 1.12 ± 0.19) in the medium-, high-dose group and SB203580 treatment group significantly decreased (P<0.01). Compared to the model group, the contents of IL-1β (20.38 ± 1.69 pg/ml, 25.73 ± 2.08 pg/ml vs. 40.22 ± 5.70 pg/ml) and TNF-α (160.39 ± 15.81 pg/ml, 198.67 ± 18.97 pg/ml vs. 282.22 ± 25.30 pg/ml), Bax/Bcl-2 (0.31 ± 0.05, 0.53 ± 0.06 vs. 1.79 ± 0.17) and expression of phosphorylated p38 MAPK (0.69 ± 0.05, 0.81 ± 0.07 vs. 1.71 ± 0.14) in the high-dose group and SB203580 treeatment group significantly decreased (P<0.01).@*Conclusions@#Curcumin can inhibit the inflammatory response and cellular apoptosis in the lungs of mice with pneumococcal pneumonia, and the mechanisms maybe related to its inhibition of p38 MAPK expression.
ABSTRACT
Objective To investigate the effects of curcumin on pneumococcal pneumonia-induced pneumonia, apoptosis and p38 MAPK expression in infant mice. Methods A total of 60 male infant C57BL/6 mice at three weeks of age were randomly divided into 6 groups: control group, model group, high-dose curcumin treatment group, middle-dose curcumin treatment group, low-dose curcumin treatment group and SB203580 treatment group. The Curcumin and SB203580 were intraperitoneally applied at doses of 200, 60, and 20 mg/kg (for curcumin) and 100 mg/kg (for SB203580) from two days before bacterial infection to three days post-infection. The control group and model group were intraperitoneally injected with an equal volume of saline. The model group, curcumin treatment groups and SB203580 treatment group were transnasally inoculated with approximately 106 CFU/ml of pneumococcal pneumonia in 50 μl of PBS applied to the tip of the nose to establish the experimental pneumococcal pneumonia. Subsequently, all the mice were killed and lung tissues were harvested for hematoxylin-eosin staining, calculation of lung score indexes, measurement of IL-1β and TNF-α contents by ELISA, and measurement of Bax, Bcl-2and p38 MAPK expression by Western blot. Results Compared to the model group, the edema score (0.50 ± 0.10, 1.51 ± 0.16, 1.38±0.11, vs. 2.50 ± 0.20), hemorrhage score (0.32 ± 0.09, 1.01 ± 0.11, 0.85±0.09 vs. 1.80 ± 0.20), inflammatory cell infiltrate score (0.35 ± 0.09, 1.61 ± 0.16, 1.52±0.10 vs. 3.21 ± 0.22), small airway damage score (0.12 ± 0.03, 0.53 ± 0.14, 0.50±0.04 vs. 1.12 ± 0.19) in the medium-, high-dose group and SB203580 treatment group significantly decreased (P<0.01). Compared to the model group, the contents of IL-1β (20.38 ± 1.69 pg/ml, 25.73 ± 2.08 pg/ml vs. 40.22 ± 5.70 pg/ml) and TNF-α (160.39 ± 15.81 pg/ml, 198.67 ± 18.97 pg/ml vs. 282.22 ± 25.30 pg/ml), Bax/Bcl-2 (0.31 ± 0.05, 0.53 ± 0.06 vs. 1.79 ± 0.17) and expression of phosphorylated p38 MAPK (0.69 ± 0.05, 0.81 ± 0.07 vs. 1.71 ± 0.14) in the high-dose group and SB203580 treeatment group significantly decreased (P<0.01). Conclusions Curcumin can inhibit the inflammatory response and cellular apoptosis in the lungs of mice with pneumococcal pneumonia, and the mechanisms maybe related to its inhibition of p38 MAPK expression.
