Reversing gastric mucosal alterations during ethanol-induced chronic gastritis in rats by oral administration of Opuntia ficus-indica mucilage

瞄准：为了学习，粘液的效果在在老鼠导致乙醇的胃炎愈合上从仙人掌属植物 ficus-indica (仙人掌科) 的叶状枝获得了。方法：长期的胃粘膜损害与粘液被对待(5 mg/kg 每天) 在它被乙醇导致以后。类脂化合物作文， 5'-nucleotidase (联系膜的 ectoenzyme ) 的活动和在胃粘膜的血浆膜的 lactate 和醇脱氢酶的 cytosolic 活动是坚定的。从试验性的组的胃的样品的组织学的研究被包括。结果：乙醇得到了表面上皮的损失和 polymorphonuclear 的渗入描绘的胃炎的组织学的侧面。Phosphatidylcholine (PC ) 减少了，胆固醇内容在胃粘膜的质膜增加了。另外，当醇脱氢酶的活动减少了时， cytosolic 活动增加了。粘液的管理即时改正了这些酶的变化。事实上，粘液乐意地在胃粘膜的质膜加速了导致乙醇的组织学的改变和骚乱的恢复，显示出只有一个意义的反煽动性的效果。5'-nucleotidase 的活动在类脂化合物作文和胃的粘膜质膜的流动性与变化相关。结论：粘液的有益的行动似乎与损坏胃粘膜的质膜的稳定相关。在粘液之间的分子的相互作用单音的糖类和膜 phospholipids，主要 PC 和 phosphatidylethanolamine (PE ) ，可以是负责在长期的胃的粘膜以后在愈合的过程期间改变依附膜的蛋白质的活动的相关特征损坏。

Effect of ultrasonic modification on the protective activity of Flammulina velutipes polysaccharide to prevent ethanol-induced injury on GES-1 cells

Flammulina velutipes(F.velutipes)polysaccharides were modified by ultrasound at the rated power of 150 W and 900 W.The monosaccharide composition,ultraviolet-visible,and Fourier transform infrared spectral characteristics of F.velutipes polysaccharides(FVP)and their ultrasonic modification products(U-FVPs)were determined.The protective effects of FVP and U-FVPs on human gastric mucosal cells GES-1 were confi rmed for the first time.The mole ratios of glucose and galactose were decreased and the mole ratio of mannose was increased after ultrasonic modification.Compared with the original FVP and the FVP modifi ed by ultrasound of 150 W(U-FVP1),the FVP modifi ed by ultrasound of 900 W(U-FVP2)could better prevent ethanol-induced damage to GES-1 cells.With increasing ultrasound intensity,the protective effect of FVPs on GES-1 cells was significantly enhanced by more effective prevention of intracellular reactive oxygen species(ROS)production and more promotion of expression of triglyceride factor 2(TFF2),prostaglandin E2(PGE2),epidermal growth factor(EGF),and transforming growth factorβ1(TGF-β1)mRNA.The ultrasonic modifi cation might be an effective way to develop novel F.velutipes polysaccharides that could effectively resist the gastric injury caused by excessive alcohol consumption.

Ligustrazine alleviates gastric mucosal injury in a rat model of acute necrotizing pancreatitis

BACKGROUND: Acute necrotizing pancreatitis (ANP) leads to a systemic inflammatory response characterized by widespread leukocyte activation and, as a consequence, distant organ injury. The aim of this study was to explore the relationship between gastric microcirculatory impairment and inflammatory mediators released in rats and to evaluate the therapeutic effect of ligustrazine extracted from Rhizoma ligusticum wallichii on gastric mucosa injury in a rat model of ANP. METHODS: Ninety-six Sprague-Dawley rats were randomly divided into three groups: normal control (group Q; ANP without treatment (group P); and ANP treated with ligustrazine (group T). The ANP model was induced by injection of 50 g/L sodium taurocholate under the pancreatic membrane (4 ml/kg). Group C was given isovolumetric injection of 9 g/L physiological saline by the same route. Group T was injected with ligustrazine (10 ml/kg) via the portal vein. The radioactive biomicrosphere technique was used to measure the blood flow 2 and 12 hours after the induction of ANP. Samples of the pancreas and stomach were taken to assess pathological changes by a validated histology score; meanwhile, the levels of serum interleukin-1 beta (IL-1 beta) were determined. Gastric tissues were also used to measure the level of myeloperoxidase (MPO), which is expressed intracellularly in the azurophilic granules of neutrophils. RESULTS: Blood flow in group P was significantly lower than that in group C (P < 0.01). Pathological changes were significantly aggravated in group P. The gastric MPO activity in group P was significantly higher than that in group C (P < 0.01). The level of serum IL-1 beta in group P increased more significantly than that in group C (P < 0.01). Blood flow of the stomach in group T was significantly higher than that in group P after 2 hours (P < 0.01). The pathological changes were significantly alleviated in group T. The MPO activity of group T was significantly lower than that of group P (P < 0.01). Although serum IL-1 beta level of group T, was higher than of group C (P < 0.01), it was lower than that of group P (P < 0.01). There was a negative correlation between gastric blood flow and MPO activity (r=-0.983, P < 0.01), and between gastric blood flow and pathological score (r=-0.917, P < 0.05). CONCLUSIONS: Decreased gastric blood flow and increased inflammatory mediators can be seen early in ANP, and both are important factors for gastric and mucosal injury. Ligustrazine can ameliorate microcirculatory disorder and alleviate the damage to the pancreas and stomach.

