萎缩性胃炎大鼠p16,bcl-2,PCNA的表达及叶酸的预防作用

目的 研究萎缩性胃炎大鼠胃黏膜中FCNA,p16,bcl-2蛋白表达情况,探讨这些调控因子改变及叶酸预防性治疗对萎缩性胃炎形成及增殖调控的影响.方法 大鼠随机分为对照组,模型组及叶酸预防组,制作萎缩性胃炎模型,叶酸预防组造模同时予叶酸溶液灌胃,共6个月.血清及组织叶酸采用化学发光法检测,胃黏膜组织分别行常规HE染色及免疫组织化学染色,免疫组化结果通过图像分析检测蛋白表达阳性面积及密度.结果 模型组较正常对照组萎缩程度重(P＜0.01);叶酸预防组较模型组萎缩程度轻(P＜0.01);与对照组比较,模型组血清及胃黏膜叶酸均无明显差异,叶酸预防组血清及胃黏膜组织叶酸均明显增高(P＜0.01);与对照组比较,模型组胃黏膜PCNA表达显著升高(P＜0.01),p16表达显著下降(P＜0.05),bcl-2表达显著增强(P＜0.01),叶酸预防组比模型组PCNA及bcl-2均有下降(P＜0.05),但PCNA仍高于对照组(P＜0.01),bcl-2表达与对照组比较无明显差异(P＞0.05),叶酸预防组p16仍低于对照组(P＜0.05),与模型组无明显差异(P＞0.05).结论 萎缩性胃炎大鼠胃黏膜细胞处于高增殖状态,并出现抑癌基因p16蛋白表达下调和凋亡抑制基因bcl-2蛋白高表达,存在细胞增殖和凋亡的不稳定状态;叶酸可在一定程度上预防胃黏膜萎缩,并能抑制bcl-2蛋白表达.     

肝硬化大鼠内脏血管一氧化氮合酶基因表达及活性的动静脉差异

目的观察肝硬化内脏血管一氧化氮合酶(NOS)表达及活性的动静脉差异在门静脉高压形成机制中的意义.方法以四氯化碳皮下注射制备大鼠门静脉高压模型,应用免疫组织化学、化学发光以及RT-PCR分别检测大鼠门静脉(PV)和肠系膜动脉(MA)组织NOS的分布、活性及基因表达.结果肝硬化组大鼠PV和MA血管各层均有iNOS分布,而eNOS则局限于内皮层.肝硬化大鼠内脏血管NOS活性[pmol.min-1.mg-1.蛋白(PV 23.82±2.48,MA 43.46±4.93)]及mRNA表达均较对照组(PV 16.48±1.54,MA 16 95±2.34)显著升高(P＜0.05与0.01);同时肝硬化大鼠MA的总NOS活性和eNOS活性及eNOS mRNA表达均显著高于PV(P＜0.01).结论内脏血管eNOS亚型活性及表达增加可能在肝硬化时NO产生增多中起主要作用,而NOS活性及表达在MA与PV之间的动静脉差异,可能是NO参与门脉高压形成的重要机制之一.     

丹参、心得安对门静脉高压症大鼠门静脉压力和胃肠激素的影响

目的:观察丹参、心得安对门脉高压症大鼠门静脉压力、胃肠激素的影响.方法:采用CCl4加酒精饮料制作大鼠门脉高压模型,造模4周后分别给大鼠服用丹参、心得安,造模结束后用Medlab-Ug4Cs生物信号采集处理系统检测正常组、模型组、丹参治疗组、心得安治疗组大鼠门静脉压力.处死大鼠后颈动脉取血,用放免法检测4组大鼠血浆胃肠激素(胃动素、胃泌素、胰高血糖素)的含量.结果:模型组大鼠门静脉压力较正常组明显升高(P＜0.01),丹参治疗组、心得安治疗组大鼠门脉压力较模型组明显下降(P＜0.01),丹参治疗组大鼠门脉压力与心得安治疗组比较差异无显著性意义(P＞0.05).心得安组大鼠与模型组比较胃动素含量无明显改善(P＞0.05),而胃泌素、胰高血糖素明显下降(P＜0.05).丹参治疗组大鼠胃泌素、胃动素、胰高血糖素含量与模型组比较明显下降(P＜0.01或P＜0.05),与心得安治疗组比较,胃动素、胰高血糖素指标下降明显(P＜0.05).结论:丹参能有效降低门脉高压症大鼠门静脉压力,调节胃肠激素,疗效优于心得安治疗组.其作用机制可能与其良好的抗肝纤维化、阻止肝硬化形成、调节胃肠激素水平、改善肝功能等作用有关.     

