Serum galectin-3 concentrations in patients with ankylosing spondylitis.

OBJECTIVE: The aim of our study was to assess potential correlations between serum galectin-3 concentrations and Ankylosing Spondylitis Disease Activity (ASDAS) index in patients with ankylosing spondylitis (AS). METHODS: A total of 112 patients with AS were included, and 130 healthy subjects were considered as controls. We collected the detailed medical history, and ASDAS index was used to assess the disease severity in patients with AS. RESULTS: The serum galectin concentrations were higher in AS patients compared to the health groups (14.1 ± 9.6 vs 9.2 ± 3.7, P < 0.001). The correlation analysis showed that serum galectin concentrations were significantly positively correlated with C-reactive protein and erythrocyte sedimentation rate (r = 0.369, P < 0.001; r = 0.240, P = 0.011). In addition, the positively correlation of serum galectin-3 with global pain index (r = 0.238, P = 0.011) was observed in AS patients. A significant positively correlation between serum galectin and ASDAS index in AS patients was found (r = 0.367; P < 0.001). In multiple linear regression analysis, the results indicated that increased serum galectin still was correlated with ASDAS index (r = 0.322, P < 0.001) in patients with AS. CONCLUSIONS: Serum galectin concentrations were found to be correlated with ASDAS index in patients with AS.

[Effects of transforming growth factor beta 3 on the histopathology and expression of collagen I in experimental hepatic fibrotic rats].

OBJECTIVE: To investgate the effects of TGFbeta3 on rat hepatic fibrosis. METHODS: The TGFbeta3 cDNA was cloned into rAAV2 vector. Rats were randomly divided into four groups: normal control group, model group, negative control group and TGFbeta3 group. Hepatic fibrosis was induced by hypodermic injection of 40% CCl(4). Recombinant AAV2-TGFbeta3 viral particles were injected via the vena caudalis one week before CCl(4) treatment. Rats were executed 8 weeks after CCl(4) treatment, global histological change was observed after HE staining, the distribution of the collagen fibers was observed after masson staining, histochemistry was done to observe the expression of collagen I; The positive area rate of the collagen fibers and the average optical rate of collagen I were quantified. RESULTS: HE staining indicated that collagen fibers were reduced in the TGFbeta3 group. Masson staining shown that the collagen fibers were distributed around the blood vessel, in the portal area and disse space. Compared to the model group (13.2%+/-2.2%) and negative control group (12.3%+/-1.5%), the collagen fibers in liver tissues of TGFbeta3 group (7.7%+/-1.5%) were significantly decreased (q = 9.456, P < 0.01; q = 8.217, P < 0.01). Histochemistry indicated that the collagen fibers of liver tissues of TGFbeta3 group (0.185+/-0.033) were significantly higher than those in the model group (0.252+/-0.042) and the negative control group (0.230+/-0.029), (q = 6.228, P < 0.01; q = 4.346, P < 0.01). CONCLUSION: TGFbeta3 alleviates the damage to hepatic cell and the level of fibrosis in CCl(4) treated rats and inhibits the expression of collagen I.