Effect of acupuncture at different meridian acupoints on changes of related factors for rabbit gastric mucosal injury

AIM: To explore the regularity of multi-meridians controlling a same viscus (MMCSV).METHODS: The rabbit gastric ulcer model was established by ethanol intragastric instillation. Fifty-six rabbits were randomly divided into normal group, model group (MG), model plus acupuncture at Foot Yangming Meridian group (YMG), model plus acupuncture at Foot Taiyin Meridian group (TYG), model plus acupuncture at Foot Shaoyang Meridian group (SYG), model plus acupuncture at Foot Jueyin Meridian group (JYG), model plus acupuncture at Foot Taiyang Meridian group (TYMG),with eight rabbits in each group. Gastric mucosal nitric oxide (NO) and nitric oxide synthase (NOS) were assayed by the nitric acid reductase method, and prostaglandin E2 (PGE2) and epidermal growth factor (EGF) were measured by radioimmunoassay. The comprehensive effects were analyzed by weighing method.RESULTS: Compared to MG, SYG, JYG and TYMG, the rabbits gastric mucosal injury index (GMⅡ) reduced very significantly in YMG (P＜0.01). Compared to MG, the GMⅡ also reduced significantly in TYG (P＜0.05). NO,NOS, PGE2 and EGF increased very significantly in YMG (P＜0.01). The EGF in YMG also increased significantly than that in TYG compared to those in MG, SYG, JYG and TYMG (P＜0.05). The PGE2 and EGF also increased very significantly in TYG than those in MG, JYG and TYMG (P＜0.01). While compared to SYG, the NOS increased significantly in TYG (P＜0.05). NOS was thehighest in YMG (P＜0.01), and was higher in TYG than in MG (P＜0.01).CONCLUSION: MMCSV is common. The Foot Yangming Meridian is most closely related to the stomach, followed by Foot Taiyin Meridian, Foot Shaoyang Meridian and Foot Jueyin Meridian. Foot Taiyang Meridian has no correlation with the stomach.

Hydrogen sulfide attenuates gastric mucosal injury induced by restraint water-immersion stress via activation of KATPchannel and NF-κB dependent pathway

AIM To explore the effect of hydrogen sulfide(H2S)on restraint water-immersion stress(RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate(ATP)-sensitive potassium(KATP)channels and nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB)pathway on such an effect.METHODS Male Wistar rats were randomly divided into a control group,a physiological saline(PS)group,a sodium hydrosulfide(Na HS)group,a glibenclamide(Gl)group,Gl plus Na HS group,a pyrrolidine dithiocarbamate(PDTC)group,and a PDTC plus Na HS group.Gastric mucosal injury was induced by RWIS for 3 h in rats,and gastric mucosal damage was analyzed after that.The PS,Na HS(100μmol/kg body weight),Gl(100μmol/kg body weight),Gl(100μmol/kg or 150μmol/kg body weight)plus Na HS(100μmol/kg body weight),PDTC(100μmol/kg body weight),and PDTC(100μmol/kg body weight)plus Na HS(100μmol/kg bodyweight)were respectively injected intravenously before RWIS.RESULTS RWIS induced serious gastric lesions in the rats in the PS pretreatment group.The pretreatment of Na HS(a H2S donor)significantly reduced the damage induced by RWIS.The gastric protective effect of the Na HS during RWIS was attenuated by PDTC,an NF-κB inhibitor,and also by glibenclamide,an ATP-sensitive potassium channel blocker,in a dose-dependent manner.CONCLUSION These results suggest that exogenous H2S plays a protective role against RWIS injury in rats,possibly through modulation of KATP channel opening and the NF-κB dependent pathway.

