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1.
[目的]研究促愈颗粒对乙酸烧灼型胃溃疡(GU)大鼠胃黏膜表皮生长因子(EGF)及其受体(EGFR)表达的影响。[方法]将大鼠随机分为4组:正常对照组,模型组,促愈颗粒组和雷尼替丁组。乙酸制备慢性GU大鼠模型后,于给药14 d和28 d后分2次处死大鼠,观察胃黏膜组织形态,免疫组织化学技术检测大鼠胃黏膜EGF及EGFR水平。[结果]与模型组比较,促愈颗粒组和雷尼替丁组囊状扩张腺体数量均显著减少(P<0.01,<0.05),EGF及EGFR水平均显著增高(P<0.01,<0.05),且促愈颗粒组作用均优于雷尼替丁组(均P<0.05)。[结论]促愈颗粒可能通过增加胃黏膜EGF和EGFR的水平,进而提高GU再生黏膜结构和功能成熟度,从而促进溃疡愈合,提高溃疡愈合质量,并防止溃疡复发。  相似文献   

2.
目的:本文肌注表皮生长因子EGF和(或)饲喂谷氨酰胺GLN防治大鼠乙酸性结肠炎。方法:Sprague-Dawley系大鼠体重200—220g,40只分为乙酸组、EGF组、GLN组、EGF GLN组各10只,从大体.光镜、电镜(透射、扫描)观察结肠粘膜的损伤情况。结果:上述4组结肠粘膜损害的指数分别为3.11±0.93,1.78±0.97,1.30±0.48及1.10±0.32(P<0.01)。镜下观察也有明显疗效,以EGF GLN组为最佳。结论:EGF及GLN对结肠粘膜细胞形态结构具有保护作用,且优于两者单独作用,这为表皮生长因子、谷氨酰胺用于防治人类溃疡性结肠炎提供了理论依据。  相似文献   

3.
Abstract Factors operative in oesophageal mucosal growth are poorly characterized. Epidermal growth factor (EGF) has been shown to stimulate mucosal growth throughout the gastrointestinal tract. The present study was performed to test the hypothesis that polyamine biosynthesis is required for stimulation of epithelial growth by EGF in oesophageal mucosa. Using an in vitro explant model, oesophageal mucosal growth was quantified in the presence or absence of EGF and α-difluoromethylornithine (DFMO), a specific inhibitor of polyamine synthesis. Administration of 50 nmol/L EGF significantly increased the rate of epithelial growth in oesophageal explants. Treatment with DFMO for 3 and 7 days not only depleted the tissue polyamines putrescine, spermidine and spermine, but also significantly impaired mucosal growth. The inhibitory effect of DFMO on mucosal growth was partially but significantly prevented when exogenous putrescine was given. Additionally, stimulation of epithelial growth by EGF was also blocked by depletion of cellular polyamines in DFMO-treated oesophageal explants. These results indicate that EGF stimulates epithelial growth of oesophageal mucosa at least partly through a process involving polyamine biosynthesis.  相似文献   

4.
Summary Renal enlargement is a characteristic feature of human and experimental diabetes mellitus that may be predictive of subsequent nephropathy. In the streptozotocin diabetic rat kidney growth rapidly follows the induction of experimental diabetes but the mechanisms responsible for this growth are poorly understood. Epidermal growth factor (EGF) is a potent mitogen for renal tubular cells. Thirty one male Sprague-Dawley rats aged 13 weeks were randomised to receive either streptozotocin (diabetic, n = 20) or buffer (control, n = 11). Animals were studied on days 1, 3, 5 and 7 following streptozotocin. Diabetes was associated with a 3-fold increase in urinary EGF excretion (223 ± 15 vs 59 ± 5 ng/day, mean ± SEM, diabetic vs control, p < 0.0001) and 3–6 fold increase in renal EGF mRNA relative to controls (p < 0.001). A transient rise in kidney EGF protein was noted on day 1. There was no difference between diabetic and control animals with regard to intrarenal sites of EGF expression or in plasma EGF. These data suggest that the increased urinary EGF excretion in diabetic animals is the result of enhanced local production and that EGF is not stored for a prolonged period within renal tubular cells but is released following its synthesis. In the context of the known intrarenal actions of EGF this growth factor may play a role in the pathogenesis of diabetes related kidney growth. [Diabetologia (1997) 40: 778–785] Received: 16 December 1996 and in revised form: 4 March 1997  相似文献   

