Association of tumor necrosis factor-α gene polymorphism with osteoarticular tuberculosis prognosis in a Hebei population.

This study investigated the association of tumor necrosis factor-α (TNF-α)-308, -238, and -863 polymorphisms with osteoarticular tuberculosis (OA-TB) prognosis in a Hebei population. Genomic DNA was extracted from venous blood samples of 120 OA-TB patients and 100 healthy volunteers. TNF-α-308, -238, and -863 were analyzed by PCR-restriction fragment length polymorphism; genotype and allele frequencies were calculated. Serum TNF-α level was significantly higher in OA-TB patients (283.16 ± 51.68 ng/L) than in control (122.54 ± 54.65 ng/L; P < 0.05). Higher frequency of TNF-α-308 GG genotype in healthy volunteers (91.0%) than in OA-TB patients (79.2%) indicated that it was a protective factor against OA-TB (OR = 0.405, 95%CI = 0.147-0.657, P = 0.007). Higher frequencies of TNF-α-308 GA genotype and TNF-α-308 allele (A) in OA-TB patients (20.8 and 10.4%, respectively) than in healthy volunteers (8.0 and 5.0%, respectively) indicated an association with increased risk of OA-TB (OR = 3.112, 95%CI = 1.520-6.343, P = 0.003; OR = 3.109, 95%CI = 1.676-6.538, P = 0.006; respectively). Haplotype association analysis of TNF-α polymorphisms (-308/-238/-863) showed a higher frequency of TNF-α AGA in OA-TB patients (12.1%) than in healthy volunteers (3.5%), indicating that it was a risk factor for OA-TB (OR = 4.201, 95%CI = 1.80-9.91, P = 0.010). TNF-α-308 G/A and TNF-α AGA (-308/-238/-863) were associated with a predisposition to OA-TB, which could aid clinical detection, prevention, and prognosis of OA-TB.

Epigallocatechin-3-gallate protects retinal vascular endothelial cells from high glucose stress in vitro via the MAPK/ERK-VEGF pathway.

Diabetic retinopathy (DR) is a frequent microvascular complication of diabetes, and one of the most common causes of legal blindness in the world. Epigallocatechin-3-gallate (EGCG) produces an anti-oxidative and anti-inflammatory effect against various human diseases. In this study, we determined the effect of EGCG on a human retinal endothelial cell (HREC) line. The cell viability was determined by a standard MTT assay, while the cell cycle and apoptosis rate were analyzed by flow cytometry. Inflammatory marker expression was detected by enzyme-linked immunosorbent assay. Treatment of HRECs with EGCG (20 and 40 mM) led to a significant decrease in the apoptosis rate (2.35 ± 0.56 and 1.24 ± 0.32%). The culture supernatant of cells treated with high glucose concentrations showed significantly higher levels of TNF-α (598.7 ± 89.7 vs 193.2 ± 38.5 pg/mL; P < 0.001), IL-6 (6.16 ± 0.51 vs 1.61 ± 0.21 ng/mL; P < 0.001), and ICAM-1 (31.6 ± 4.4 vs 14.8 ± 2.9 ng/mL; P < 0.001) compared to the cells in the control group. EGCG decreased the expression level of phosphorylated p38-mitogen activated protein kinase (MAPK) and extracellular regulated kinase (ERK)1/2. Moreover, EGCG was shown to significantly inhibit the expression of vascular endothelial growth factor (VEGF). Therefore, EGCG treatment ameliorated the negative effect of high glucose concentrations on the cell viability and apoptotic rate. The protective effects of EGCG under high glucose conditions may be attributed to the regulation of inflammatory cytokines and inhibition of the MAPK/ERK-VEGF pathway.