Total triterpenes from fruits of Chaenomeles speciosa(Sweet) Nakai protect against indomethacin-induced gastric mucosal injury: involvement of TFF1-mediated EGF/EGFR and apoptotic pathways

OBJECTIVE Gastric ulcers affect people of all ages and half of the world's population,which is being considered as the new"plague of the 21st century".As is well known,gastric mucosa is known as the first guard to protect the stomach from ulcer injury,while the aetiology of gastric ulcer is relative to imbalances between gastric mucosal protective and aggressive factors.Therefore,reducing or eliminating the aggressive factors,returning to the balance of between mucosal protective and aggressive factors,and then restoring the normal functional of gastric mucosal barrier could be crucial for treating the gastric ulcer.The fruits of Chaenomeles speciosa(TCS),also known as"mugua",might be processed into edible and health care derived products,and used as a commonly used traditional medicine in China for thousands of years.In China folk,there is a saying that"apricot one benefit,pear two benefits,mgua hundred benefits",so it has a"hundred-benefit"fruit reputation.Tujia nationality inhabitants in Southwestern China should have rheumatic diseases and peptic ulcers for living in the damp environments and bingeing on spicy and pungent foods.For the exis⁃tence of the fruit derived products of Chaenomeles speciosa as their complementary foods or snacks,the habit makes them rarely suffer from the two kinds of diseases.Enlightened by these,we had investigated the structure-activity rela⁃tionships,screened out CSTT with gastroprotective activity.Our previous studies demonstrated that TCS owned effec⁃tively therapeutic effects on gastric ulcer patients and animals,and further confirmed that TFF1 and apoptotic pathway were closely interrelated with its exerting gastroprotection.However,its underlying molecular mechanisms involved have not been fully elucidated.The current study was to further investigate its protective effect on indomethacin(IND)-damaged RGM-1 cells and rats and its underlying mechanisms through modulating TFF1-mediated EGF/EGFR and apoptotic pathways.METHODS The gastroprotection of TCS was evaluated with IND-induced gastric lesions model in RGM-1 cells and rats.In vitro,the proliferation,migration,mitochondrial viability and apoptosis were assessed,In vivo,ulcer index,ulcer inhibition rate,gastric juice acidity,gastric wall mucus(GWM),histopathology of gastric mucosa were detected.The gastroprotective effects of TCS through the TFF1-mediated EGFR/EGFR and apoptotic pathways were presented and measured by qRT-PCR and Western blotting assays.RESULTS TCS had gastroprotective function,which was related to the amelioration in promoting IND-damaged RGM-1 cell proliferation and migration,hoisting gastric juice acidity and GWM,improving ulcer index and ulcer inhibition rate,attenuating the hemorrhage,edema,epithelial cell loss and inflammatory cell infiltration of gastric mucosa,upregulating proliferation cell nuclear antigen,Bcl-2,Bcl-xl mRNA and TFF1,EGF,p-EGFR,p-Src,pro-caspase-3,pro-caspase-9 protein expressions,mitochondrial viability,mitochondrial cytochrome C concentration and p-EGFR/EGFR,p-Src/Src,Bcl-2/Bax,Bcl-xl/Bad ratioes,downregulating Bax,Bad,Apaf-1 mRNA and cleaved-caspase-3,cleaved-caspase-9,cleaved-PARP-1 protein expressions,cytosol cytochrome C concentration.CONCLUSION TCS′s gastroprotective effect was closely connected with boosting TFF1 expression,acti⁃vating TFF1-mediated EGF/EGFR pathway,thus restraining mitochondrial-dependent apoptosis,which provided new insights into interpreting its underlying mechanism and promised to act as a candidate drug to treat gastric mucosal injury.

