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Objective To investigate the effects of high-fat diet on the formation of colorectal adenomas in rats.Methods Twenty Wistar rats were evenly divided into two groups,one group were fed with common food and the other group were fed with high fat-diet.The rats of two groups were intraperitoneally injected with 1,2-dimethyl-hydrazine (DMH) (40 mg/kg) once a week for 10 consecutive weeks.Rats with common diet and DMH were assigned to SDT group,and those with high-fat diet and DMH were assigned to HFDT group.The expression of Ki-67 was detected by immunohistochemistry and the expression of proliferating cell nuclear antigen (PCNA) and cyclooxy-genase 2 (COX2) was detected by immunofluorescence.The levels of serum triglyceride,cholesterol,insulin like growth factor-1 (IGF-1),insulin,leptin and tumor necrosis factor-α were determined by enzyme linked immunosorbent assay.Student's t test and Mann-Whitney test were performed for statistical analysis.Results At the 18th week,the numbers of Ki-67 positive cells of SDT group and HFDT group were 24.00± 1.84 and 75.17 ± 3.17,respectively,and the difference was statistically significant (t=13.960,P＜0.01).The fluorescence intensity of PCNA of SDT group and HFDT group was 213.70±21.61 and 333.30±30.44,respectively,and the difference was statistically significant (t =4.987,P＜0.01).The levels of serum triglyceride of SDT group and HFDT group were (0.43 ± 0.05) mmol/L and (1.14±0.07) mmol/L,respectively,and the difference was statistically significant (t=8.366,P＜0.01).The levels of cholesterol were (3.75±0.'26) pmol/L and (7.77±0.79) pmol/L,respectively,and the difference was statistically significant (t=4.851,P＜0.01).Conclusion High-fat diet can promote the genesis and development of adnomas through influencing the body's endocrine metabolism,increasing cell proliferation cycle and regulating inflammatory reaction.
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Objective To explore the effect of fat on 1,2-dimethylhydrazine (DMH)-induced colon tumors.Methods A total of 50 7-week-old male Wistar rats were further divided into four groups:standard diet feed control group (n =10),standard diet feed plus DMH-induced tumor group (SDT,n =15),high-fat diet feed control group (n =10) and high-fat diet feed plus DMH-induced tumor group (HFDT,n =15).Rats were killed 18 weeks later,and enzyme-linked immunosorbent assay was used to detect serum triglyeeride,tumor necrosis factor (TNF-α),and colonic TNF-α,interleukin-6.After the intestinal tracts were removed,the location,amount,and size of the tumors were observed.The pathological changes of the tissue sections were observed,and the distributions of TNF-α and Ki-67 in the normal tissues and tumors were detected by immunohistochemistry.Results Upon the completion of the study,the mortality rate of rats was 20.00％ in the SDT group and 26.67％ in the HFDT group,the tumor formation rate was 75.00％ in the SDT group and 81.82％ in the HFDT group,and the tumor-bearing rate was 117％ in the SDT group and 191％ in the HFDT group.No statistical significance difference between the two groups in mortality rate,tumor formation rate (P =0.545) and tumor bearing rate (x2 =1.343,P =0.247).The average tumor volume was significantly different between the standard diet feed control group and high-fat diet feed control group (28.57％ vs 66.67％,P =0.030).Also,the serum triglyceride and TNF-α levels significantly differed between the SDT group and HFDT group [TG (1.39 ± 0.31) mmol/L and TNF-α (124.80 ± 21.69) ng/L in the HFDT group and TG (0.46 ±0.20) mmol/L and TNF-α (85.83 ± 17.45) ng/L in the SDT group] (P =0.000).The expressions of TNF-α,IL-6,and Ki-67 in colonic mucosa were significantly higher in the high-fat diet feed control group than in the standard diet feed control group [TNF-α:(6.22 ± 0.63) ng/g vs (2.33 ± 0.44) ng/g,P=0.020; IL-6:(13.50±0.67) ng/gvs (7.31 ±0.41) ng/g,P=0.000; and Ki-67:40％ vs 10％,P =0.028].The Ki-67 expression rate was 90.48％ in the HFDT group,compared to 50％ in the SDT group (P =0.015).Conclusions High-fat diet can increase the serum triglyceride and TNF-α levels in rats,upregulate the expressions of TNF-α,IL-6 and Ki-67,and thus promote inflammation and cell proliferation,and ultimately affect the tumor formation and development.However,the effect of fat on DMH-induced colon tumors warrants further studies.
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Objective To clarify the anatomical and pathlogical implications of Denonvilliers' fascia.Method In this study,thirty pelvic specimens (17 males and 13 females) were incised through the median sagittal plane and carried for regional anatomy study; Denonvilliers' fascia was identified by immunohistochemistry.Results Denonvilliers' fascia could be found in all male specimens:it had an anterior leaf and a posterior leaf,with the anterior one attaching to seminal vesicle,seminiferous duct,prostate and the bottom of bladder firmly.The fascia originated at the fold of the peritoneum and ended at the perineum fascia,fusing into the pelvic parietal fascia laterally.It was not obvious in females,only to find a thin and transparent membrane between vagina and rectum.The maximum height of Denonvilliers' fascia in left pelvis was (3.2 ± 0.3) cm,compared with (3.3 ± 0.3) cm in the right pelvis (t =0.965,P ＞ 0.05).Immunohistochemistry study revealed that there was no lymph node in the fascia and its lateral parts were enriched of nerve fibers,which were few in its middle part.Conclusions The unique anatomical and pathlogical characteristics of Denonvilliers' fascia are of vital importance to the avoidance of nerve injury during rectal surgery.
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In the process of epithelial-mesenchymal transition (EMT),cell-cell adherence is disrupted,apico-basal polarity is lost,the ability of anti-apoptosis,migration and invasion is acquired.Y-box-binding protein 1 (YB-1) is a member of the cold-shock protein superfamily,containing a structurally and functionally conserved cold shock domain.Studies indicate that YB-1 can promote the occurrence and development of tumors by regulating EMT.In the process of EMT mediated by YB-1,various transcription factors and signal pathways play important roles.
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Chemokines are a class of functional chemotactic peptide. CXC chemokine class is a large family of chemokines in a sub- tribe. In the occurrence and development of tumor cells, there often accompanied by a series of molecular and biology change. CXC chemokine subfamily is closely related to the body' s immune response to tumor and biological behaviors of tumor. In this paper, CXC chemokine sub-Several members of the tribe and their receptor and tumor biological relationship are reviewed.