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1.
Journal of Peking University(Health Sciences) ; (6): 239-244, 2019.
Article in Chinese | WPRIM | ID: wpr-941798

ABSTRACT

OBJECTIVE@#To investigate the effect of sulfur dioxide (SO2) on the apoptosis of alveolar macrophage (AM) in lung protection of limb ischemia/reperfusion (I/R) induced acute lung injury (ALI), and to find a new target for the control of inflammatory response.@*METHODS@#Twenty pathogen-free, adult male Sprague-Dawley (SD) rats (180-230 g) were used in this study. Five rats were to be used for limb ischemia/reperfusion, then plasma was extracted as ischemia/reperfusion serum stimulation. Fifteen rats were to be used for extracting AM by bronchoalveolar lavage. The AM was isolated and cultured, then the cell count was adjusted to 1×106/mL, and randomly divided into the following 4 groups (n=6): control group, I/R group, SO2 group, and I/R+SO2 group. The I/R group was given ischemia/reperfusion serum (500 μg/L) to stimulate 6 h; the SO2 group was given an SO2 donor, Na2SO3/NaHSO3 [(0.54 mmol/kg) / (0.18 mmol/kg)]; and the I/R+SO2 group was given the same ischemia/reperfusion serum and Na2SO3/NaHSO3 at the same time. The level of mitochondrial membrane potential, the state of mitochondrial permeability transition pore (mPTP), the rate of AM apoptosis, the expression of Bcl-2 and Caspase-3 proteins were detected by flow cytometry, microplate reader and Western blotting.@*RESULTS@#Compared with the control group, in the I/R group, the ratio of red to green fluorescence and the absorbance decreased significantly, the percentage of apoptotic cells increased obviously, the apoptotic rate was 43.81%±2.40%, Caspase-3 protein expression increased, Bcl-2 protein expression decreased. While compared with the I/R group, in the I/R+SO2 group, the ratio of red to green fluorescence and the absorbance increased significantly; the apoptotic rate decreased to 37.01%±1.93%, Caspase-3 protein expression decreased, Bcl-2 protein expression increased.@*CONCLUSION@#Exogenous SO2 has the effect of accelerating AM apoptosis by stimulating mPTP to open and mitochondrial membrane potential to decrease; besides, exogenous SO2 could stimulate AM to secrete more anti-inflammatory cytokines and less inflammatory cytokines. In conclusion, exogenous SO2 can reduce macrophage apoptosis by inhibiting mitochondrial pathways.


Subject(s)
Animals , Male , Rats , Acute Lung Injury , Apoptosis , Ischemia , Macrophages, Alveolar , Rats, Sprague-Dawley , Reperfusion Injury , Sulfur Dioxide
2.
Chinese Journal of Traumatology ; (6): 193-198, 2016.
Article in English | WPRIM | ID: wpr-235749

ABSTRACT

<p><b>PURPOSE</b>To assess the effects of lipopolysaccharide (LPS) pretreatment on wound infection mouse model and evaluate the biological safety of the optimal pretreatment dose in vivo.</p><p><b>METHODS</b>Mice were pretreated with LPS of different doses at 48 and 24 h before femoral medial lon- gitudinal incision was made and infected with different bacteria.</p><p><b>RESULTS</b>It is showed that 0.5 mg/kg/time of LPS pretreatment can significantly alleviate the inflammation in mouse model infected with methicillin-resistances Staphylococcus aureus, methicillin-sensitive S. aureus, Pseudomonas aeruginosa,or Escherichia coli compared with doses of 0.25 mg/kg/time, 1 mg/ kg/time, and 1.5 mg/kg/time.</p><p><b>CONCLUSIONS</b>LPS pretreatment can alleviate the inflammation in mouse model and the optimal dose is 0.5 mg/kg/time, and meanwhile it does not damage organs' function.</p>


Subject(s)
Animals , Female , Mice , Disease Models, Animal , Inflammation , Lipopolysaccharides , Therapeutic Uses , Mice, Inbred BALB C , Surgical Wound Infection , Drug Therapy , Toll-Like Receptor 4 , Physiology
3.
Chinese Journal of Oncology ; (12): 835-837, 2012.
Article in Chinese | WPRIM | ID: wpr-307283

ABSTRACT

<p><b>OBJECTIVE</b>We have identified a SNP within the seed-binding region for miR-502 in the 3'-UTR of the SET8 gene that codes for a methyltransferase for histone H4. SET8 methylates TP53 and thus regulates cell proliferation and genome stability. This study is to investigate the role for this SNP and its interaction with the TP53 codon 72 SNP in the age of onset of breast cancer.</p><p><b>METHODS</b>We conducted a case-only study of 1, 110 breast cancer cases. PCR-RFLP was used for SNP genotyping. Ages of onset of breast cancer among different genotypes were analyzed using SAS software.</p><p><b>RESULTS</b>Our analysis revealed that the SET8 CC and TP53 GG genotypes were independently associated with earlier age of onset of breast cancer in an allele-dose dependent manner. Moreover, individuals with both SET8 CC and p53 GG genotypes developed cancer at age of 47.74 years, compared with 54.55 years for individuals with both SET8 TT and TP53 CC genotypes.</p><p><b>CONCLUSIONS</b>miR-502-binding SNP in SET8 may modulate SET8 expression and contribute to early development of breast cancer either independently or together with the TP53 codon 72 SNP.</p>


Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Middle Aged , Young Adult , 3' Untranslated Regions , Genetics , Age of Onset , Binding Sites , Genetics , Breast Neoplasms , Genetics , Codon , Gene Frequency , Genetic Predisposition to Disease , Genotype , Histone-Lysine N-Methyltransferase , Genetics , MicroRNAs , Genetics , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , Polymorphism, Single Nucleotide , Tumor Suppressor Protein p53 , Genetics
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