5.
目的探讨糖皮质激素治疗老年鼻息肉患者的效果及其对息肉组织中表皮生长因子(EGF)和表皮生长因子受体(EGFR)表达水平的影响。方法纳入2014年1月至2016年8月在我院接受糖皮质激素治疗的60例老年鼻息肉患者(息肉组)及鼻中隔偏曲患者20例(对照组)。息肉组患者采用布地奈德喷剂治疗12周,分别于治疗前、治疗后采集息肉组织及对照组鼻黏膜组织进行免疫组化染色及逆转录-多聚酶链反应(RT-PCR)检查,对比两组EGF和EGFR蛋白及信使核糖核酸(mRNA)表达水平。计量资料以均数±标准差表示,两组间比较采用t检验。结果息肉组患者的鼻息肉病变评分情况:治疗前(2.48±0.77)分,治疗2周后(2.11±0.68)分,治疗6周后(1.57±0.49)分,治疗12周后(1.29±0.64)分;鼻息肉病变评分呈逐渐降低趋势,各时间点比较差异具有统计学意义(P0.05)。息肉组在治疗前、治疗后的EGF、EGFR蛋白表达水平和mRNA表达水平均高于对照组(P0.05);息肉组治疗12周后鼻息肉组织中EGF和EGFR蛋白表达水平和mRNA表达水平较治疗前均显著降低(P0.05)。结论糖皮质激素治疗老年鼻息肉患者的效果肯定,其作用机制与抑制鼻息肉组织中EGF及EGFR表达有关。  相似文献   

6.
OBJECTIVE : To study the effect of epidermal growth factor (EGF) on pathological changes of the gastric mucosa in rats with chronic atrophic gastritis (CAG). METHODS : The established CAG rat models were divided into groups A and B. The rats in group A received 10 μg/kg EGF subcutaneously. In group B, rats were subcutaneously injected with the same quantity of normal saline. Twelve weeks later, all rats were killed by cervical dislocation and their gastric mucosa were examined microscopically. RESULTS : The grading of the inflammatory cell infiltration in group A was lower than that in group B (P < 0.01). The thickness of the gastric mucosal gland layer was 215.0 ± 20.7 μm in group A and 139.2 ± 13.8 μm in group B (P < 0.01). The ratio of the thickness of the gastric mucosal glands to that of the muscularis mucosa (L1/L2) was 2.70 ± 0.34 in group A and 1.27 ± 0.27 in group B (P < 0.01). The number of gastric glands in a 1‐mm length of mucosal layer was 26.20 ± 1.27 in group A and 19.90 ± 1.78 in group B (P < 0.01). In group A, the gastric glands were rearranged, without signs of malignant proliferation. The width of gastric mucosa expressing proliferating cell nuclear antigen (PCNA) was larger in group A than in group B (77.70 ± 4.16 μm vs 54.40 ± 4.54 μm; P < 0.01). CONCLUSIONS : Epidermal growth factor plays a therapeutic role in reversing gastric mucosal atrophy in rats with CAG. It promotes the expression of PCNA, which induces a protective proliferation in gastric mucosal lesions in rats with CAG.  相似文献   

7.
The effect of salivary epidermal growth factor (EGF) on the growth and metabolism of gastrointestinal mucosa was examined by comparing DNA synthesis, DNA and RNA content, and weight of mucosa of salivarectomized and sham operated male rats. DNA synthesis of gastric mucosa was suppressed at 2 days after salivarectomy. Both weight and DNA content of oxyntic mucosa in the salivarectomized group were significantly lower than that of the sham operated group. Although salivarectomy suppressed DNA synthesis of jejunal mucosa, the difference was not significant statistically. The effect of salivarectomy on colonic mucosa was least in the gastrointestinal tract. Such a result suggested that the gradient-oriented antitrophic effect was brought about by salivarectomy. Urinary EGF excretion after salivarectomy was examined by radioreceptor assay. Although the antitrophic effect of salivarectomy on oxyntic mucosa was highest on day 2, no significant difference of urinary EGF concentration was detected on day 2. From these results it is suggested that the effect of salivarectomy on the gastrointestinal tract was not due to the change of EGF in systemic circulation but due to the change of luminal EGF.  相似文献   