ABSTRACT
Objective To evaluate the clinical improvements after autologous bone marrow mononuclear cells (BMMNCs) percutaneously injected into coronary artery in patients with heart failure due to non-ischemic cardiomyopathy using PET myocardial peffusion/metabolic imaging.Methods From February 2011 to October 2012,40 patients with heart failure due to non-ischemic cardiomyopathy were selected.The test group including 15 patients (13 males,2 females,average age (57.5±14.5) years) received the autologous BMMNCs intracoronary injection on the basis of drug treatment.The other 25 cases (21 males,4 females,average age (58.0±12.0) years) were taken as the control group and only received the drug treatment.All patients were followed up for 24 months,and the myocardial perfusion/metabolism imaging,echocardiography,brain natriuretic peptide (BNP) test,6-minute walking experiment were performed.The data were analyzed by two-sample t test.Results During the follow-up period,the test group had no ventricular arrhythmia and other serious complications,and the patients' symptoms had been improved.There was no change in myocardial perfusion after treatment of autologous BMMNCs,but the myocardial metabolic defect by volume reduced from (43.79± 17.99) cm3 to (28.19±9.27) cm3 (t =3.33,P＜0.01) 24 months after the treatment.The myocardial metabolic defect by volume at the baseline and after 24 months in the control group was (43.30±15.70) cm3,(48.51±15.77) cm3 respectively (t=1.01,P＞0.05).In the test group,the left ventricular end-diastolic diameter decreased from (64.0±8.0) mm to (59.0±7.0) mm 24 months after the treatment (t=2.04,P＜0.05),and the left ventricular ejection fraction was significantly higher than that before treatment:(45.0±4.0) ％ vs (27.0±6.0) ％ (t =10.81,P＜0.01).Conclusion PET myocardial perfusion/metabolic imaging can be used as tools in evaluating the therapeutic effect of autologous BMMNCs in patients with heart failure due to non-ischemic cardiomyopathy.
ABSTRACT
Objective To describe and analyze the distribution of medical expenditure of Liaoning province in 2014 in terms of population beneficiary based on the System of Health Accounts 2011(SHA 2011).Methods By means of multistage and stratified sampling, a total of 252 medical institutions were selected from four cities in Liaoning province according to their economic status and geographical distribution.Macro data including the outpatient income and hospitalization income were taken into account, to calculate the beneficiary population of the province in 2014 according to SHA2011.Results GBD classification found that the highest medical expenditure category was non-communicable diseases, accounting for 63.02% in total medical expenditure.ICD classification found that respiratory disease as consuming the highest medical expenses (43.76%).The average medical expenditure of the elderly population was the highest per person, up to 3 041.70 yuan per person.Conclusions Medical expenses of non-communicable diseases, respiratory disease and elderly population were still high.Thus we need to emphasize disease prevention, and take efficient measures against such key diseases to curb the medical expenses.The elderly population calls for specific and effective measures to reduce their medical expenses.
ABSTRACT
High‐speed economic development and progress of medical technologies in China have significantly benefitted people′s health conditions.Significantly higher life expectancy in average ,as a result ,also contributed to population aging process.How to deal with the contradictions between population aging and rapid growth of medical costs is challenging the healthcare sector of the country.Analysis of medical costs at three tertiary hospitals in Liaoning Province discovered problems in out‐of‐pocket medical expenses of elderlies ,and proposed on measures to effectively ease their burden in medical expenditure .
