Serious Selenium Deficiency in the Serum of Patients with Kashin-Beck Disease and the Effect of Nano-Selenium on Their Chondrocytes.

To investigate selenium (Se) concentrations in serum of patients with rheumatoid arthritis (RA), osteoarthritis (OA), and Kashin-Beck disease (KBD), together with the effect of Se supplement (chondroitin sulfate [CS] nano-Se [SeCS]) on CS structure-modifying sulfotransferases in KBD chondrocyte. Fifty serum samples from each group with aged-matched (40-60 years), normal control (N), RA, OA, and KBD (25 males and females, respectively) were collected to determine Se concentrations. Furthermore, the KBD chondrocytes were divided into two groups following the intervention for 24 h: (a) non-treated KBD group and (b) SeCS-treated KBD group (100 ng/mL SeCS). The ultrastructural changes in chondrocytes were observed by transmission electron microscopy (TEM). Live/dead staining was used to observe cell viability. The expression of CS-modifying sulfotransferases including carbohydrate sulfotransferase 12, 13, and 15 (CHST-12, CHST-13, and CHST-15, respectively), and uronyl 2-O-sulfotransferase (UST) were examined by quantitative real-time polymerase chain reaction and western blotting analysis after SeCS intervention. The Se concentrations in serum of KBD, OA, and RA patients were lower than those in control. In OA, RA, and control, Se concentrations were higher in male than in female, while it is opposite in KBD. In the cell experiment, cell survival rate and mitochondrial density were increased in SeCS-treated KBD groups. Expressions of CHST-15, or CHST-12, and CHST-15 on the mRNA or protein level were significantly increased. Expression of UST slightly increased on the mRNA level, but no change was visible on the protein level. Se deficiency in serum of RA, OA, and KBD was observed. SeCS supplemented in KBD chondrocytes improved their survival rate, ameliorated their ultrastructure, and increased the expression of CS structure-modifying sulfotransferases.

The clinical implication of serum cyclophilin A in patients with chronic obstructive pulmonary disease.

Background: Cyclophilin A (CyPA) is a secreted molecule that is regulated by inflammatory stimuli. Although inflammation has an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD), little is known regarding the relationship between serum CyPA and COPD. Methods: Ninety-three COPD patients with acute exacerbation were enrolled in the study and were reassessed during the convalescence phase. Eighty-eight controls were matched for age, gender, body mass index, smoking index and comorbidity. The basic clinical information and pulmonary function of all participants were collected. Serum levels of CyPA and other inflammation indexes were further measured. Results: Serum CyPA was significantly increased in convalescent COPD patients compared to healthy controls, and further elevated in COPD patients with acute exacerbation. Serum CyPA positively correlated with serum interleukin-6, matrix metalloproteinase-9 and high-sensitivity C-reactive protein in both the exacerbation and convalescence phases of COPD. Furthermore, it negatively correlated with percent value of forced expiratory volume in 1 second (FEV1%) predicted and FEV1/forced vital capacity in convalescent COPD patients. Conclusion: These results suggest that serum CyPA can be used as a potential inflammatory biomarker for COPD and assessment of serum CyPA may reflect the severity of inflammation in COPD.

Curcumin ameliorates alveolar epithelial injury in a rat model of chronic obstructive pulmonary disease.

AIMS: To investigate the effects of curcumin on alveolar epithelial injury in a rat model of chronic obstructive pulmonary disease (COPD) and its potential mechanism. MAIN METHODS: The rat COPD model was established by cigarette smoke exposure combined with intratracheal administration of lipopolysaccharide. Thirty-eight male Sprague-Dawley rats were randomly divided into four groups: control, COPD model, COPD with curcumin and COPD with solvent groups. Neutrophil and macrophage infiltration in bronchoalveolar lavage fluid (BALF) was evaluated, and the levels of IL-6, IL-8 and TNF-α in BALF and serum were determined by ELISA. Histopathological examination and TUNEL staining were used to assess the alveolar epithelial injury. The protein expression of p66Shc and p-p66Shc in the lung tissues was determined by immunohistochemistry and western blot. KEY FINDINGS: Curcumin significantly decreased the numbers of total cells, neutrophils and macrophages in BALF from COPD rats. In addition, the levels of IL-6, IL-8 and TNF-α in BALF and serum of COPD rats were significantly decreased after treatment with curcumin. Moreover, curcumin ameliorated emphysema and ultrastructural damage of alveolar epithelial cells in COPD rats. The apoptosis index of alveolar epithelial cells in the COPD with curcumin group was significantly lower than that in the COPD model group. Furthermore, the protein expression of p66Shc and p-p66Shc in alveolar epithelia was significantly decreased in the COPD with curcumin group compared with COPD model group. SIGNIFICANCE: Curcumin attenuates alveolar epithelial injury in COPD rats, which may be partially due to the down-regulation of p66Shc.

D-dimer as a potential biomarker for the progression of COPD.

BACKGROUND: D-dimer is a manifestation of endogenous fibrinolytic activity and associated with inflammation process. Despite chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by a hypercoagulable state, D-dimer levels in COPD patients are still conflicting. METHODS: Forty-three participants were investigated at admission for an acute exacerbation of COPD, and reassessed when stable. Forty-three controls were matched for age, gender, body mass index, smoking index, comorbidities and medication use. Participants underwent pulmonary function and laboratory testing, including the measurements of D-dimer and high-sensitivity C-reactive protein (hsCRP). RESULTS: The median of D-dimer was 2839 µg/l (IQR: 2078-4389 µg/l) and 1799 µg/l (IQR: 1205-2196 µg/l) in exacerbated and stable COPD patients respectively. The median of D-dimer in the control subjects was 433 µg/l (IQR: 369-456 µg/l). D-dimer level was significantly increased in stable COPD patients compared with healthy controls, and further increased in those patients with an acute exacerbation (both P<0.001). D-dimer was positively correlated with the well-known inflammatory marker hsCRP both in the exacerbated and stable phases of COPD (r=0.392 P=0.009 and r=0.411 P=0.006, respectively), and negatively correlated with FEV1% predicted and FEV1/FVC in stable COPD (r=-0.409 P=0.006 and r=-0.343 P=0.024, respectively). CONCLUSIONS: D-dimer is increased in COPD patients, and could be considered as an inflammatory marker for the assessment of inflammation in the progression of COPD.