8.
[目的]观察健中愈疡片对乙酸诱导胃溃疡大鼠血清表皮生长因子(EGF)水平和胃溃疡边缘表皮生长因子受体(EGFR)表达的影响。[方法]制备乙酸诱导大鼠胃溃疡模型,分别予健中愈疡片、雷尼替丁和0.85%氯化钠液治疗14d,用放射免疫分析法测定大鼠血清EGF水平,免疫组织化学染色法检测胃溃疡边缘EGFR表达。[结果]造模3d时,胃溃疡模型组大鼠的血清EGF水平明显高于正常对照组,胃溃疡边缘EGFR表达比正常对照组明显增加。治疗14d后,与雷尼替丁组和0.85%氯化钠液组比较,健中愈疡片组的血清EGF水平显著减少(P〈0.01),而胃溃疡边缘EGFR表达显著增加(P〈0.01)。[结论]血清EGF水平可以作为反映胃肠黏膜完整性的一个监控指标,健中愈疡片能够减少血清EGF水平和增加胃溃疡边缘EGFR表达,这可能是其加速乙酸诱导胃溃疡愈合的主要作用机制。  相似文献   

9.
糖尿病大鼠的肾脏肥大和尿EGF变化   总被引:2,自引:0,他引:2  
本文观察了大黄对链脲菌素所致糖尿病大鼠肾脏肥大、尿表皮生长因子(EGF),以及肾功能的影响.结果表明,糖尿病大鼠肾脏肥大和尿EGF呈明显相关性,大黄抑制肾脏肥大,其尿EGF排泄量也明显降低;同时肾小球滤过率降低,大黄并能部分地减少近曲小管Na~+的再吸收.说明大黄抑制肾脏肥大的作用与大黄减少肾EGF生成和近曲小管增殖和肥大有关.  相似文献   

10.
目的 探讨表皮生长因子 (EGF)及其受体 (EGFR)在甲状腺增殖性疾患中的表达及其作用。方法 应用免疫组化ABC染色方法观察 70例甲状腺组织切片EGF及EGFR的表达。结果(1)EGF在正常、肿瘤及非肿瘤组织中几乎均无表达。 (2 )乳头状、滤泡型甲状腺癌及其混合癌EGFR阳性表达高于非癌疾患及正常组织 (P <0 .0 5 ) ,阳性表达程度以强阳性为主。 (3)在正常组织、良性腺瘤、结节性甲状腺肿及桥本病 ,弱或中度的EGFR阳性表达率各组间差异无显著性。正常组织阳性表达率虽高达 83.3 % ,但 2 / 3表达为弱阳性。 (4 )乳头状甲状腺癌以细胞浆表达EGFR占优势 ,滤泡型及混合型甲状腺癌主要为混合着色 ,但与非癌混合着色不同的是多数以胞浆表达占优势 ;良性疾患以混合染色为主 ,但结节性甲状腺肿以膜着色居多。正常组织为浆、膜混合着色。结论  (1)对EGFR强阳性表达尤其细胞浆为主者应高度疑及甲状腺癌。 (2 )各甲状腺良性疾患均有不同程度EGFR表达 ,虽无统计学意义上的差别 ,却可说明EGFR对于良性肿瘤及非肿瘤增殖性疾患的生成均有不应忽视的作用。  相似文献   

11.
Epidermal growth factor (EGF) up-regulation of glucose absorption via increased Na+/glucose cotransporter (SGLT-1) activity has previously been described in rabbit jejunal brush-border membrane and in differentiated Caco-2 cells. The goal of the present study was to assess the in vitro effect of EGF (200 ng/ml) on glucose uptake in human mucosal specimens, and we describe a simple procedure that uses endoscopic biopsies for short-term gludose uptake measurements. Uptake values for the EGF-treated biopsies ranged from 2.7 to 29.0, with a mean uptake of 10.65, while uptake values for the untreated biopsies ranged from 0.9 to 17.5, with a mean uptake of 7.99 (P < 0.05, paired t test). This early effect of EGF on human enterocytes may have important therapeutic implications. A role in increasing the rate of internal rehydration is suggested.  相似文献   