EFFECT OF ELECTROACUPUNCTURE OF "ZUSANLI" ON VIP CONTENTS OF THE PERIPHERAL BLOOD, GASTRIC MUCOSAL AND BRAIN TISSUES IN GASTRIC MUCOSAL INJURY RATS

Objective: To observe the therapeutic effect of electroacupuncture (EA) of "Zusanli"(ST 36) on vasoactive intestinal peptide (VIP) levels in the peripheral blood, gastric mucosal and brain tissues in experimental gastric injury rats. Methods: Gastric mucosal injury model was established by using cold restraining stress method. 40 Wistar rats were randomly and evenly divided into normal control group, model group, EA group and non acupoint group. VIP contents of plasma and gastric mucosal and medulla oblongata tissues were assayed using radioimmunoassay and gastric mucosal blood flow (GMBF) was measured by employing hydrogen clearing method. Results: In cold restraining stress rats, spot and strip like bleeding necrosis foci in the gastric mucous primarily in the gastric antrum could be seen clearly, GMBF and VIP contents in plasma, gastric mucous and brain tissues declined significantly (P<0.05, 0.01), while the gastric mucosal lesion index (LI) raised significantly (P<0.05) in comparison with those of normal control group. Following EA of "Zusanli" (ST 36), GMBF decreased pronouncedly, VIP contents of the plasma, bulba and gastric mucosal tissues increased strikingly in comparison with model group (P<0.01). Conclusion: EA of "Zusanli" (ST 36) possesses a protection effect on gastric mucous under stress condition and VIP is involved in the effect of EA.

Protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats

Objective:To observe the protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats.Methods:All rats were randomly divided into normal control group,cirrhosis and treatment group.Thioacetamide was used to establish rat model of cirrhotic portal hypertension.The necrotic tissue of gastric mucosa ulcer focus,degree of neutrophils infiltration at the ulcer margin,portal pressure,portal venous flow,abdominal aortic pressure,abdominal aortic blood flow at front end,gastric mucosal blood flow(GMBF),glycoprotein(GP)of gastric mucosa,basal acid secretion,H' back-diffusion,gastric mucosal damage index,NO,prostaglandin E_2(PGE_2) and tumor necrosis factor-α(TNF-α) were determined respectively,and the pathological changes of gastric mucosa were also observed by microscope.Results:Compared with cirrhosis group and the control group,the ulcer bottom necrotic material,gastric neutrophil infiltration and UI of the treatment group were all decreased significantly(P<0.01),GMBF value,GP values,serum NO,PGE_2,TNF- a were all significantly increased.Conclusions:Omeprazole has an important protective effect on gastric mucosal and it can increase gastric mucosal blood flow and related to many factors.

Protective role of fruits of Rosa odorata var. gigantea against WIRSinduced gastric mucosal injury in rats by modulating pathway related to inflammation, oxidative stress and apoptosis

Objective: Rosa odorata var. gigantea is a popular medicinal plant. Some studies have demonstrated that ethanolic extract of the fruits of R. odorata var. gigantea(FOE) has gastroprotective properties. The aim of this study was to investigate the gastroprotective activity of FOE on water immersion restrained stress(WIRS)-induced gastric mucosal injury in a rat model and elucidate the possible molecular mechanisms involved.Methods: A rat stress ulcer model was established in this study using WIRS. After rats were treated with FOE orally for 7 d, the effect of FOE treatment was analyzed by hematoxylin and eosin(H&E) staining, and the changes of inflammatory factors, oxidative stress factors, and gastric-specific regulatory factors and pepsin in the blood and gastric tissues of rats were examined by ELISA assay. Molecular mechanism of FOE was investigated by immunohistochemical assay and Western blot.Results: Compared with the WIRS group, FOE could diminish both the macroscopic and microscopic pathological morphology of gastric mucosa. FOE significantly preserved the antioxidants glutathione peroxidase(GSH-PX), superoxide dismutase(SOD) and catalase(CAT) contents;anti-inflammatory cytokines interleukin-10(IL-10) and prostaglandin E2(PGE2) levels as well as regulatory factors tumor necrosis factor-a(TGF-a) and somatostatin(SS) contents, while decreasing malondialdehyde(MDA), nitric oxide synthase(i NOS), tumor necrosis factor(TNF-a), interleukin-1β(IL-1β), interleukin-6(IL-6), gastrin(GAS)and endothelin(ET) levels. Moreover, FOE distinctly upregulated the expression of Nrf2, HO-1, Bcl2 and proliferating cell nuclear antigen(PCNA). In addition, FOE activated the expression of p-EGFR and downregulated the expression of NF-ΚB, Bax, Cleaved-caspase-3, Cyto-C and Cleaved-PARP1, thus promoting gastric mucosal cell survival.Conclusion: The current work demonstrated that FOE exerted a gastroprotective activity against gastric mucosal injury induced by WIRS. The underlying mechanism might be associated with the improvement of anti-inflammatory, anti-oxidation and anti-apoptosis systems.

