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Esophageal cancer is a type of upper gastrointestinal malignant tumor with a high degree of malignancy， strong invasion ability， and poor prognosis， which belongs to the category of "dysphagia" in traditional Chinese medicine （TCM）. In addition to tumor resistance， Chinese herbal prescription plays a role in sensitization. In light of information in literature， the syndrome elements of esophageal cancer include Qi stagnation， phlegm， Qi deficiency， blood stasis， and Yin deficiency. After clinical differentiation， the syndromes of esophageal cancer are divided into phlegm and Qi obstruction， Qi and Yin deficiency， fluid deficiency and heat accumulation， Qi deficiency and phlegm dampness， combined phlegm and heat， combined phlegm and stasis， combined heat toxin and stasis， healthy Qi deficiency and toxin accumulation， et al. Dabanxiatang， Qigesan， Xuanfu Daizhetang， Liujunzitang， Shashen Maidongtang， and Tongyoutang are the common clinical prescriptions， where Qigesan， Liu Junzitang， and Tongyoutang have been proved by in vitro and in vivo experiments to exert anti-esophageal cancer effect by directly inhibiting tumor cell proliferation， promoting apoptosis， affecting tumor microenvironment， regulating cell energy metabolism， and inhibiting angiogenesis. In addition， an increasing number of studies have been conducted on anti-esophageal cancer effect of Chinese herbal prescription by targeting non-coding single-stranded microRNA. The specific mechanisms of Da Banxiatang， Shenzhe Peiqitang， Xiao Xianxiongtang， Renshen Banxiatang， and Liushenwan have been scarcely reported despite good clinical efficacy. Wuzhuyu Tang and Tongguansan recorded in ancient books have been rarely applied in modern times. Therefore， the present study reviewed the special drugs and prescriptions mentioned in ancient TCM classics， the commonly used Chinese herbal prescriptions in modern clinical practice， and experimental research progress， to promote treatment methods of Chinese herbal prescriptions against esophageal cancer.
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Objective::To study the forming process of the gynandrium-like in Amomum villosum. Method::The flowerets were divided into 8 growth periods from 0.5 cm in length to the day after flowering. Fresh sample were anatomized, and paraffin sectioning was performed on the flowerets. The height of anther chamber, the pollen sac angles, the width of anther gap, the diameter of style, the filament-labellum angle (α), and the filament-anther angle (β) were determined. Result::The angle of the pollen sac had no obvious change before flowering, but decreased from 32° to 17° after flowering. The width of anther gap increased to 0.29 mm in the 5th growth period, while the diameter of style was 0.32 mm in the same period, the ratio of them was 92%. Compared with the day before flowering, the angle α decreased from 83° to 42° during flowering, and the angle β decreased from 186° to 147°. In the filament, the abaxial side had 1 to 5 layers of cells more than the adaxial side. In the style, it was found that the adaxial side had 1 to 6 layers of cells more than the abaxial side. Conclusion::The asymmetry of the cell structure at abaxial and adaxial sides of the filament and style is the basis of the movement. In the 5th growth period, the width of anther gap increased almost to the size of style, so the style was able to slide in. When blossoming, the pollen sacs quickly squeezed to the gap in middle, and the entrance for style to access was blocked. Therefore, the style had to remain in the gap of the pollen sacs. Meanwhile, angles α and β drastically decreased, resulting in the stamen sandwiched the pistil and bending together toward the labellum. The gynandrium-like structure was formed.
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Objective: To set up a callus induction system for Amomum villosum by tissue culture. Method: The rhizome buds of A. villosum and stem segments,root tip segments of sterile A. villosum plantles were used as explants and cultured in MS media with different concentrations of 6-BA,NAA and 2,4-D (the pH of each medi is about 5.8). A callus induction system was established to explore the effect of different explants and different medium on callus induction for A. villosum. Result:The findings showed that the rhizome buds and sterile plantlet stems and root tip segments of three different explants can be successfully induced into calli. The most suitable medium for callus induction from rhizome buds and sterile plantlet stems was MS with 6-BA (1.5 mg·L-1),2,4-D (1.0 mg·L-1) and NAA (0.5 mg·L-1) with the highest induction rates of 15% and 60% respectively. MS medium combined with 6-BA (2.0 mg·L-1),2,4-D (1.0 mg·L-1) and NAA (1.0 mg·L-1) was the most suitable proposal for inducing the callus from sterile root tip segments with the highest induction rate of 76%. Conclusion:Under certain culture conditions,rhizome buds,stem or root tip segments of sterile plantlet can be effectively induced into callus. The callus induction system of A. villosum is preliminarily established, and root tip segments of sterile plantlet are the optimal explant.