汉防己甲素对肝硬化大鼠胃黏膜微循环及超微结构的影响

目的:观察汉防己甲素降低大鼠肝硬化门脉高压(PHT)的疗效和对胃黏膜微循环及其超微结构的影响.方法:制作肝硬化PHT模型,成模后分为模型(M)组、汉防己甲素(T)组、普萘洛尔组(P)及正常对照(N)组,治疗15 d后进行各指标的测定.结果:与M组比较,T组门静脉压力(PVP)明显降低(P<0.01),ALT,HA及PCⅢ指标下降(P<0.05),平均动脉压(MAP)和心率(HR)无明显变化;P组引起了PVP明显降低(P<0.01)和HR的减慢(P<0.05),MAP,ALT,HA及PCⅢ无明显变化;T组、P组光镜下胃黏膜毛细血管最大直径及面积明显减小(P<0.01),透射电镜下胃黏膜超微结构的损伤明显减轻.结论:汉防己甲素能有效、安全地降低大鼠肝硬化门脉压力,可有效改善其胃黏膜微循环及超微的变化,为临床治疗门脉高压性胃病提供实验依据.     

肝硬化门脉高压大鼠胃粘膜屏障功能的观察

建立两组门脉高压症(PH)动物模型,并与对照组(SO组)比较,以观察胃粘膜屏障功能的改变.结果显示,与SO组比较,门静脉狭窄组(PVS组)大鼠内脏血流量明显增加(Ρ＜0.001),胃粘膜处于缺血状态,胃壁结合粘液(GP)显著下降(P＜0.01);肝硬化门脉高压症组(PL组)较PVS组降低更明显(P＜0.05);三组间胃基础泌酸量(BAS)无差异.PVS组、PL组大鼠H+返渗量(H+BD)均明显高于SO组(P＜0.001),表明PVS大鼠胃粘膜屏障功能破坏严重,尤以PL大鼠为甚;门脉高压胃病(PHG)与胃粘膜屏障功能严重减弱有关,其肝功能受损参与胃粘膜病变的发生.     

选择性iNOS抑制剂对肝硬化大鼠门脉高压性胃黏膜病变的影响

目的:探讨选择性诱导型一氧化氮合酶抑制剂氨基胍(aminoguanidine,AG)对肝硬化大鼠门脉高压性胃黏膜病变的防治作用及其机制.方法:将SD大鼠30只随机分为对照组( n =10)、模型组( n = 10)和AG组( n = 10),予400mL/L CCl4皮下注射12 wk建立肝硬化大鼠模型,AG组为皮下注射CCl4同时予AG饮用.观察比较各组大鼠胃黏膜形态及组织学变化,应用免疫组化法检测胃黏膜诱导型一氧化氮合酶(iNOS)的表达,并测定胃黏膜溃疡指数、门静脉压力.结果:AG组胃黏膜病变程度较模型组减轻,溃疡指数明显低于模型组(3.00±2.31 vs 10.60±3.47,P<0.01);模型组胃黏膜iNOS吸光度、面密度值均较对照组增高(0.64±0.04 vs 0.25±0.03;0.344±0.068 vs 0.017±0.008,均P<0.01),AG组胃黏膜iNOS吸光度值、面密度值(0.46±0.09,0.159±0.021)均较模型组明显下降(均P<0.01).AG组门脉压力较模型组降低.结论:AG可在一定程度上减轻门脉高压性胃黏膜病变,其机制可能主要通过抑制胃黏膜iNOS表达.     