党参多糖对慢性萎缩性胃炎大鼠胃黏膜损伤的影响

目的探究党参多糖(CPP)调节核转录因子红系2相关因子2(Nrf2)/血红素加氧酶1(HO-1)信号通路对慢性萎缩性胃炎(CAG)大鼠胃黏膜损伤的影响。方法将大鼠随机分为对照组,模型组,CPP低、中、高剂量组(CPP 10、20、40 mg/kg)及ML385组(Nrf2抑制剂ML38530 mg/kg联用CPP 40 mg/kg),每组10只,采用N-甲基-N′-硝基-N-亚硝基胍联合不规律饮食法建立CAG大鼠模型后,连续给药6周。HE染色观察胃黏膜组织病理形态变化;检测血清胃泌素(GAS)、胃动素(MTL)、胃蛋白酶(PP)及胃黏膜组织肿瘤坏死因子α(TNF-α)、白细胞介素8(IL-8)、丙二醛(MDA)、超氧化物歧化酶(SOD)水平;TUNEL染色观察胃黏膜组织细胞凋亡情况;免疫组化法观察胃黏膜组织Nrf2、B淋巴细胞瘤-2(Bcl-2)相关X蛋白(Bax)表达;Western blot法检测胃黏膜组织Nrf2、HO-1、Bax、Bcl-2蛋白表达。结果与对照组比较,模型组大鼠胃黏膜组织损伤;GAS、MTL、PP、SOD水平,Nrf2、HO-1、Bcl-2蛋白表达水平均显著降低(P<0.05);MDA、TNF-α、IL-8水平,细胞凋亡指数,Bax蛋白表达水平均显著升高(P<0.05)。与模型组比较,CPP低、中、高剂量组胃黏膜组织病理有不同程度改善;各定量指标均显著逆转(P<0.05);Nrf2抑制剂ML385可显著减弱高剂量CPP对CAG大鼠上述指标的改善作用(P<0.05)。结论CPP能改善CAG大鼠胃黏膜损伤,抑制氧化应激、炎症反应和细胞凋亡,其作用机制可能与激活Nrf2/HO-1信号通路有关。

葛根熟大黄复配提取物对乙醇致急性胃黏膜损伤大鼠的保护作用

为研究葛根熟大黄复配提取物对无水乙醇诱导的急性胃黏膜损伤大鼠模型辅助保护作用,将60只大鼠随机分为正常对照组、模型对照组、葛根熟大黄复配提取物低、中、高剂量组,每组12只,连续灌胃32 d,末次给药后禁食不禁水24 h,无水乙醇造模。记录动物体质量、胃损伤积分、胃黏膜损伤程度以及充血、出血、上皮细胞变性坏死积分及病变总积分。与正常对照组相比,模型对照组和葛根熟大黄复配提取物组大鼠体质量无显著性差异(P>0.05),模型对照组胃损伤积分显著升高(P<0.05)。与模型对照组相比,葛根熟大黄复配提取物中、高剂量组能减少胃充血、出血、上皮细胞变性和坏死,降低大鼠胃黏膜急性酒精损伤病理组织学病变总积分(P<0.01);高剂量组能显著降低大鼠胃黏膜急性酒精损伤积分(P<0.05)。葛根熟大黄复配提取物对无水乙醇诱导的急性胃黏膜损伤模型具有辅助保护作用。

