柴胡桂枝汤对大鼠乙酸胃溃疡愈合质量的影响

目的：研究柴胡桂枝汤对大鼠乙酸胃溃疡愈合质量的影响。方法：用冰醋酸制备大鼠慢性胃溃疡模型,随机分为Ａ、Ｂ、Ｃ三组,分别灌服柴胡桂枝汤、西咪替丁、生理盐水。用苏木精－伊红染色和粘液组织化学染色对大队愈合性胃溃疡再生粘膜进行定量观察。用硝酸还原酶法检测胃粘膜ＮＯ含量。结果：柴胡桂枝汤组和西咪替丁组再生粘膜厚度、粘液指数高于生理盐水组（Ｐ〈０．０１）,粘膜肌层缺损宽度小于生理盐水组（Ｐ〈０．０１）,ＮＯ     

柴胡桂枝汤对大鼠乙酸胃溃疡愈合质量的影响

目的研究柴胡桂枝汤对大鼠乙酸胃溃疡愈合质量的影响。方法用冰醋酸制备大鼠慢性胃溃疡模型,随机分为A、B、C三组,分别灌服柴胡桂枝汤、西咪替丁、生理盐水。用苏木精-伊红染色和粘液组织化学染色对大鼠愈合性胃溃疡再生粘膜进行定量观察。用硝酸还原酶法检测胃粘膜NO含量。结果柴胡桂枝汤组和西咪替丁组再生粘膜厚度、粘液指数高于生理盐水组(P＜0.01),粘膜肌层缺损宽度小于生理盐水组(P＜0.01),NO含量高于生理盐水组(P＜0.01～0.05);柴胡桂枝汤组粘液指数及NO含量高于生理盐水组(P＜0.01～0.05)。结论柴胡桂枝汤能提高溃疡愈合质量,是临床抗消化性溃疡复发的可能机制之一。     

胃灵颗粒对大鼠乙酸胃溃疡愈合质量的影响

目的 :研究胃灵颗粒对大鼠乙酸慢性胃溃疡愈合质量的影响。方法 :用冰醋酸制备大鼠乙酸慢性胃溃疡模型 ,随机分为 5组 ,分别灌服蒸馏水 ,雷尼替丁 ,低、中、高剂量胃灵颗粒 ,用苏木精 -伊红染色对大鼠愈合性胃溃疡再生粘膜进行定量观察 ,并测胃壁结合粘液量、胃酸、胃蛋白酶活性。结果 :胃灵颗粒组改善胃粘膜的组织损伤 ,并提高胃壁结合粘液量 ,减少胃酸的排出。结论 :胃灵颗粒能提高溃疡愈合质量 ,是临床抗消化性溃疡复发的可能机制之一。     

七方胃痛胶囊对大鼠乙酸胃溃疡愈合质量的影响

[目的]观察七方胃痛胶囊对大鼠实验性胃溃疡愈合质量(QOUH)的影响.[方法]予冰醋酸注射制作大鼠胃溃疡模型后,随机分为5组:分别予0.85%氯化钠液、雷尼替丁胶囊、七方胃痛胶囊(小、中、大3个剂量),连续灌胃14 d,处死大鼠,制作病理切片,予苏木精-伊红染色和黏液组织化学染色,在光镜下观察溃疡指数、再生黏膜厚度、黏膜肌层缺损宽度、表面黏液厚度、再生组织结构.[结果]七方胃痛胶囊能增加再生黏膜厚度及表面黏液厚度,减少再生黏膜肌层缺损宽度(P＜0.01),有量效关系(P＜0.01),能明显改善再生组织结构.[结论]七方胃痛胶囊能改善再生组织结构,从而提高QOUH,达到抗溃疡复发的作用.     

胃肠粘膜提取物对大鼠胃溃疡治疗的实验研究

胃肠粘膜含有多种生物活性物质，具有抗粘膜损伤和促进组织修复的作用，对胃粘膜细胞有正向保护效益。本研究从新生小牛胃肠粘膜制备出分子量＜10KD的组织提取物，观察其对实验性大鼠胃溃疡的治疗作用，并初探与胃粘液分泌的关系。     

