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1.
Chinese Medical Journal ; (24): 347-356, 2017.
Article in English | WPRIM | ID: wpr-303149

ABSTRACT

<p><b>BACKGROUND</b>15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), one of the major metabolites from prostaglandin D2 in arachidonic acid metabolic pathway, has potential anti-inflammatory properties. The objective of this study was to explore the effects of 15d-PGJ2-loaded poly(D,L-lactide-co-glycolide) nanocapsules (15d-PGJ2-NC) on inflammatory responses and bone regeneration in local bone defect.</p><p><b>METHODS</b>The study was conducted on 96 Wistar rats from June 2014 to March 2016. Saline, unloaded nanoparticles, free 15d-PGJ2or 15d-PGJ2-NC, were delivered through a collagen vehicle inside surgically created transcortical defects in rat femurs. Interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) levels in the surrounding soft tissue were analyzed by Western blot and in the defect by quantitative real-time polymerase chain reaction over 14 days. Simultaneously, bone morphogenetic protein-6 (BMP-6) and platelet-derived growth factor-B (PDGF-B) messenger RNA (mRNA) in the defect were examined. New bone formation and EphrinB2 and osteoprotegerin (OPG) protein expression in the cortical defect were observed by Masson's Trichrome staining and immunohistochemistry over 28 days. Data were analyzed by one-way analysis of variance. Least-significant difference and Dunnett's T3 methods were used with a bilateral P< 0.05.</p><p><b>RESULTS</b>Application of l5d-PGJ2-NC (100 μg/ml) in the local bone defect significantly decreased IL-6, IL-1β, and TNF-α mRNA and protein, compared with saline-treated controls (P < 0.05). l5d-PGJ2-NC upregulated BMP-6 and PDGF-B mRNA (P < 0.05). New bone formation was observed in the cortical defect in l5d-PGJ2-NC-treated animals from 7th day onward (P < 0.001). Expression of EphrinB2 and OPG presented early on day 3 and persisted through day 28 in 15d-PGJ2-NC group (P < 0.05).</p><p><b>CONCLUSION</b>Stable l5d-PGJ2-NC complexes were prepared that could attenuate IL-6, IL-1β, and TNF-α expression, while increasing new bone formation and growth factors related to bone regeneration.</p>


Subject(s)
Animals , Male , Rats , Bone Morphogenetic Protein 6 , Metabolism , Bone Regeneration , Inflammation , Drug Therapy , Interleukin-1beta , Metabolism , Interleukin-6 , Metabolism , Platelet-Derived Growth Factor , Metabolism , Prostaglandin D2 , Therapeutic Uses , Rats, Wistar , Tumor Necrosis Factor-alpha , Metabolism
2.
Chinese Journal of Medical Genetics ; (6): 86-88, 2006.
Article in Chinese | WPRIM | ID: wpr-263844

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the correlation between polymorphism at position -511C/T in the promoter region of interleukin 1B (IL1B) and the severity of coronary heart disease (CHD).</p><p><b>METHODS</b>The polymerase chain reaction-restriction fragment length polymorphism technique was applied to analyze the polymorphisms of IL1B -511C/T in 127 patients with CHD and 152 controls. And the serum level of lipoproteins was detected by enzymology method.</p><p><b>RESULTS</b>The distribution of IL1B -511C/T polymorphism between acute coronary syndrome (ACS) patients and controls was significantly different (chi-square test=5.72, P<0.01). CT and TT genotype carriers were in increased risk of ACS with more double ratio to CC genotype (OR=2.56, 95%CI=1.17-5.59). In CHD group, total cholesterol and low density lipoprotein-cholesterol levels of patients with CT and TT genotypes (6.09+/-0.97 mmol/L and 3.97+/-0.92 mmol/L) were significantly higher than those of patients with CC genotype (5.12+/-0.56 mmol/L and 2.87+/-0.71 mmol/L, P<0.05).</p><p><b>CONCLUSION</b>The polymorphism at position -511C/T in IL1B is associated with the severity of CHD, and the DNA variation at this position may affect the secretion of IL1B, and aggravate the reaction of inflammation and dyslipoidemia.</p>


Subject(s)
Female , Humans , Male , Middle Aged , Coronary Disease , Genetics , Interleukin-1 , Genetics , Interleukin-1beta , Polymorphism, Genetic , Polymorphism, Single Nucleotide , Promoter Regions, Genetic , Genetics , Severity of Illness Index
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