杏鲍菇发酵苦荞提取物对小鼠酒精性肝、胃损伤的保护作用

目的:研究杏鲍菇发酵苦荞提取物的体外抗氧化活性及体内对酒精性肝脏、胃黏膜损伤的保护作用。方法:本实验检测杏鲍菇发酵苦荞提取物中功能成分的含量,并分析提取物的抗氧化能力;以Lieber-DeCarli酒精液体饲料建立小鼠慢性酒精性肝脏、胃黏膜损伤模型,考察发酵后的苦荞提取物在低、高剂量(1.5 g/kg B.W.、3.0 g/kg B.W.)对肝脏和胃粘膜损伤的保护作用。结果:杏鲍菇发酵苦荞提取液中含有较多的抗氧化成分,其中多酚、黄酮、三萜含量分别为11.40±0.32 mg GAE/g DW、17.19±0.30 mg RE/g DW、7.59±0.24 mg/g,黄酮类物质:芦丁和槲皮素含量分别为13.55±0.05、0.665±0.01 mg/g;杏鲍菇发酵苦荞提取液的铁离子还原抗氧化能力及其对DPPH和ABTS+自由基清除率分别为:16.66±0.65、33.49±1.26、15.68±1.17μmol Trolox/g DW;与模型组相比,高、低剂量组均能显著降低丙二醛(P<0.05)、天冬氨酸氨基转移酶(P<0.01)、丙氨酸氨基转移酶(P<0.01)、乳酸脱氢酶(P<0.05)、白细胞介素1β(P<0.05)水平,并显著提高超氧化物歧化酶(P<0.01)、谷胱甘肽过氧化物酶(P<0.01)水平,下调了活性氧(P<0.01)、鼠肉瘤蛋白(P<0.01)、丝氨酸/苏氨酸激酶(P<0.01)、细胞外信号调节激酶(P<0.05)、丝裂原活化蛋白激酶激酶(P<0.05)的蛋白表达量。结论:杏鲍菇发酵苦荞提取物具有较好的抗氧化活性,并对小鼠慢性酒精性肝脏、胃黏膜损伤具有明显的保护作用。

普洱熟茶活性成分对胃的保护作用研究进展

随着社会饮食结构的变化和生活节奏的加快,胃部不适逐渐成为影响人们健康的一种疾病。而早在清朝时期,就有文字记载喝普洱茶可以“养胃”。随着饮用人群的增加,普洱熟茶的胃保护作用被越来越多的消费者所感知。然而,目前普洱熟茶的胃保护作用研究较少,其物质基础和作用机制也不明确。从内含物质变化来看,普洱熟茶中的茶多酚衍生物、茶多糖、没食子酸、鞣花酸、槲皮素的含量在发酵后显著升高,且研究证实这些物质对胃损伤都有一定的保护作用,因此普洱熟茶胃保护作用的发挥极有可能是这些内含物质综合作用的结果,鉴于此,文章通过大量相关文献调研结果,进一步分析推测普洱熟茶可能通过抗胃黏膜损伤、抗炎症、抗氧化、抑制幽门螺杆菌、抗胃癌等多种方式发挥其胃保护作用,具有“多物质、多靶点、多机理”的特点。

基于Nrf2/HO-1通路探讨针灸预处理对急性胃黏膜损伤大鼠的影响及机制

目的:观察针灸预处理对急性胃黏膜损伤大鼠的影响,并探讨其机制。方法:将52只SPF级大鼠随机分为正常组、模型组、灸预组和针预组,每组13只,先分别对灸预组和针预组大鼠施以艾灸和针刺中脘、足三里,每次20 min,每日1次,连续7 d;然后对模型组、灸预组和针预组采用无水乙醇与阿司匹林混悬液灌胃制备大鼠急性胃黏膜损伤模型。比较各组大鼠胃黏膜损伤指数(UI)和病理学变化,酶联免疫吸附测定(ELISA)法检测各组大鼠胃黏膜组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPX)含量和肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)水平,免疫组织化学法检测核因子E2相关因子2(Nrf2)和血红素氧合酶-1(HO-1)蛋白表达。结果:与正常组相比,模型组大鼠UI升高(P<0.01),胃黏膜组织出现充血和糜烂等病理表现,提示模型制备成功,血清SOD、GPX含量下降(P<0.01),血清MDA、TNF-α、IL-6水平及胃黏膜组织Nrf2、HO-1蛋白表达水平上升(P<0.01)。与模型组相比,灸预组和针预组UI显著降低(P<0.01);灸预组大鼠胃黏膜未见明显病理改变,针预组大鼠胃黏膜大部分完整,只有少量红细胞渗出。与模型组相比,灸预组和针预组血清SOD、GPX含量上升(P<0.01),血清MDA、TNF-α、IL-6水平及胃黏膜组织Nrf2、HO-1蛋白表达水平下降(P<0.05或P<0.01)。与针预组相比,灸预组血清SOD、GPX含量上升(P<0.01),血清MDA、TNF-α、IL-6水平及胃黏膜组织Nrf2、HO-1蛋白表达水平下降(P<0.05或P<0.01)。结论:针灸预处理可以预防大鼠急性胃黏膜病理损伤,其作用机制可能与调控Nrf2/HO-1通路、缓解氧化应激反应和减轻炎症反应有关。