促愈颗粒对大鼠乙酸胃溃疡愈合质量的影响

目的:观察促愈颗粒对大鼠乙酸胃溃疡愈合质量的影响.方法:用冰醋酸制备大鼠慢性胃溃疡模型,所有大鼠随机分为4组(空白模型组、促愈颗粒组、雷尼替丁组和正常对照组).HE染色观察大鼠愈合性胃溃疡再生黏膜腺体成熟度和炎症细胞浸润情况;硝酸还原法检测血清NO含量;放射免疫法检测血浆PGE2含量;免疫组织化学技术检测大鼠胃黏膜EGF的表达情况;透射电镜观察大鼠再生黏膜超微结构的变化.结果:给药28d后与模型组和雷尼替丁组比较,促愈颗粒组再生黏膜囊性扩张腺体数量及炎细胞数量明显减少(再生黏膜囊性扩张腺体数量:1.43±0.53 vs 3.84±1.08.2.36±0.79,P<0.01和P<0.05;炎细胞数量:9.92±2.66 vs 28.32±6.96,17.92±4.76,P<0.01和P<0.05);血清NO及血浆PGE2含量显著增高(NO:105.41±8.02μmol/g vs 67.35±16.85,79.1 8±28.05μmol/g,P<0.0 1或P<0.05;PGE2:125.50±11.95 ng/L vs 97.33±11.84,118.83±13.25 ng/L,P<0.01和P>0.05);胃黏膜EGF表达明显增强(25.38±5.17 vs 16.82±2.13,21.12±6.08,P<0.05和P<0.05);促愈颗粒组超微结构的恢复亦优于模型组和雷尼替丁组.结论:促愈颗粒能提高溃疡再生黏膜结构,功能成熟度及电镜下成熟度,从而提高溃疡愈合质量.     

止血愈疡颗粒剂对大鼠乙酸型胃溃疡及环核苷酸的影响

自制止血愈疡颗粒剂对乙酸型胃溃疡大鼠有显著的抗溃疡作用。检测雷尼替丁组及模型组大鼠胃粘膜环磷酸腺苷／环磷酸鸟苷（cAMP／cGMP）比值分别为7．2±3．5和24．8±20．8，两组比较差异有显著性意义（P＜0．05）。表明，雷尼替丁能使大鼠胃粘膜cAMP／cGMP水平下降，提示可能cAMP／cGMP比值降低则胃酸分泌减少。止血愈疡颗粒剂表现出与雷尼替丁相同的效应。     

模拟失重对大鼠实验性胃溃疡愈合的影响

目的:探讨模拟失重对乙酸诱导的大鼠实验性胃溃疡愈合的影响及可能机制.方法:32只SD大鼠随机分为4组,即尾部悬吊7d组、尾部悬吊14d组和相应的同步对照组.采用乙酸烧灼法制备大鼠慢性胃溃疡模型,造模后第3天悬吊组大鼠采用尾悬吊法建立模拟失重动物模型.游标卡尺检测胃溃疡面积,电镜下观察再生黏膜结构,放免法检测胃液EGF含量,观察大鼠胃溃疡愈合分期.结果:与对照7d组相比,悬吊7d组大鼠溃疡面积明显增大(6.0mm2±1.7mm2vs2.2mm2±0.7mm2,t=5.661,P<0.01),溃疡分期明显降低(χ2=12.771,P<0.01);与对照14d组相比,悬吊14d组溃疡面积明显增大(3.0mm2±1.2mm2vs1.1mm2±0.4mm2,t=4.233,P<0.01),胃液EGF含量明显增高(0.155ng/mL±0.052ng/mLvs0.103ng/mL±0.019ng/mL,t=2.635,P<0.05);与悬吊7d组比较,悬吊14d组溃疡面积明显减小(3.0mm2±1.2mm2vs6.0mm2±1.7mm2,t=3.805,P<0.01),胃液EGF含量明显降低(0.155ng/mL±0.0...     

