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Objective To investigate the effect of ursolic acid (UA) on the colorectal tumor and microenvironment in mice,and to provide a theoretical basis for the clinical application of UA.Methods The models of subcutaneous transplanted tumor of mouse CT26 cells was established.The models were divided into four groups:control group,tumor bearing group,tumor beating dimethyl sulfoxide (DMSO) group and tumor beating UA group.Tbe serum levels of interleukin-6 (IL-6) were detected by enzyme linked immunosorbent assay (ELISA).The number and percentage of myeloid-derived suppressor cell (MDSC) in the spleen of mice were analyzed by flow cytometry.The mRNA levels of IL-6 and signal transducer and activator of transcription 3 (STAT3) in tumor were examined by real-time quantitative polymerase chain reaction (RT-PCR).The protein levels of STAT3 and p-STAT3 in tumor were detected by Western blotting.Results The results showed that UA could significantly decrease the number of spleen MDSC.The accounts of spleen MDSC of tumor bearing UA group (249.60 ± 17.12) was lower than that of tumor beating DMSO group (366.40 ± 34.08),and the difference was statistically significant (P =0.021).The serum level of IL-6 in tumor bearing UA group [(46.40 ± 17.05) pg/ml] was decreased than that in tumor bearing DMSO group [(94.27 ±21.51) pg/ml],and the difference was statistically significant (P =0.012).The expression levels of IL-6 and STAT3 mRNA in tumor tissues of tumor bearing UA group (0.12 ±0.01,0.21 ±0.08) were lower than those of tumor bearing DMSO group (0.69 ± 0.14,0.79 ± 0.06),and the differences were statistically significant (P =0.008;P =0.003).The protein expression levels of STAT3 and p-STAT3 in tumor tissues of tumor bearing UA group (0.81 ±0.02,0.28 ±0.04) were lower than those of tumor bearing DMS0 group (0.98 ±0.02,0.91 ±0.22),and the differences were statistically significant (P =0.027;P =0.029).Conclusion UA may inhibit the activation of STAT3 signaling pathway and the amplification of MDSC in microenvironment by reducing IL-6,thus to enhance the function of immune-killing tumor cells to regulate tumor immune microenvironment and inhibit the immune escape of mouse colorectal cancer cells.
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Objective To observe the effect of EGFR‐TKI combined with chemotherapy on the changes of serum insulin‐like growth factor1(IGF‐1)and anterior gradient‐2(AGR2)levels in the patients with advanced non‐small cell lung cancer(NSCLC) ,and to investigate whether IGF‐1 and AGR2 can serve as a potential indicator of the prognosis and efficacy of chemotherapy in NSCLC . Methods Sixty‐eight patients with advanced NSCLC were selected as the experimental group treated by EGFR‐TKI combined chemotherapy and 30 healthy people served as the healthy control group .(treatment group) .The levels of serum IGF‐1 and AGR2 before chemotherapy and at 3 weeks after chemotherapy were detected by ELISA .The influence of serum IGF‐1 and AGR2 levels on the prognosis was analyzed by using Kanplan‐Meier method .Results (1)The disease control rate(DCR)in the EGFR‐TKI com‐bined chemotherapy was 52 .9% ;(2)the level of serum IGF‐1 before treatment in the experimental group was (329 .35 ± 88 .13)μg/L ,which was significantly higher than (146 .36 ± 41 .27)μg/L in the healthy control group(P<0 .01);the level of serum AGR2 in experimental group was(16 .72 ± 6 .23)ng/mL ,which was significantly higher than (4 .38 ± 2 .17)ng/mL in the healthy control group(P<0 .01);serum levels of IGF‐1 and AGR2 after treatment were(211 .53 ± 52 .31)μg/L and (9 .72 ± 3 .56)ng/mL respec‐tively ,which were significantly lower than those before treatment (P<0 .01);serum IGF‐1 and AGR2 in NSCLC patients were pos‐itively correlated(r=0 .489 ,P<0 .01);(3)serum levels of IGF‐1 and AGR2 after chemotherapy were(128 .62 ± 48 .24)μg/L and (7 .22 ± 4 .27)ng/mL respectively ,which were obviously lower than(334 .23 ± 82 .11)μg/L and(18 .43 ± 6 .17)ng/mL before chem‐otherapy(all P<0 .01) .The Kanplan‐Meier analysis revealed that serum IGF‐1 and AGR2 levels in advanced NSCLC had an obvi‐ous influence on the prognosis .Conclusion Serum IGF‐l and AGR2 levels may have a potential clinical value to assess the therapeu‐tic efficacy of EGFR‐TKI combined chemotherapy and prognosis in advanced NSCLC .
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Objective To study the relationship between soluble CD147 (sCD147) level in peripheral blood and serum lipid level and explore the effect of sCD147 on atherosclerosis in rheumatoid arthritis (RA). Methods The level of sCD147 in 36 patients with RA,36 patients with coronary artery disease (CAHD) and 30 healthy volunteers was detected by enzyme linked immunosorbent assay (ELISA) .The disease activity score (DAS28) in RA patients was evaluated and the correlation between sCD147 level and DAS28 score was analyzed.The serum lipid level of RA patients was detected by an automatic biochemical analyzer and the cor relation between sCD147 level and serum lipid level was analyzed.Results The level of sCD147 in serum of RA patients was significantly higher than that in patients with CAHD and healthy volunteers,sCDI47 level in the RA group with high DAS28 score was significantly higher than that with low or medium DAS28 score.In RA patients,elevated total cholesterol (TC) and triglyceride (TG) level was positively correlated with serum sCDI47 level (r=0.84,P＜0.05;r=0.87,P＜0.05;while slightly elevated,normal TC and normal TG had no correlation with serum sCDI47 level (r=0.41,P=0.21;r=0.14,P=0.57;r=0.49,P=0.87).Elevated or slight ly elevated LDL-C was positively correlated with serum sCD147 level (r=0.86,P＜0.05;r=0.81,P＜0.05), while no correlation could be found in the group with normal LDL-C level (r=0.78,P=0.22).The high density lipoprotein-cholesterol (HDL-C) level decrease in RA patients had no correlation with serum sCD147 level (r--0.04,P=0.96;r=0.13,P--0.87).Conclusion sCD147 may be involved in the pathogenesis of RA and associate with disease activity.Elevated sCD147 level may be associated with abnormal serum lipid in RA.