Objective To explore the clinical value of expression levels of serum COX-2 in patients with advanced NSCLC before and after EGFR-TKI treatment. Methods The serum was collected from 58 cases. Before and after targeted therapy , the serum COX-2 level was examined by ELISA. Meanwhile , CT scan was exercised to evaluate the treatment. Follow-up interview was done. The relationship among the change in expression level of serum COX-2 , efficacy and PFS was analyzed. Results The serum COX-2 level significantly decreased in the response group (t = 11.258, P = 0.000) and increased in the PD group (t = -7.759, P =0.000) after EGFR-TKI treatment, and not significantly changed in the SD group (t = 1.424, P = 0.170). Before treatment, the baseline serum COX-2 level in the response group was significantly higher than that in the SD group and the PD group (F = 20.852, P = 0.000 ). Before the targeted therapy, the higher the level of serum COX-2 was, the longer PFS patients would enjoy. Conclusion Detection of the serum COX-2 contributes to the judgment of therapeutic effect of EGFR-TKI and can be used as a prediction of EGFR-TKI drugs outcomes for patients with advanced NSCLC.

Objective:To study the effects of modified citrus pectin (MCP) on the viability and gene expressions of synovial fibroblasts (SF) as well as SF treated by galectin-3 (Gal-3).Methods:Rabbit SF was isolated and cultured in vitro. Then SF was treated with different concentrations of MCP (0, 250, 500, and 750 mg/L). In addition, SF was further treated with the same different concentrations of MCP after treatment with 10 μg/ml Gal-3 for 24 h. The viability of SF was detected by CCK-8 on the first, third, and fifth day after treatment. The mRNA expression of transforming growth factor-β1 (TGF-β1), type I collagen (COL1A2), and Gal-3 in SF was detected by real-time quantitative PCR. The synthesis of type I collagen in SF was investigated by immunofluorescence staining. Results:MCP, especially at a concentration of 500 mg/L can inhibit the proliferation of SF significantly (all P < 0.05) on the first, third, and fifth day after treatment. Compared with the control group, MCP at different concentrations induced different gene expression profiles. In particular, MCP at high concentrations can upregulate the expression of TGF-β1, COL1A2 and Gal-3 in SF. However, MCP shows no significant effect on the synthesis of type I collagen in SF. MCP can down-regulate the expression of TGF-β1, COL1A2, and significantly reduce the synthesis of type I collagen in SF after Gal-3 treatment. Particularly, the effect of MCP at a concentration of 500 mg/L on inhibiting the expression of TGF-β1, COL1A2, and Gal-3 in SF is significant. Conclusions:MCP can inhibit the excessive proliferation of SF and regulate gene expression in SF.