大鼠移植静脉再狭窄过程中黏着斑激酶的活化及奥美沙坦的干预作用

目的 研究黏着斑激酶(FAK)在大鼠移植静脉再狭窄过程中的作用,并研究奥美沙坦的干预效应.方法 建立大鼠颈外静脉移植模型,将40只雄性大鼠随机分成:1)假手术组;2)模型组;3)奥美沙坦组;4)生理盐水组等4组.观察各组血管壁内膜厚度及内膜/中膜(I/M);采用免疫组化方法观察各组血管平滑肌细胞增殖核抗原(PCNA)及平滑肌肌动蛋白(α-SM actin)表达;采用western-blot方法检测FAK及磷酸化FAK的表达.结果 模型组与假手术组相比,内膜明显增厚(P＜0.01),I/M明显增加(P＜0.01),PCNA表达明显增加(P＜0.01),α-Smactin、FAK、磷酸化FAK明显增加(P＜0.05);奥美沙坦组与模型组相比,内膜厚度、I/M明显减轻(P＜0.05),PCNA、α-SM actin、磷酸化FAK表达明显降低(P＜0.05).结论 FAK活化参与了大鼠移植静脉再狭窄过程,奥美沙坦可以抑制大鼠移植静脉再狭窄,这种作用可能与减轻局部FAK活化有关.     

肾上腺髓质素在肝硬化大鼠肝脏、门静脉的表达及意义

目的　探测肾上腺髓质素(ADM)在肝硬化大鼠门静脉血浆浓度及在肝脏、门静脉的表达。方法　以CCL4诱导肝硬化大鼠模型,正常大鼠作对照。造模完成后于门静脉采血,同时取门静脉及肝组织。以放射免疫法测定大鼠门静脉血浆ADM浓度。免疫组化染色(SABC法)检测ADM在大鼠肝脏及门静脉的表达,并以Ridit分析作半定量分析。结果　肝硬化大鼠门静脉血浆ADM浓度明显高于正常大鼠(5 3 .61±18.2 7对3 6.84±12 .67,t=3 .2 1,P <0 .0 1)。正常大鼠除肝窦外,肝细胞内也有ADM表达,肝硬化时肝脏和门静脉表达均明显增加(U肝脏=2 .69,P <0 .0 5 ;U门静脉=2 .2 7,P <0 .0 5 )。结论　肝硬化时ADM在肝细胞、肝窦内皮细胞,门静脉血管的表达及门静脉血浆浓度均较正常大鼠升高。肝细胞、肝窦内皮细胞,门静脉表达ADM增加可能是循环ADM浓度增高的一个因素。肝硬化时ADM可能在门静脉压力的调节中发挥重要作用。     

应用组织芯片技术研究Delta-like 4在胃癌组织中的表达及意义

目的:研究Delta-like 4(DLL4)在胃癌中的表达及其与血管生成的关系.方法:采用免疫组化EnVision法检测胃癌组织芯片中DLL4的表达,用CD34进行微血管内皮细胞染色,计算微血管密度(MVD),分析其相关性.结果:DLL4在胃癌中的表达明显高于正常胃黏膜(85.9% vs 35.3%.P＜0.01).DLL4的高表达与胃癌的转移(r=0.612,P＜0.01)和胃壁浸润深度(r=0.482,P＜0.01)呈正相关,与胃癌的组织病理及Borrmann分型无关.胃癌组织MVD明显高于正常胃黏膜组织(66.5±18.6 vs 34.2±16.4.P＜0.01).MVD值与胃癌的组织病理分型(r=0.506,P＜0.01)和转移有关(r=0.426,P＜0.01),与胃癌胃壁浸润深度和Borrmann分型无明显相关性.DLL4表达阳性组的MVD指数明显高于DLL4表达阴性组(70.5±16.2 vs 32.5±10.4,P7＜0.01),DLL4表达与MVD呈正相关(r=0.521.P＜0.01).结论:DLL4表达促进血管分化,对胃癌的转移、浸润起重要作用.     

细胞凋亡和增殖在大鼠应激性溃疡发病中的作用

目的　从生化及形态学角度研究应激性溃疡 (SU)发生发展过程中胃黏膜细胞的死亡形式及增殖功能的变化。方法　原位末端标记 (TUNEL)法检测水浸 束缚应激 (WRS)结束前后不同时间点细胞凋亡的发生 ;透射电镜下观察细胞形态的变化 ;免疫组化ABC法原位检测增殖细胞核抗原(PCNA)蛋白的表达。结果　正常大鼠胃黏膜上皮散在TUNEL阳性细胞 ,PCNA蛋白主要在胃腺颈部近胃小凹处呈中等阳性表达。WRS 2h～WRS结束后 5hTUNEL阳性细胞较对照组明显增多 (P <0 .0 1)并逐渐达高峰 ,而PCNA表达较正常对照组显著减少 (P <0 .0 1) ;WRS后 8～ 12hTUNEL阳性细胞逐渐减少 ,而PCNA表达达高峰 ;WRS后 2 4hTUNEL阳性细胞仍高于正常水平 (P <0 .0 5 ) ,PCNA表达基本恢复至正常水平 (P >0 .0 5 )。透射电镜下可见正常胃黏膜细胞形态规则 ,核形规整 ;而发生凋亡的细胞形态各异。结论　应激期胃黏膜细胞凋亡明显增加 ,增殖能力下降 ,它们之间的失衡是溃疡发生的重要原因 ;在应激性损伤恢复的早期阶段 ,大量细胞发生凋亡可能是启动细胞增殖的必要条件。     

