Background and aims: Cholesterol crystals have been shown to cause inflammation. As a response to cholesterol crystal accumulation, the NLRP3 inflammasome is activated to produce IL-1β which eventually leads to atherosclerotic lesions. As a part of innate immunity, CARD8 is involved in the modulation of above mentioned inflammatory activities. The primary objective of this study was to investigate the association between polymorphism of CARD8 rs2043211 and susceptibility to arteriosclerosis obliterans (ASO) in Chinese Han male population. Methods: 758 male arteriosclerosis obliterans patients and 793 male controls were genotyped for rs2043211 with the TaqMan allele assays. Fasting blood-glucose (FBG), total cholesterol (TC), triglycerides (TG), urea nitrogen, creatinine, Serum uric acid, high density lipoprotein, low density lipoprotein, ALT, AST, and IL-1β in the blood were detected for all subjects. Clinical data were recorded to analyze the genotype-phenotype. Independent samples t-test was used to perform the comparisons between two groups. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to measure the strength of relationship in the genotype distribution and allele frequencies between patients and controls. The analysis of variance was used for a genotype-phenotype analysis of the ASO patients. Results: The genotypic and allelic frequencies in the ASO group were significantly different from that in the control group (P = 0.014 by genotype, P = 0.003 by allele). Those carrying the genotype TT had a higher risk for ASO than those carrying the genotype AA (OR = 1.494, 95%CI1.131-1.974, P = 0.005).The difference was also significant after the adjustment for the history of smoking, TC, LDL, fasting blood glucose, systolic blood pressure and BMI(OR = 1.525, 95%CI1.158-2.009, P = 0.003). Conclusion: Our finding suggests that the polymorphism of CARD8 rs2043211 is probably associated with the development of ASO in Chinese Han male population.

Epigallocatechin-3-gallate (EGCG) is a kind of polyphenol compound, called catechin, and is extracted from green tea. EGCG has a wide range of biological activities. The present study aimed to evaluate the effect of EGCG on neointimal hyperplasia in a rat model of carotid artery balloon injury and to explore the molecular mechanisms involved. Various experiments were performed to assess the effects of EGCG on thickening of neointima, expression levels of high mobility group box 1 protein (HMGB1) and receptor of advanced glycation end products (RAGE), the inflammatory response, oxidative stress and activation of nuclear factor (NF)-κB. Results demonstrated that EGCG decreased the intimal area and the ratio of intimal area/medial area compared with the balloon injury group. The expression levels of HMGB1 and RAGE induced by balloon injury were markedly inhibited by EGCG treatment. Furthermore, the inflammatory response and oxidative stress damage, which have close correlations with HMGB1, were restrained by EGCG. Finally, EGCG treatment markedly inhibited NF-κB activation. The present data provided evidence that EGCG attenuates neointimal hyperplasia in a model of carotid artery balloon injury, which indicated that EGCG may serve as a potential drug for restenosis in clinics.

No abstract

Postoperative fractionated radiotherapy after an ePTFE graft replacement of the abdominal aorta did not affect the healing of the anastomotic stoma. However, it suppressed the development of hyperplasia in the anastomotic stoma neointima and graft neointima formation in the short term.

No abstract