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Objective@#To evaluate the diagnostic efficiency and accuracy of endoscopic ultrasonography (EUS) on vascular involvement of pancreatic cancer.@*Methods@#Patients, suspected pancreatic cancer with vascular involvement by CT scan in Huashan Hospital, Fudan University from January 2014 to March 2019, were enrolled prospectively in the study. EUS was performed to evaluate the vascular involvement compared with surgical pathological results.@*Results@#A total of 132 patients with pancreatic cancer were enrolled in the study, and they all underwent EUS observation and radical resection with vessels resection. There were 103 cases of cancer in pancreatic head, 19 cancers in pancreatic neck and 10 cancers in distal pancreas. The diagnostic sensitivity, specificity and accuracy of EUS was 97.4% (113/116), 81.2% (13/16), and 95.5% (126/132), respectively for pancreatic cancers with vein involvement; while was 33.3% (2/6), 90.0% (81/90), and 86.5% (83/96), respectively, for pancreatic cancers with superior mesentery artery involvement.@*Conclusion@#EUS may play a key role in diagnosis of vascular involvement of pancreatic cancer, and be helpful for the surgical decision marking.
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Objective To evaluate the diagnostic efficiency and accuracy of endoscopic ultrasonography ( EUS ) on vascular involvement of pancreatic cancer. Methods Patients, suspected pancreatic cancer with vascular involvement by CT scan in Huashan Hospital, Fudan University from January 2014 to March 2019, were enrolled prospectively in the study. EUS was performed to evaluate the vascular involvement compared with surgical pathological results. Results A total of 132 patients with pancreatic cancer were enrolled in the study, and they all underwent EUS observation and radical resection with vessels resection. There were 103 cases of cancer in pancreatic head, 19 cancers in pancreatic neck and 10 cancers in distal pancreas. The diagnostic sensitivity, specificity and accuracy of EUS was 97. 4％ ( 113/116 ) , 81. 2％ (13/16), and 95.5％ (126/132), respectively for pancreatic cancers with vein involvement;while was 33.3％ ( 2/6 ) , 90. 0％ ( 81/90 ) , and 86. 5％ ( 83/96 ) , respectively, for pancreatic cancers with superior mesentery artery involvement. Conclusion EUS may play a key role in diagnosis of vascular involvement of pancreatic cancer, and be helpful for the surgical decision marking.
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Objective: Through analyzing the development practice and restricting factors of social capital running medical institutes in ethnic minority areas, it explored the regulation path for social capital running medical institutes in ethnic minority areas. Methods: Through researching the policy practice, hold practice and operation practice, it selected 8 ethnical provinces as research areas and summarized the development practice of social capital running medical institutes in ethnic minority areas. Results: The current constraints of social capital running medical institutes in China’s ethnic areas mainly reflected in the constraints of the economic depth of poverty to restrict the medical treatment of the patients in the society, the lack of policy guarantee restricted the competitiveness of the social medical market and the agglomeration of social medical personnel. Conclusion: Social capital running medical institutes in ethnical areas should regulate the path of institutional construction, the regulatory path of the industry and the regulatory path of PPP (Public Private Partnership) path.