Microvascular abnormalities of the portal hypertensive gastric mucosa

Compared with normotensive mucosa, the portal hypertensive gastric mucosa has increased susceptibility to injury by noxious agents such as alcohol and aspirin, but the mechanism of this phenomenon is unclear. Since the microvasculature of the normal gastric mucosa is an important target of injury by these agents, we studied the histologic and ultrastructural features of gastric vasculature and mucosal microvasculature in rats with portal hypertension (produced by staged portal vein ligation) and in sham-operated rats. In portal hypertensive rats, the gastric mucosa was swollen and hyperemic and the endothelial cells of mucosal microvessels had very prominent enlarged cytoplasm obstructing capillary lumina. Quantitative analysis of transmission electron micrographs demonstrated that in portal hypertensive rats the gastric mucosal capillary endothelium had significantly increased cytoplasmic area (236%), increased pinocytic vesicular area (416%) and increased capillary basement membrane thickness (143%) compared to respective parameters in sham-operated control rats. Arterioles in the muscularis mucosae and in submucosa were thickened, and submucosal veins demonstrated features of arterialization. All these findings indicate that portal hypertension produces definite microvascular changes in the gastric mucosa resulting in compromise of the capillary lumina. These changes may be the basis for the observed morphologic and functional abnormalities of the portal hypertensive mucosa and its increased predisposition to injury.     

The role of epidermal growth factor in gastric epithelial proliferation in portal hypertensive rats exposed to stress

BACKGROUND/AIMS: This study was designed to determine whether epidermal growth factor may have a role in the stomach of portal hypertensive rats after exposure to water immersion and restraint stress. METHODOLOGY: Rats with portal hypertension (portal vein partial ligation) were studied to determine the proliferative response of the gastric epithelium to epidermal growth factor (EGF) during stress. The portal hypertensive rats received EGF (0, 10, 25, 50, and 100 microg/kg/day) subcutaneously for 7 days before water immersion restraint stress. Each rat was subjected to water immersion restraint stress for 6 hours, at the end of which the stomachs were excised to evaluate gross and microscopic mucosal damage, and gastric epithelial proliferation using proliferating cell nuclear antigen (PCNA) immunoreactivity. RESULTS: The gross and microscopic mucosal damage were significantly greater in control or low dose EGF-pretreated (10 or 25 microg/kg/day) rats than in high dose EGF-pretreated (50 or 100 microg/kg/day) rats (p<0.01). These changes were accompanied by parallel alterations in the PCNA labeling index. The PCNA labeling index between high dose EGF-pretreated and control or low dose EGF-pretreated rats differed significantly (p<0.01). CONCLUSIONS: This study clearly indicates that the influence of EGF on the proliferative response of the portal hypertensive (PHT) gastric epithelium to stress in rats was dose-dependent, suggesting an important role for EGF in the protection of PHT gastric mucosa from stress injury.     

Are humoral factors involved in the colonic mucosal lesion in portal hypertensive rats?