ABSTRACT
The activation and deactivation of Ca(2+)- and calmodulindependent neuronal nitric oxide synthase (nNOS) in the central nervous system must be tightly controlled to prevent excessive nitric oxide (NO) generation. Considering plasma membrane calcium ATPase (PMCA) is a key deactivator of nNOS, the present investigation aims to determine the key events involved in nNOS deactivation of by PMCA in living cells to maintain its cellular context. Using time-resolved Förster resonance energy transfer (FRET), we determined the occurrence of Ca(2+)-induced protein-protein interactions between plasma membrane calcium ATPase 4b (PMCA4b) and nNOS in living cells. PMCA activation significantly decreased the intracellular Ca(2+) concentrations ([Ca(2+)]i), which deactivates nNOS and slowdowns NO synthesis. Under the basal [Ca(2+)]i caused by PMCA activation, no protein-protein interactions were observed between PMCA4b and nNOS. Furthermore, both the PDZ domain of nNOS and the PDZ-binding motif of PMCA4b were essential for the protein-protein interaction. The involvement of lipid raft microdomains on the activity of PMCA4b and nNOS was also investigated. Unlike other PMCA isoforms, PMCA4 was relatively more concentrated in the raft fractions. Disruption of lipid rafts altered the intracellular localization of PMCA4b and affected the interaction between PMCA4b and nNOS, which suggest that the unique lipid raft distribution of PMCA4 may be responsible for its regulation of nNOS activity. In summary, lipid rafts may act as platforms for the PMCA4b regulation of nNOS activity and the transient tethering of nNOS to PMCA4b is responsible for rapid nNOS deactivation.
Subject(s)
Animals , Humans , Rats , Brain , Metabolism , Calcium , Metabolism , Cells, Cultured , Cerebellum , Cell Biology , Fluorescence Resonance Energy Transfer , HEK293 Cells , Nitric Oxide , Metabolism , Nitric Oxide Synthase Type I , Metabolism , PDZ Domains , Plasma Membrane Calcium-Transporting ATPases , Metabolism , Protein Interaction Maps , Protein Isoforms , Metabolism , Rats, Sprague-DawleyABSTRACT
AIM: To investigate the role of Smad7 in the Smad2 expression induced by transforming growth factor-?_1(TGF-?_1) in rat peritoneal mesothelial cells(PMCs).METHODS: Rat PMCs were cultured at different doses of TGF-?_1 (0,1.25,2.5,10 ?g/L) for different time(0,5,15,30,60,120 min).PCDNA3-Smad7 was then transfected into cultured rat PMCs by lipofectamine,and the cells were stimulated like the above.Endogenous Smad2 and Smad7 expression was evaluated by RT-PCR and Western blotting.RESULTS: TGF-?_1 induced increase in Smad2 mRNA and protein expression at 5 min,peaked at 30 min,and declined to baseline levels at 120 min, which was in a time-dependent manner.TGF-?_1 also induced Smad7 mRNA expression at 5 min,and then declined,down to the lowest at 30 min,but at 60 min it increased again.Smad2,Smad7 mRNA and protein expression induced by TGF-?_1 were also dose-dependent.After transfection,overexpressions of Smad7 mRNA and protein in rat PMCs were observed,which did not decline with time.The expression of Smad2 mRNA significantly decreased by 33%,56%,67%,71%,63% and 57%(P
ABSTRACT
AIM: To investigate the expression of Smad2 signal protein in peritoneal mesothelial cells and how transforming growth factor ?1 (TGF-?1) affects its expression. METHODS: Rat peritoneal mesothelial cells were cultured in different levels of TGF-?1 (0,1.25,2.5,10 ?g/L) for different time (0,5,15,30,60,120 min). Endogenous Smad2 expression was evaluated by RT-PCR and immunohistochemical assay. The alteration of subcellular location of Smad2 was determined by immunohistochemical assay. RESULTS: TGF-?1 induced Smad2 mRNA expression, which increased at 5 min, peaked at 30 min, and declined to baseline levels by 120 min, in a time-dependent manner. Smad2 mRNA expression induced by TGF-?1 was also in a dose -dependent manner. TGF-?1 induced Smad2 phosphorlylation and nuclear localization in both time-dependent and dose-dependent manner, which was concordant with mRNA expression. Smad2 translocated from cytoplasm to nuclear accumulation in response to TGF-?1, and peaked at 30 min. CONCLUSIONS: Smad2 is present in peritoneal mesothelial cells. TGF-?1 may activate Smad2 expression and translocation to nuclear in a time-dependent and dose-dependent manner. [