原花青素对幽门螺杆菌所致小鼠胃黏膜损伤的作用及机制

背景原花青素(proanthocyanidins,PAs)可改善乙醇诱导的胃溃疡,而目前尚不清楚其能否在幽门螺杆菌(Helicobacter pylori,H.pylori)感染所致的胃黏膜损伤发挥修复作用.目的探讨PAs对H.pylori所致小鼠胃黏膜损伤的保护作用及作用机制.方法选取SPF级雄性C57BL/6小鼠43只,随机分为对照组、模型组、及低、中、高剂量PAs干预组(PAs-L、PAs-M、PAs-H).通过灌胃法定植H.pylori构建小鼠胃炎模型,并灌胃给予PAs干预4 wk.快速尿素酶试验及Warthin-Starry染色法评估H.pylori感染情况,HE染色观察小鼠胃黏膜组织的病理学表现,试剂盒测定小鼠胃黏膜组织氧化应激水平及血清中炎症因子[肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白介素(interleukin,IL)-1β,IL-8]的水平,TUNEL染色检测黏膜上皮细胞凋亡,Western blot检测胃黏膜组织中B细胞淋巴瘤-2(B cell lymphoma-2,Bcl-2)、Bcl-2相关X蛋白(Bcl-2 assaciated X protein,Bax)及裂解的半胱氨酸蛋白酶3(cleaved cysteine protease 3,cleaved-caspase 3)的表达.结果H.pylori定植感染可致小鼠胃黏膜出现损伤,表现为黏膜明显的出血点、糜烂及溃疡面,同时腺体数量减少,排列紊乱,有明显的炎性浸润;PAs干预可显著改善H.pylori所致的胃黏膜损伤.与模型组相比,PAs干预组小鼠血清中的TNF-α、IL-1β和IL-8水平以及胃黏膜组织中的氧化应激水平、胃黏膜细胞凋亡、Bax和cleaved-caspase3的表达均显著降低,而Bcl-2的表达明显增加,并且这种变化呈现出剂量依赖性.结论PAs可改善H.pylori感染所致的胃黏膜损伤,机制可能与其降低H.pylori感染所致的胃黏膜氧化应激和炎症反应并调控凋亡相关蛋白的表达抑制胃黏膜细胞凋亡有关.

解酒护肝胶囊对大鼠酒精性肝损伤保护作用研究

目的评价解酒护肝胶囊对酒精性肝损伤的防治作用以及增强酒精代谢功效研究。方法各实验组灌胃给予不同浓度受试样品后,建立酒精性肝损伤及急性酒精中毒模型。测定血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、谷氨酰氨基转移酶(GGT)、乙醇和乙醛含量;检测肝脏中三酰甘油(TG)、超氧化物歧化酶(SOD)水平;HE染色观察肝脏和胃组织的病理变化。结果与模型组比较,解酒护肝胶囊中剂量组能显著降低血清中ALT含量(P<0.05),中、高剂量组能显著降低AST和GGT含量(P<0.01),低、中、高剂量组均能显著降低肝脏组织中TG含量(P<0.01),高剂量组显著提高SOD水平(P<0.01)。肝脏组织病理切片显示,模型组大鼠肝细胞大小不均,肝索排列紊乱,有较多小泡性脂肪空泡,同时伴有炎症浸润、细胞坏死,各剂量给药组均可不同程度改善大鼠肝脏组织病变情况;与模型组比较,解酒护肝胶囊高剂量组在醉酒后8 h内乙醇和乙醛含量均显著下降(P<0.01)。解酒护肝胶囊低、高剂量组肝脏和胃组织的病变情况均有所缓解。结论解酒护肝胶囊可抑制氧化应激反应,降低脂质过氧化,加速酒精代谢,对肝组织和胃黏膜具有一定的保护作用。