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Great changes in drug metabolizing enzyme (DME) expression occur in the fetus and child during development. Individual hepatic DME ontogeny can be categorized into one of three groups based on developmental trajectories.Some enzymes such as CYP3A7,are expressed at highest level in the fetus dur-ing the first trimester and either remain elevated or slightly de-crease during gestation,but are silenced or reduced to relatively low levels within one to two years after birth.SULT1 A1 is an ex-ample of the second group of DME.These enzymes are ex-pressed at relatively constant levels throughout gestation and into adulthood.CYP3A4 belongs to the third DME group .These en-zymes are expressed at negligible or low levels in the fetus.Sig-nificant increases in enzyme levels are exhibited within the first one to two years after birth.The epigenetic regulation refers to genomic modifications that do not involve changes in DNA se-quence and include DNA methylation,histone modifications, and non-coding RNAs.The epigenetic regulation mechanisms are responsible for the developmental expression of DME genes dur-ing liver maturation.This review will provide a summary of DME developmental expression profiles and reveal epigenetic mecha-nisms underlying variable drug metabolism and drug response. Thus,knowledge regarding DME ontogeny has permitted im-proved capability to predict drug disposition in pediatric pa-tients,which is crucial for improving drug dosing leading to opti-mal safety and efficacy in children.
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This study was designed to investigate effects of pargyline on histone methylation in the promoter and enhancer regions and transcription of cytochrome P450 3A4/3A7 (CYP3A4/3A7) gene. Human primary fetal liver cells were isolated, cultured and randomly divided into several groups including control, solvent, pargyline low, middle, high dose (treated with 0.6, 1.2, 2.4 mmol·L-1). HepG2 cells were cultured and treated with 0.03, 0.3, 3 mmol·L-1 pargyline. After 48 hours, total RNAs were prepared from the cells to determine the expression of CYP3A mRNA in primary fetal cells and HepG2 cells with real-time quantative PCR (qPCR). HepG2 cells were cultured and then treated with 3 mmol·L-1 pargyline for 48 hours. The chromatin immunoprecipitation (ChIP) assay was performed with dimethylation of histone H3 at lysine 4 (H3K4me2), and IgG antibodies respectively. The precipitated DNA was resuspended and used for qPCR. Primers were used to detect different regions of CYP3A4/3A7 promoter and enhancer. Occupancy of H3K4me2 was shown as percent of input DNA relative to control cells. The results suggested that pargyline has an effect on primary fetal liver cells and HepG2 cells proliferation. The level of CYP3A7 was markedly enhanced in human primary fetal liver cells by treatment with 1.2, 2.4 mmol·L-1 of pargyline (P-1 of pargyline in HepG2 cells (P<0.001) compared with solvent control. Occupancy of H3K4me2 on human CYP3A4 promoter (-362 to +53) and enhancer segment (-7 836 to -6 093) harbored the overlapping hepatocyte nuclear factors 4A (HNF4A) binding site compared with a negative control. Occupancy of H3K4me2 on human CYP3A7 promoter (-163 to +103) and enhancer segment (-4 054 to -3 421, -6 265 to -6 247) overlapped with glucocorticoid receptor (GR) binding site. In conclusion, the enriched H3K4me2 in the promoter and enhancer regions was induced by pargyline with HNF4A or GR binding site in CYP3A4/3A7 gene to activate the corresponding genes.
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Objective α?Asarone has the effect of relieving cough and asthma as well as sedative, hypnotic and anticonvul?sive function. Our study was designed to explore the effects of apoptosis induced by α? Asarone on human esophageal carcinoma Eca?109 cell line as well as the expression levels of GADD153 and Smac mRNA. Methods Human esophageal carcinoma Eca?109 cells were cultured in vitro, which were divided into blank control group, 5?FU group( 500μg/mL) andα?Asarone group of different dosages ( 25,50,100μg/mL) . After cultivation, MTT method and Annexin V?PI were used to measure cell proliferation rate and apoptosis rate. Expression levels of GADD153 and Smac protein and mRNA were detected by western blotting and real? time quantitative PCR. Results Compared with blank control group, the cell proliferation rates in other groups decreased significantly (P<0.01), and cell apoptosis rate increased significantly ( P<0.01) . Compared with blank control group, the expression levels of GADD153 and Smac pro?tein and mRNA in other groups increased significantly( P<0.05) . Conclusion α? Asarone can inhibit cell proliferation and induce the apoptosis of human esophageal carcinoma Eca?109 by regulating the expression levels of GADD153 and Smac gene.