AIMS: With a prehepatic portal hypertensive rat model, we explored the involvement of humoral factors to the occurrence of portal hypertensive colopathy (PHC), another clinical entity besides portal hypertensive gastropathy (PHG) in portal hypertension, by investigating the expression of inducible nitric oxide synthase (iNOS), endothelial constitutive NOS (ecNOS), endothelin-1 (ET-1), tumour necrosis factor alpha (TNF-alpha) and vascular endothelial growth factor (VEGF) in the colonic and gastric mucosa. METHODS: Portal hypertension was produced by a two-stage ligation of portal vein plus ligation of the left adrenal vein in male Sprague-Dawley rats. Two weeks after complete obstruction of the portal vein, the portal pressure was measured and the expression of iNOS, ecNOS, ET-1, TNF-alpha and VEGF in the colonic and gastric mucosa were detected by RT-PCR and immunohistochemistry methods. RESULTS: A 1.8 fold (P < 0.01) elevation of the portal pressure was detected in the portal hypertensive rats as compared to control. Significantly up-regulation of the mRNA levels of iNOS (P < 0.01), ET-1 (P < 0.05) and TNF-alpha (P < 0.01), but not ecNOS and VEGF, were detected in the colonic mucosa of portal hypertensive rats compared with control. The mRNA of iNOS, ecNOS, ET-1, TNF-alpha and VEGF were all significantly increased at varied levels in the gastric mucosa as compared to control (P all < 0.05). No difference of the appearance and localization of immunostaining of iNOS, ecNOS, ET-1, TNF-alpha and VEGF in the colonic and gastric mucosa were seen between two groups. CONCLUSIONS: These data suggest the involvement of the upregulation of iNOS, ET-1 and TNF-alpha in the colonic mucosal lesion of portal hypertensive rats.     

Immunohistochemical localization of vascular endothelial growth factor in the rat portal hypertensive gastropathy

BACKGROUND AND AIMS: Portal hypertensive gastropathy (PHG) is now recognized to be a distinct entity. Recently, angiogenesis has been noticed as a key factor in clarifying the pathophysiology of various diseases. Angiogenesis in the PHT of explored gastric mucosa has yet to be explored. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor. The aim of the present study was thus to investigate whether the hypoxic state exists in PHG, and whether VEGF appears more strongly in PHG than in normal gastric mucosa and, if so, what exactly is the role of the hypoxic state and VEGF in PHG. METHODS: At 1, 3, 7 and 14 days after either a portal ligation or sham operation, the portal venous pressure, the gastric mucosal blood flow volume and the blood gas were measured and, the expression of VEGF and antiproliferating cell nuclear antigen (PCNA) in gastric mucosal specimens was immunohistochemically assessed. RESULTS: The portal pressure (PP) and the gastric mucosal blood flow (GMBF) in the PHT rats were significantly greater than in the control (CTR). Both the SaO2 and PaO2 of the arterial blood gas were lower in the PHT rats than in the control rats. The percentage of VEGF expression in the PHG was found to be higher than that in the control gastric mucosa. The percentage of PCNA expression in the PHG was higher than that in the control gastric mucosa. CONCLUSION: The levels of SaO2 and PaO2 were lower in the PHT rats. There is a possibility that a kind of portal hypertensive gastric change may trigger an enhanced histochemical expression of VEGF. The increased activity of VEGF may have a possibility of the hypoxic gastric mucosal state caused by the presence of active congestion. This damaged mucosal state 'PHG' may thus facilitate the fragility in PHG and such lesions may be slow and insidious, which may therefore lead to sudden and severe anemia, thus causing massive and sometimes fatal hemorrhaging.     

Effects of propranolol and sucralfate on ethanol-induced gastric mucosal damage in chronic portal hypertensive rats

In a rat model of chronic portal hypertension we studied ethanol-induced gastric mucosal damage and the effects of pretreatment by propranolol and sucralfate. Susceptibility to ethanol was increased in chronic portal hypertensive rats compared with sham-operated rats (55 +/- 8% vs. 25 +/- 4%). Both acute pretreatment (10 min) and chronic pretreatment (3 weeks) with propranolol reduced gastric mucosal injury induced by ethanol in portal hypertensive rats, compared with saline-treated rats. Acute and chronic pretreatment with propranolol had no protective effect in sham-operated rats. In portal hypertensive rats, sucralfate in two different doses (500 and 125 mg/kg) protected the gastric mucosa against ethanol-induced gastric injury compared with animals receiving saline (2 +/- 1% and 3 +/- 2% vs. 25 +/- 3%). Sucralfate at the higher dose did not reduce portal pressure in portal hypertensive rats. We conclude that: (1) chronic portal hypertension increases ethanol-induced gastric damage; (2) acute and chronic propranolol treatment reduces ethanol-induced gastric injury in portal hypertensive rats, probably by decreasing portal hypertension; (3) sucralfate has a cytoprotective effect in portal hypertensive rats without reducing portal pressure. These results suggest a potential application of sucralfate in patients otherwise treated by sclerotherapy.     