四逆泻心汤对慢性乙酸胃溃疡大鼠溃疡愈合的影响

[目的]观察四逆泻心汤（SNXX）对慢性乙酸胃溃疡大鼠溃疡愈合的影响。[方法]SD大鼠40只，随机取10只作空白对照（A）组，行假手术处理，剩余大鼠用乙酸腐蚀法制慢性胃溃疡模型，造模后存活大鼠随机分为模型对照（B）组，SNXX治疗（C）组，雷尼替丁治疗（D）组。治疗3周后，测量溃疡体积、面积；光镜下评价溃疡愈合质量（QOUH），测定血清一氧化氮（NO）、表皮生长因子（EGF）水平。[结果]C组溃疡体积缩小优于B组（P〈0．01）、D组（P〈0.05）；D组溃疡面积缩小优于B组（P〈0．01），C组溃疡面积较B组有缩小趋势，但无统计学意义。C组光镜下QOUH优于B、D组；血清NO水平低于B组（P〈0．01）、D组（P〈0．05）；血清EGF水平高于A组（P〈0．01）、B组（P〈0．05），较D组有升高趋势，但无统计学意义。[结论]SNXX可促进大鼠慢性乙酸胃溃疡愈合，溃疡体积缩小及QOUH明显优于雷尼替丁，溃疡面积缩小与雷尼替丁的差异无统计学意义，降低NO水平，升高EGF水平可能为其机制之一。     

健胃汤抗大鼠乙酸胃溃疡及泼尼松再损伤的实验研究

目的 :从溃疡愈合质量 (QOUH )角度探讨健胃汤抗消化性溃疡 (PU )复发的可能机制。方法 :采用大鼠乙酸胃溃疡模型 ,观察健胃汤对该模型及泼尼松诱导的再损伤胃粘膜的影响 ,并测定其一氧化氮 (NO)、表皮生长因子 (EGF)的含量。结果 :健胃汤能改善胃粘膜的组织损伤并提高溃疡周围组织的 NO、EGF含量。结论 :健胃汤能提高 QOUH ,增强溃疡瘢痕处抗泼尼松再损伤能力 ;提高溃疡周围组织的 NO、EGF含量 ,这可能是其抗 PU复发的机制之一。     

健中愈疡片对乙酸致胃溃疡大鼠胃粘膜细胞动力学的影响

目的研究健中愈疡片对乙酸致大鼠胃溃疡边缘粘膜细胞凋亡和细胞增殖的影响.方法制备乙酸致大鼠胃溃疡模型.分别予健中愈疡片、雷尼替丁和生理盐水治疗14 d后,测量溃疡面积,检测胃溃疡边缘粘膜细胞凋亡指致、增殖细胞核抗原标记指数和Bcl-2蛋白表达.结果健中愈疡片组和雷尼替丁组的溃疡面积明显小于生理盐水组(P＜O.O1).与胃溃疡模型组、雷尼替丁组和生理盐水组比较,健中愈疡片组的溃疡边缘细胞凋亡指数明显下降(P＜O.01),Bcl-2蛋白表达和增殖细胞核抗原标记指数均显著增加(P＜O.01).结论健中愈疡片具有减少胃溃疡边缘粘膜细胞凋亡和促进细胞增殖的作用,这可能是其治疗胃溃疡的作用机制之一.     

Impairment of Gastric Ulcer Healing by Alendronate,a Nitrogen-Containing Bisphosphonate,in Rats

Bisphosphonates such as alendronate have been developed as antiresorptive agents capable of treating diseases related to bone remodeling. In the present study, we examined the effect of alendronate on the healing of acetic acid-induced gastric ulcers in rats and investigated the mechanism involved in this action both in vivo and in vitro using the rat gastric epithelial cell line (RGM1). Acetic acid-induced gastric ulcers healed spontaneously, with up-regulation of COX-2/prostaglandin E₂ production as well as expression of vascular endothelium-derived growth factor (VEGF) and basic fibroblast growth factor (bFGF) in ulcerated mucosa. The healing of ulcers was impaired by indomethacin (2 mg/kg, s.c.) or alendronate (60 mg/kg, p.o.) given once daily for 7 days, starting 3 days after acid application. Indomethacin, but not alendronate, inhibited mucosal prostaglandin E₂ production. Alendronate as well as indomethacin decreased the protein expression of both VEGF and bFGF in ulcerated mucosa, resulting in a reduction of angiogenesis in the ulcer base. Supplementation of recombinant bFGF significantly reverted the delay in ulcer healing caused by alendronate. On the other hand, the size of cell-free areas in RGM1 cells in vitro decreased with time after wound induction, and this process was promoted by epidermal growth factor (EGF; 10 ng/ml). Co-incubation with alendronate (1 mM) did not affect the spontaneous healing but significantly suppressed the accelerated wound healing caused by EGF. These results suggest that alendronate impairs the healing of gastric ulcers in rats, and this effect may be related to down-regulation of VEGF and bFGF, the important growth factors for vascularization/granulation, as well as suppression of the stimulatory action of EGF on epithelial proliferation/migration.     