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Objective To confirm the main pathway of chemokine-chemokine receptor which mediates the accumulation of regulatory T cell ( Treg) in pancreatic cancer .Methods The concentrations of protein of FOXP3 and chemokines of CCL2, CCL3, CCL5, CCL17, CXCL8 in human and mouse pancreatic cancer and adjacent normal pancreatic tissue were measured by the method of enzyme-linked immunosorbent assay (ELISA).The receptor of chemokine CCL5 (CCR5) in human and mouse pancreatic cancer were determined by the immunofluorescent stain .Results The concentration of FOXP 3 protein in human pancreatic cancer and adjacent normal pancreatic tissue as (487.5 ±534.1) and (162.6 ±42.0) pg/mg, respectively, while they were (84.6 ±54.1) and (14.4 ±7.6) pg/mg, respectively in mouse.The concentration of FOXP3 protein were significantly higher in pancreatic cancer than those in adjacent normal pancreatic tissue .The concentration of CCL2 in human pancreatic cancer and adjacent normal pancreatic tissue as (76.9 ±37.5), (40.8 ±25.5) pg/mg, and the concentration of CCL3 as (38.0 ±22.6), (21.3 ±16.5) pg/mg, and the concentration of CCL5 were (390.2 ±158.5), (59.1 ±22.8) pg/mg, and the concentration of CCL17 as (7.2 ±2.0), (4.1 ±2.4)pg/mg, and the concentration of CXCL8 as (9.3 ±5.5), (6.3 ±5.2)pg/mg.The concentration of CCL2, CCL5, CCL17 in pancreatic cancer was significantly higher than those in adjacent normal pancreatic tissue (P<0.05).The concentration of CCL2 in mouse pancreatic cancer and adjacent normal pancreatic tissue as (77.9 ±30.5), (43.6 ±16.6) pg/mg, and the concentration of CCL3 was (27.4 ±18.2), (14.0 ±4.5)pg/mg, and the concentration of CCL5 was (302.2 ±55.8), (64.5 ±30.3) pg/mg; and the concentration of CCL17 was (4.4 ±1.4), (2.2 ±1.0)pg/mg;and the concentration of CXCL8 was (55.1 ± 55.1), ( 93.4 ±7.3 ) pg/mg.The concentration of CCL2, CCL5, CCL17 in pancreatic cancer were significantly higher than those in adjacent normal pancreatic tissue , and the difference between the two groups was statistically significant (P<0.05).The level of FOXP3 in pancreatic cancer was positively correlated with the concentration of chemokine CCL 5 both in human and mouse pancreatic cancer .Immunofluorescent staining indicated that the FOXP3 +cells also expressed CCR5.Conclusions The CCL5-CCR5 is the main chemokine-chemokine receptor pathway mediating the accumulation of Treg cells in pancreatic cancer .
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Pancreatic adenocarcinoma is a severe-invasive, early-metastasis and malignant neoplasm with latent pathogenesis, while its biological behaviors are the highlight of current tumor study.In present study,through reviewing the studies related to expression profile of pancreatic cancer up to now.This artical summarized the achievement, challenge and trend of development of expression profile in pancreatic cancer.In conclusion, exploring the mechanism of carcinogenesis and development of pancreatic cancer based on the breakthrough of expression-profiling studies and establishing ideal models of pancreatic cancer, will promote systemic diagnosis and treatments of pancreatic cancer and do favor to the prognosis of the patients.