12.
ABSTRACT— Expression of epidermal growth factor (EGF) and fibroblast growth factor (FGF) was examined in 56 patients with hepatocellular carcinoma (HCC) using an immunohistochemical method. EGF and FGF were expressed on carcinoma cells in 14 (25%) and 23 cases (41%), respectively. In the 23 FGF-positive cases, 11 cases were positive for both acidic and basic FGF, while 18 were positive for acidic FGF, and 16 were positive for basic FGF. In non-cancerous hepatic tissues, FGF was weakly positive in macrophages, hepatocytes and vascular endothelial cells in some cases, while EGF was totally negative. There were no significant correlations between the expression of EGF or FGF on carcinoma cells and the various clinicopathologic factors examined. These data suggest that EGF and FGF are produced by human HCC cells in vivo. The roles of the expression of these growth factors in the development and progression of HCC remain only speculative.  相似文献   

13.
表皮生长因子对SD大鼠萎缩性胃炎的作用   总被引:13,自引:0,他引:13  
目的探讨表皮生长因子(EGF)对大鼠慢性萎缩性胃炎(CAG)胃黏膜病变的作用。方法将已经建立的SD大鼠CAG模型随机分成治疗组和对照组,治疗组给予EGF10μg/kg皮下注射,每日1次;对照组给予等容生理盐水皮下注射,每日1次,刺激12周后取出全胃,观察各组大鼠胃黏膜病理变化。结果治疗组大鼠胃黏膜炎性细胞浸润程度较对照组明显减轻(P<0.01);两组大鼠胃黏膜腺体层厚度分别为(215.0±20.7)μm和(139.2±13.8)μm(P<0.01),胃黏膜腺体层厚度/黏膜肌层厚度分别为2.70±0.34和1.27±0.27(P<0.01),单位长度内胃黏膜腺体数目分别为26.20±1.27和19.90±1.78(P<0.01);治疗组胃黏膜腺体增殖细胞核抗原(PCNA)表达阳性的宽度(77.70±4.16)μm较对照组(54.40±4.54)μm明显增加(P<0.01)。治疗组大鼠胃黏膜腺体排列规则,未发现有恶性增殖现象。结论EGF对SD大鼠CAG模型的胃黏膜萎缩有逆转治疗作用。EGF促进大鼠胃黏膜细胞PCNA阳性表达是其对大鼠CAG损伤的保护性增殖作用。  相似文献   

14.
15.
NTRODUCTIONEpidermalgrowthfactor(EGF)isasinglechainpolypeptidethatissecretedbysubmandibularandBrunner′sglandsandisapowerfulm...  相似文献   

16.
[目的]观察参七消痞方(SQ)对慢性萎缩性胃炎(CAG)大鼠组织病理形态及血清生长激素(GH)、表皮生长因子(EGF)的影响.[方法]通过N-甲基-N’-硝基-N-亚硝基胍(MNNG)综合其他因素建立CAG大鼠模型(14周),之后再随机分为模型组、摩罗丹组、叶酸组、参七消痞组.模型组给予0.9%氯化钠1 ml/0.1 kg灌胃,摩罗丹组摩罗丹3.6 g/kg灌胃,叶酸组叶酸2 mg/kg灌胃,参七消痞组参七消痞汤9 g/kg灌胃,共计8周.另从实验开始造模时设立空白对照组.每周监测大鼠体重,第22周取材,观察大鼠胃病理组织学改变,测量胃窦区褶皱处胃黏膜腺体厚度(L1)/黏膜肌层厚度(L2)的比值;腹主动脉取血分离血清,放免法检测血清GH、EGF水平.[结果]参七消痞组与模型组相比,肉眼及镜下观察均大鼠胃黏膜组织病理形态有不同程度的改善,L1/ L2比值提高(P<0.01);血清GH水平有升高趋势(P<0.05),血清EGF水平显著升高[(0.84±0.17)、(0.72±0.17)μg/L,P<0.01].[结论]复方参七消痞汤能明显改善CAG大鼠的胃黏膜病变,其治疗机制可能与升高血清EGF水平有关.  相似文献   

