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Objective To investigate the expression of CCL2 in colorectal cancer and its carcinogenesis mechanism associated with macrophages.Methods The expression level of CCL2 mRNA in 17 cases of colorectal cancer tissues and corresponding adjacent tissues were analyzed by PCR,and the phenotypes of macrophages in tumor infiltrating lymphocytes (TIL) were analyzed by flow cytometry.Human peripheral blood mononuclear cells were isolated and induced to differentiate into macrophages.After 12 h incubation with CCL2,the phenotypic changes of macrophages were analyzed by flow cytometry.The expression level of VEGF,COX-2 and IL-6 in the supernatant were measured by ELISA assay.Results The expression level of CCL2 in colorectal cancer tissues was significantly higher than that in corresponding adjacent mucosal tissues (t =4.017,P ＜ 0.05),and the macrophages in TIL had a high proportion of CCR2 phenotype.CCL2 was shown to induce increased CCR2 expression in macrophages (t =5.070,P ＜ 0.05),and promote the secretion of the tumor growth-associated factors such as VEGF,COX-2 and IL-6 (all P ＜ 0.05).Conclusion The levels of CCL2 in colorectal cancer were up-regulated suggesting that CCL2 may play a key role in tumor promotion by recruiting macrophages and influencing their function.
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<p><b>OBJECTIVE</b>To realize the oxidative damage of kidney mitochondrial complex in obese rats induced by high-fat diet and investigate the protective effects of sulforaphane against the damage.</p><p><b>METHODS</b>Eighty-eight adult male SD rats were used, after 1 week adaptability feeding, 8 rats were selected as control group and given low-fat diet. The other 80 rats were given high-fat diet. After 2 weeks, the 32 diet-induced obesity models were choosen whose weight gain was higher than 40%. The 32 rats were randomly divided into 4 groups, i.e. high fat group, high fat+sulforaphane low dose group, high fat+sulforaphane middle dose group and high fat+sulforaphane high dose group. The rats in the sulforaphane low, middle and high dose groups were orally administered with sulforaphane 5, 10 and 20 mg/kg, all the 4 groups were kept feeding high-fat diet for 5 weeks. All rats were sacrificed and their kidneys were removed to assay the index of oxidative damages.</p><p><b>RESULTS</b>The content of ROS (0.26 ± 0.04) and MDA((0.87 ± 0.05) U/mg) in the hight-fat group were significantly higher than those in the control group((0.20 ± 0.02),(0.57 ± 0.08) U/mg)(t values were -3.02 and -4.72, P < 0.05). The activity of T-AOC((0.43 ± 0.04) U/mg) and MMP (12.09 ± 1.56) were lower than the control group ((0.48 ± 0.04 U/mg, (16.08 ± 3.12) )(t values were 2.06 and 2.28, P < 0.05). Gavage intervention with sulforaphane, the MDA amount ((0.67 ± 0.05), (0.55 ± 0.05), (0.56 ± 0.07) U/mg) in the sulforaphane low, middle and high dose groups were lower than the hight-fat group ((0.87 ± 0.05) U/mg (t values were 3.65, 5.71 and 5.60. P < 0.05). The activity of T-AOC ((0.49 ± 0.05), (0.55 ± 0.05), (0.54 ± 0.04) U/mg), T-SOD ((61.07 ± 2.79), (55.95 ± 2.39), (60.26 ± 6.02) U/mg) and the level of MMP ((17.17 ± 2.52), (18.24 ± 2.54), (18.21 ± 3.65)) were higher than in the high-fat group ((0.43 ± 0.04) U/mg,(47.22 ± 2.43) U/mg,(12.09 ± 1.56)) (tT-AOC values were -2.36, -4.83 and -4.30; tT-SOD values were -6.37, -4.71 and -5.99; tMMP values were -2.90, -3.52 and -3.50, P < 0.05). The activity of GSH-Px in the sulforaphane low and middle dose groups ((69.12 ± 8.63), (64.43 ± 6.58) U/mg) were higher than those in the high-fat group((53.03 ± 5.70) U/mg)(t values were -3.82 and -2.71, P < 0.05). But there were no significant difference between the high dose group ((60.02 ± 7.05) U/mg) and the high-fat group (t = -1.66, P > 0.05).</p><p><b>CONCLUSION</b>High-fat diet can induce the mitochondrial oxidative dysfunction in kidney, and sulforaphane shows protective effect on the kidney mitochondrial complex from oxidative damage in obese rats induced by high-fat diet.</p>
Subject(s)
Animals , Male , Rats , Diet , Diet, High-Fat , Isothiocyanates , Kidney , Mitochondria , Obesity , Oxidative Stress , Rats, Inbred StrainsABSTRACT
Objective To study the clinical effect of tamoxifen on the treatment of breast cystic hyperplasia.Methods 288 cases of breast cystic hyperplasia were entered randomly as experimental group,it was given tamoxifen 10mg～20mg Bid for 1～3 months;and control group,was given methyltestosterone l0mg Bid,the clinical effect of the two groups was compared.Results In experimental group,the cure rate was 45 5%(131/288),the obviously effective rate was 39 9%(115/288),the effective rate was 12 2%(35/288),and the inffective rate was 2 4%(7/288),the total efficiency was 97 6%(281/288),while the total efficiency in control group was 88%(132/150).There was significant difference in the two groups(P