Impaired Adaptive Cytoprotection to Ethanol-Induced Damage in Gastric Mucosa of Portal Hypertensive Rats

Portal hypertension predisposes gastric mucosato increased damage by noxious agents. Adaptivecytoprotection has not been studied in portalhypertensive gastric mucosa. We evaluated adaptivecytoprotection in the gastric mucosa of portal hypertensiverats by exposure to ethanol. The injury index (percentgross lesions) was significantly higher in portalhypertensive rats than in sham-operated rats. The ratio of adaptive cytoprotection, calculated as thedegree of decrease in the injury index caused bypre-absolute-ethanol administration of 20% ethanol, wassignificantly impaired in portal hypertensive rats. Basal levels of gastric mucosal hexosamine werelower in portal hypertensive rats than in controls, anda blunted response to 20% ethanol was associated withportal hypertension. Nitric oxide inhibition (L-NAME, 5 mg/kg) reduced the ratio of adaptivecytoprotection in sham-operated but not in portalhypertensive rats. These results suggest that impairedadaptive cytoprotection in portal hypertensive gastric mucosa may be caused by blunted mucusproduction.     

The effect of prostacyclin on the gastric mucosa in portal-hypertensive rats

BACKGROUND/AIMS: This study investigates the effect of prostacyclin, which is thought to be involved in the hemodynamic circulation, on the gastric mucosa of rats with portal hypertension. METHODOLOGY: Various gastric functions were evaluated in portal vein ligated rats after the intraperitoneal administration of either a placebo or prostacyclin for 7 days. RESULTS: The gastric mucosal damage induced by the instillation of 90% ethanol was significantly greater in the prostacyclin-treated group than in placebo-treated group. The portal pressure was similar in both groups. There was no significant difference between the two groups in plasma concentration of 6-keto-PGF1a (a stable metabolite of prostacyclin), whereas the mucosal content of 6-keto-PGF1a was significantly higher in the prostacyclin-treated group than in the placebo-treated group. Prostacyclin pretreatment significantly increased the gastric mucosal blood flow, estimated by laser-Doppler flowmetry, and the hemoglobin content of the gastric mucosa, measured by reflectance spectrophotometry, whereas the oxygen content remained unchanged. CONCLUSIONS: We speculate that the increased gastric mucosal perfusion induced by a high content of prostacyclin in the portal hypertensive gastric mucosa may play a role in the pathogenesis of ethanol-induced gastric mucosal damage.     

Zinc L-carnosine protects against mucosal injury in portal hypertensive gastropathy through induction of heat shock protein 72

BACKGROUND AND AIMS: Increased susceptibility to gastric mucosal injury is observed in portal hypertensive gastropathy (PHG). In this study, the effects of zinc L-carnosine, an anti-ulcer drug, were evaluated on expression of heat shock protein (hsp) 72 and cytoprotection in gastric mucosa in a rat model of PHG. METHODS: Portal hypertensive gastropathy with liver cirrhosis was induced by bile duct ligation for 4 weeks in male Sprague-Dawley rats. Expression of gastric mucosal hsp72 was evaluated by Western blotting at 6 h after intragastric administration of L-carnosine, zinc sulfate, or zinc L-carnosine. Blood was also collected for determination of serum zinc level. Mucosal protective abilities against hydrochloric acid (HCl) (0.6N) followed by pretreatment with L-carnosine, zinc sulfate or zinc L-carnosine were also studied. RESULTS: L-carnosine, zinc sulfate, and zinc L-carnosine induced hsp72 in gastric mucosa of rats with bile duct ligation. Zinc sulfate and zinc L-carnosine suppressed HCl-induced mucosal injury. However, L-carnosine could not suppress HCl-induced mucosal injury. Serum zinc levels were significantly elevated after zinc L-carnosine administration. Furthermore, pretreatment with zinc L-carnosine (30-300 mg/kg) increased the expression of hsp72 in gastric mucosa and prevented HCl-induced mucosal injury in rats with bile duct ligation in a dose-dependent manner. CONCLUSIONS: Zinc derivatives, especially zinc L-carnosine, protected portal hypertensive gastric mucosa with increased hsp72 expression in cirrhotic rats. It is postulated that zinc L-carnosine may be beneficial to the mucosal protection in PHG as a 'chaperone inducer'.