17.
目的探讨电针足阳明胃经原穴足三里穴对胃酸分泌的调节作用及机制.方法采用完全随机方法分组.在清醒状态下电针大鼠足三里穴,并与空白对照组及非经非穴组相对比,在针剌不同时间点测胃酸分泌及取血,放免法检测胃液及血浆促胃液素(GAS)和表皮生长因子(EGF)浓度.结果电针足三里穴后空腹胃液量显著减少(P<0.01)pH值上升(P<0.05),酸度变化不大.足三里穴组胃液及血浆GAS浓度均降低,分别为239 ng/L±61 ng/L vs 294 ng/L±32ng/L(P<0.05)和81 ng/L±22ng/L vs 102ng/L±30 ng/L(P<0.01).胃液EGF浓度显著升高3.16μg/L±1.05 μg/L vs 1.65μg/L±0.35μg/L(P<0.01).血浆EGF浓度显著降低0.25μg/L±0.01μg/L vs 0.54 μg/L±0.11μg/L(P<0.01).其他组无显著变化.结论电针足三里穴明显抑制胃酸分泌并使胃液pH升高,与血浆、胃液GAS下降有关;电针足三里穴诱导上消化道EGF分泌增加,EGF参与抑制胃酸分泌,具有重要意义.  相似文献   

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19.
目的 探讨采用体外化学合成的针对表皮生长因子受体(EGFR)设计的双链RNA(double-stranded RNA,dsRNA),是否能诱导肺非小细胞肺癌(NSCLC)细胞出现序列特异性基因沉默,及抑制EGFR基因表达后NSCLC细胞的生物学特征。方法 体外合成EGFR序列特异性dsRNA(dsRNA-EGFR),结合脂质体2000转染肺腺癌SPC-A-1细胞,用荧光显微镜及流式细胞仪测定转染细胞的EGFR受体数量;适时定量聚合酶链反应检测其EGFR基因表达水平。采用集落形成试验检测SPC-A-1细胞的增殖和集落形成能力。建立裸鼠肿瘤模型,计算肿瘤抑制率。结果 dsRNA-EGFR可使EGFR在蛋白水平表达下降71.3%、基因水平表达下降50.0%,SPC-A-1细胞集落形成下降66.8%,并显著抑制在体肿瘤生长,肿瘤抑制率为75.0%。结论 dsRNA-EGFR可序列特异性下调NSCLC细胞EGFR在基因及蛋白水平的表达,有效抑制肿瘤生长。  相似文献   

20.
Summary Background. EGF and EGF-R are frequently overexpressed in the tissue of patients suffering from ductal pancreatic cancer and to lesser degree in patients with chronic pancreatitis. The aim of this study was to determine the value of serum measurements in these patients to detect malignant pancreatic disease. In cases of pancreatic cancer, the tissue expression of EGF and EGF-R was evaluated by immunohistochemistry. Method. Thirty-five patients with chronic pancreatitis and 31 patients with pancreatic cancer were evaluated; 71 patients admitted for routine surgery (hernia repair, cholecystectomy, goiter surgery) served as controls. Results. EGF and EGF-R values were not significantly different in pancreatic cancer as compared to controls and did not correlate with other tumor markers (CA 19-9, carcinoembryonic antigen [CEA], tumor polypeptide antigen [TPA]) or with the stage of the disease. Fourteen patients (67%) with pancreatic cancer displayed tissue overexpression for EGF and 11 patients for EGF-R (52%). These patients, however, also failed to exhibit any significant pathological changes in serum concentration. In chronic pancreatitis, EGF and EGF-R were significantly decreased as compared to pancreatic cancer and controls. This was an unexpected finding. There was a positive correlation to clinical exocrine insufficiency. Conclusion. The results of this study show that routine measurements of epidermal growth factor (EGF) and epidermal growth factor receptor (EGF-R) cannot improve screening for pancreatic cancer despite the frequently present tissue overexpression. Both values fail to reveal this malignancy in a serum test. Patients with chronic pancreatitis exhibit no or very low concentrations of EGF. In cases where preoperative diagnosis is difficult the noninvasive EGF and EGF-R serum measurements may be helpful in discriminating between pancreatic cancer and chronic pancreatitis.  相似文献   

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