Epidermal Growth Factor in Gastric Ulcer Healing by Nocloprost,a Stable Prostaglandin E2 Derivative

Background: The gastroprotective and ulcer-healing properties of prostaglandins, especially in gastric ulcers induced by non-steroidal anti-inflammatory drugs, are well established. Ulcer healing is an active process of filling the mucosal defect with migrating and proliferating epithelial cells combined with angiogenesis in granulation tissue at the ulcer bed. Growth factors, especially epidermal growth factor (EGF) and transforming growth factor alpha (TGFa) are crucial in the regulation of the reconstruction of damaged mucosal structures. Methods: In this double-blind, randomized, prospective study 40 patients with gastric ulcer were treated with nocloprost, a stable prostaglandin E₂ derivative, or with ranitidine. All subjects underwent endoscopy before and after 4 and 8 weeks of anti-ulcer therapy. During endoscopy mucosal biopsies were performed for determination of EGF content in gastric mucosa at the ulcer margin and in the intact mucosa. Additionally, EGF output in saliva and its plasma concentrations were determined in all subjects before and during the treatment. Results: The gastric ulcer healing rate after 4 weeks was significantly higher in patients treated with nocloprost than in those treated with ranitidine (63% versus 39%, respectively). At initial examination the EGF content in the gastric mucosa obtained from the ulcer edge was significantly higher than that in the intact mucosa. There was a significant increase in the EGF content in both the ulcer margin and the intact mucosa in subjects treated with nocloprost but not in patients under treatment with ranitidine. Similarly, patients treated with nocloprost had significantly higher EGF output in saliva and higher EGF concentration in plasma throughout the anti-ulcer therapy. Conclusion: Nocloprost is superior to ranitidine in the treatment of chronic gastric ulcers, and these effects could be due, at least in part, to higher expression and mucosal content of EGF in the ulcer area.     

胃舒合剂对大鼠乙酸实验性胃溃疡的保护作用及其机理探讨

本实验发现大鼠乙酸实验性胃溃疡模型，存在着血液流变学的异常和自由基反应的失衡，其全血比粘度及全血还原粘度高于正常组（Ｐ＜０．０１），血浆超氧阴离子、红细胞超氧阴离子，血过氧化脂质（ＬＰＯ）也明显高于正常组（Ｐ＜０．０１），血过氧化物歧化酶（ＳＯＤ）则低于正常组（Ｐ＜０．０１）。中药胃舒合剂可明显地改善大鼠血液流变学的异常及氧自由基的失衡，对乙酸所致的大鼠实验性胃溃疡有显著的保护作用，且其作用优于三九胃泰（Ｐ＜０．０１）。     

Gastric Mucosal Cell Cycle Regulation with Ulcer Healing by Sulglycotide

Background: The progression of the events associated with gastric mucosal repair is controlled in an orderly manner by a plethora of the extracellular cues exerting their effect on the cell cycle regulatory proteins, cyclins, and cyclin-dependent kinases, the expression of which varies through the cycle stages. The purpose of this study was to evaluate the expression of cyclin-dependent kinase (Cdk2) and proliferating cell nuclear antigen (PCNA) during chronic ulcer healing with sulglycotide. Methods: Rats with experimentally induced gastric ulcers were treated twice daily for 14 days either with sulglycotide at 200 mg/kg or vehicle, and at different stages of the treatment their stomachs were used for macroscopic damage assessment and quantitation of gastric mucosal Cdk2 and PCNA expression. Results: The assays showed that the ulcer healing was accompanied by an increase in mucosal expression of Cdk2 and PCNA. The maximum increase in Cdk2 (2.3-fold) occurred by the 4th day of healing, whereas the expression of PCNA reached a maximum increase (4.7-fold) on the 2nd day of healing. An accelerated ulcer healing (10 days) with sulglycotide treatment was reflected in a marked enhancement in Cdk2 and PCNA. In comparison with the controls, sulglycotide caused a 2.2-fold enhancement in PCNA expression by the 2nd day of treatment and a 2.5-fold enhancement by the 6th day, whereas the Cdk2 expression attained a maximum 2.1-fold increase by the 6th day of treatment and remained substantially increased for up to 10 days. Conclusions: The findings show a complex interplay between the extracellular cues and cell cycle regulatory proteins, an orderly progression that drives the mucosal repair process. We also show that the gastroprotective agent sulglycotide is capable of affecting the expression of the cell cycle regulatory proteins that control cell cycle progression through Gl and into S phase.