Objective To understand the clinical significance and diagnosis value of serum interleukin-6(IL-6) levels in the patients with respiratory infection and non-small cell lung cancer(NSCLC).Methods The serum levels of IL-6 in 61 patients with NSCLC,and 36 patients with respiratory infection and 30 of the healthy was measured by enzyme-linked immunosorbent assay(ELISA).Results The data showed that mean serum IL-6 levels in patients with NSCLC was higher than in the healthy( P 0 05).Conclusion We consider that increased IL-6 level could be used as one of differential diagnostic marker of NSCLC;Serum IL-6 levels may be a reference of judging each stage of NSCLC and predicting prognosis.

Objective To investigate the effects and mechanisms of prostaglandin E2 receptor subtype 3 (EP3) on transforming growth factor β1 (TGF-β1)-induced mouse mesangial cells damage. Methods Primary mouse mesangial cells were separated and cultured. Three siRNAs were synthesized and transfected into mesangial cells for silencing EP3 by LipofectamineTM 2000 and the best one was chosen. MCs were grouped into: (1)control group; (2)TGF-β1 (10 μg/L) group; (3)NC-siRNA plus TGF-β1 (10 μg/L) group; (4) EP3-siRNA group; (5)EP3-siRNA plus TGF-β1 (10 μg/L). Then the proliferation of MCs was evaluated by CCK-8 assay. The expression of PGE2 and cAMP in cell supernatant were detected by ELISA. The mRNA and protein expression of fibronectin (FN), connective tissue growth factor (CTGF), cyclooxygenase-2 (COX2), membrane-bound prostaglandin E2 synthase 1 (mPGES1) were detected by real - time quantitative PCR and Western blotting. The phosphorylation of p38 MAPK and ERK1/2 was decected by Western blotting. Results Compared with control group, the cell proliferation induced by TGF-β1 was increased (P<0.05), the expression of PGE2 and cAMP were improved, mRNA and protein expression of FN, CTGF, COX2 and mPGES1 were up-regulated (all P<0.05). Compared with TGF-β1 group, the cell proliferation in EP3-siRNA plus TGF-β1 group was reduced, the expression of FN, CTGF, COX2 and mPGES1 mRNA and protein were downregulated (all P<0.05), the phosphorylation of ERK1/2, p38 MAPK were also declined (P<0.05). Conclusion EP3-siRNA may reduce TGF-β1-induced cell damage through upregulating the expression of cAMP, repressing the activity of ERK1/2 and p38 MAPK, inhibiting the expression of COX2 mPGES1 and PGE2 by feedback, then decreased the expression of FN and CTGF.

OBJECTIVE: To observe the effects of Pollen Typhae total flavone (PTF) on glucose and lipid metabolism in 3T3-L1 adipocytes. METHODS: The content of glucose which disappeared from the culture medium after incubation with drugs for 24 hours was determined as glucose consumption of the cells. The activity of cells was detected by XTT method. The transport of glucose was observed by (3)H-glucose uptake method. The efflux of free fatty acid (FFA) from adipocytes was observed by the concentration of FFA in the culture medium. RESULTS: The glucose concentration in culture medium was significantly decreased with a concentration-dependent effect, when PTF concentrations were from 0.025 g/L to 0.4 g/L. The toxic effect on cells appeared while PTF concentration was 0.4 g/L, and the MTT value decreased. PTF also significantly increased glucose transportation in the 3T3-L1 adipocytes as rosiglitazone (ROS) did. At the same time, FFA concentration in culture medium was significantly decreased as compared to the normal control group, while ROS-treated group did not show any difference. CONCLUSION: PTF can increase insulin sensitivity by increasing glucose transportation and consumption in the 3T3-L1 adipocytes as well as decreasing the FFA efflux from the cells.

Objective To explore the effects and mechanisms of prostaglandin E2 (PGE2) receptor 1 antagonist (SC-19220) on proliferation,prostaglandin synthase and extracellular regulated protein kinases (ERK) signal pathway induced by transforming growth factor β1(TGF-β1) in glomerular mesangial cells.Methods Mouse glomerular mesangial cells (GMCs) were divided into 5 groups:control group,TGF-β1 (10 μg/L) group,TGF-β1 (10 μg/L) plus SC-19220 group (0.1,0.5,1.0 μmol/L).The proliferation of GMCs was measured by CCK-8.The PGE2 in supernatant was measured by ELISA.The expression of connective tissue growth factor (CTGF),laminin (LN),cyclooxygenase 2(COX2),membrane-bound prostaglandin E2 synthase 1 (mPGES1) protein and mRNA was examined by Westem blotting and real-time quantitative PCR,ERK1/2 or phospho-ERK1/2 was measured by Western blotting as well.Results TGF-β1 induced the proliferation of GMCs and increased the secretion of PGE2.Besides,TGF-β1 significantly up-regulated the expression of CTGF,LN,COX2 and mPGES1 mRNA and protein (P ＜ 0.05),and increased the expression of phospho-ERK1/2 protein (P ＜ 0.05).However,SC-19220 significantly attenuated the changes of above-mentioned parameters and their activities (P ＜ 0.05).All the effects of SC-19220 were in dose-dependent manner.Conclusions SC19220 may reduce TGF-β1-induced cell damage by suppressing the activity of ERK1/2,and feedback inhibition of COX2,mPGES1 and PGE2,thus decreases the expression of LN and CTGF.

SARS-CoV-2 main protease (M^pro) is one of the most extensively exploited drug targets for COVID-19. Structurally disparate compounds have been reported as M^pro inhibitors, raising the question of their target specificity. To elucidate the target specificity and the cellular target engagement of the claimed M^pro inhibitors, we systematically characterize their mechanism of action using the cell-free FRET assay, the thermal shift-binding assay, the cell lysate Protease-Glo luciferase assay, and the cell-based FlipGFP assay. Collectively, our results have shown that majority of the M^pro inhibitors identified from drug repurposing including ebselen, carmofur, disulfiram, and shikonin are promiscuous cysteine inhibitors that are not specific to M^pro, while chloroquine, oxytetracycline, montelukast, candesartan, and dipyridamole do not inhibit M^pro in any of the assays tested. Overall, our study highlights the need of stringent hit validation at the early stage of drug discovery.