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<p><b>OBJECTIVE</b>To investigate the effects of icariin on the GRP78 mRNA expression of vascular smooth muscle cell in vitro and to elucidate the anti-atherosclerosis mechanism of icariin.</p><p><b>METHOD</b>The model was established by using half cystine in vitro. The vascular smooth muscle cell had been incubated with various concentrations of icariin for 48 hours. The apoptosis rate was detected by flow cytometry using Annexin/PI-staining and GRP78 mRNA expression was tested by RT- PCR. These differentially expressed fragments were cloned, identified and sequenced.</p><p><b>RESULT</b>Icariin at concentrations of 0.2 and 0.4 mg x L(-1) obviously promoted the apoptosis of vascular smooth muscle cell. The early apoptosis rate was raised magnificently in a dose dependent manner compared with that of the half cystine group (P < 0.01). Furthermore, the fragment, 648 bp, was similar to the gene of glucose regulated protein GRP78 from VSMC. Icariin could magnificently increase the GRP78 mRNA expression compared with that of the halfcystine group (P < 0.05).</p><p><b>CONCLUSION</b>The anti-atherosclerosis mechanism of icariin might be partly due to the promotion of apoptosis and the promotion of the GRP78 mRNA expression of vascular smooth muscle cell.</p>
Subject(s)
Animals , Rabbits , Apoptosis , Cell Proliferation , Cells, Cultured , Flavonoids , Pharmacology , Gene Expression , Heat-Shock Proteins , Genetics , Metabolism , Homocysteine , Pharmacology , Myocytes, Smooth Muscle , Cell Biology , MetabolismABSTRACT
Objective:To select the differentially expressed vascular smooth muscle cell(VSMC) apoptosis gene induced by icariin,glucose regulated protein 78(GRP78),to observe the expression of GRP78 in atherosclerosis tissue and to the elucidate the mechanism of anti-atherosclerosis of icariin.Methods:The model was established by using halfcystine in viro.The vascular smooth muscle cell was incubated with various concentrations of icariin for 48 hours.The apoptosis was detected by TUNEL assay.GRP78 gene was amplificated by PCR,recombinant plasmid were constructed,transfected into E.coli,positive clonings were selected and conf irmed by restriction endonucleas analysis,and sequence-ed.Tissue situ hybridization was used to observe the GRP78 expression in atherosclerosis tissue.Results:Icariin promoted obviously vascular smooth muscle cell apoptosis.Furthermore,the fragment,648bp,was similar to the gene of GRP78 from VSMC,and the expression level was signif icantly higher in high cholesterol group than in control nroup.Conclusions:The GRP78 plays a key role in inducing atherosclerotic lesions.The mechanism of anti-atherosclerosis of icariin might be partly due to promoting apoptosis of vascular smooth muscle cell.
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AIM: To select differentially the expressed gene,glucose regulated protein 78(GRP78),to observe the expression of GRP78 in atherosclerosis tissue and to elucidate the mechanism for anti-atherosclerosis of puerarin.METHODS: The model was established by using homocysteinemia in vitro.The vascular endothelial cells were incubated with various concentrations of puerarin(10 -7 mol/L,10 -6 mol/L,10 -5 mol/L) for 48 h.The apoptosis rate was detected by flow cytometry using Annexin/PI-staining.GRP78 gene was amplificated by PCR.These differentially expressed fragments were cloned,selected,confirmed,and sequenced.Digoxigenin-labeled DNA Probe and cholesterol-rich rabit model were prepared,GRP78 mRNA was determined by in situ hybridization in atherosclerotic lesions and normal tissue.RESULTS: Three concentrtions of puerarin significantly inhibited the apoptosis of endothelial cells.The early apoptosis rate was decreased magnificently in a dose dependent manner compared with that of HCY group (P
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AIM: To investigate the effect of curcumin on the binding activity of hepatic nuclear factor-kappa B(NF-?B) and the expression of peroxisome proliferator-activated receptor-?(PPAR-?) in rats with liver fibrosis induced by carbon tetrachoride. METHODS: A total of 60 clean male rats were randomly and averagely divided into group A,B,C,D,E and F.The rats in group A served as normal controls,while those in other five groups were injected subcutaneously 40% CCI_4 for seven weeks to induce the model of liver fibrosis.After seven weeks,the rats in group C,D,E,F were intragastrically administered with 50 mg/kg silibinin,100 mg/kg cur,200 mg/kg cur,400 mg/kg cur once per day for six weeks,respectively.HE staining was used to observe the pathological changes of liver tissues under light microscope,and immunohistochemistry and reverse transcriptase polymerase chain reaction(RT-PCR) were performed to detect the activity of NF-?B,PPAR-? and mRNA expression of PPAR-?.RESULTS: The inflammatory and fibrotic degrees were obviously alleviated in group C,D,and E compared with group B.The expression of NF-?B p65 was significantly decreased in liver tissue in group C,D and E,compared with model control group B(P