基于JAK2/STAT3信号通路探讨红芪多糖对糖尿病胃轻瘫大鼠炎症反应的影响

目的研究红芪多糖(hedysarum polybotrys polysacchcaide,HPS)对糖尿病胃轻瘫(diabetic gastroparesis,DGP)大鼠胃黏膜炎症反应的影响及可能作用机制。方法62只雄性Wistar大鼠随机分为Control组12只及造模组50只,除Control组外,其余大鼠采用小剂量多次腹腔注射链脲佐菌素(25 mg·kg^(-1),连续3 d)联合高糖高脂饲料不规则喂养复制DGP模型,将成模大鼠随机分为Model组(灌胃纯净水)、HPS低、中、高剂量组(50、100、200 mg·kg^(-1)·d^(-1))及Metformin组(90 mg·kg^(-1)·d^(-1))分别灌胃处理,Control组给予等体积纯净水灌胃,每日1次,连续8周。HE染色观察各大鼠胃黏膜病理形态;ELISA检测大鼠胃黏膜TNF-α、IL-6、GAS、MTL含量;RT-PCR检测胃黏膜JAK2、STAT3 mRNA表达;Western blot检测胃黏膜JAK2、STAT3蛋白及磷酸化水平。结果与Control组相比,Model组大鼠HE染色胃黏膜有大量炎性细胞浸润;TNF-α、IL-6含量明显增加(P<0.01),GAS、MTL含量明显减少(P<0.01);JAK2、STAT3 mRNA表达明显升高(P<0.05);p-JAK2、p-STAT3明显升高(P<0.01)。与Model组相比,各给药组大鼠胃黏膜炎性表现有所改善;TNF-α、IL-6含量明显减少,GAS、MTL含量明显增加;JAK2、STAT3 mRNA表达明显降低;p-JAK2、p-STAT3表达明显降低(P<0.05)。结论HPS可改善大鼠胃黏膜炎症反应,修复胃黏膜损伤,其机制可能与调控JAK2/STAT3信号通路有关。

DIAPH3对cagA^(+)Hp诱导的胃黏膜上皮GES-1细胞EMT及紧密连接蛋白表达的影响

目的研究Diaphanous相关成蛋白3(DIAPH3)对细胞毒素相关蛋白A(cagA^(+))幽门螺杆菌(Hp)诱导的胃黏膜上皮GES-1细胞上皮间质转化(EMT)及紧密连接蛋白表达的影响。方法H.pylori J99毒株(cagA^(+)Hp)与GES-1细胞株共培养,使用DIAPH3干扰片段对细胞进行干预。观察细胞增殖、侵袭、凋亡情况,并检测EMT相关蛋白和紧密连接蛋白变化。结果显微镜下显示cagA^(+)Hp共培养的GES-1细胞大小不一,形态发生异变。与对照组比较,模型组、DIAPH3-NC组和DIAPH3组干预后不同时间的OD_(570)值、侵袭细胞数量均增加,凋亡率降低,N钙黏附蛋白(N-cadherin)、波形蛋白(Vimentin)相对表达量升高,E-钙黏附蛋白(E-cadherin)和紧密连接蛋白(occludin、claudin-1、ZO-1)相对表达量降低(P<0.05);与模型组、DIAPH3-NC组比较,DIAPH3组的OD_(570)值、侵袭细胞数量均降低,凋亡率增加,N-cadherin、Vimentin相对表达量降低,E-cadherin、occludin、claudin-1、ZO-1相对表达量升高(P<0.05)。结论抑制NIAPH3表达能抑制胃黏膜上皮GES-1细胞的EMT,阻止细胞的侵袭和转移,提高凋亡率,上调紧密连接蛋白表达。

甘草甜素对大鼠幽门螺杆菌相关性胃炎的改善作用及机制

目的探讨甘草甜素(GL)对大鼠幽门螺杆菌(HP)相关性胃炎的改善作用及机制。方法以接种1×10^(9) cfu/mL HP建立HP相关性胃炎大鼠模型,将造模成功大鼠随机分为模型组、阳性对照组(HP标准四联方案)和GL低、中、高剂量组(5、20、50mg/kg),每组12只;另取12只正常大鼠作为正常对照组。除正常对照组和模型组大鼠灌胃等体积生理盐水外,其他各组大鼠灌胃相应药物,每天1次,连续30 d。给药结束后大鼠行13C尿素呼气试验,记录超基准值(DOB);观察大鼠胃黏膜组织病理变化和细胞形态学变化,并进行病理评分;检测大鼠胃黏膜组织中白细胞介素8(IL-8)、IL-1β、肿瘤坏死因子α(TNF-α)、活性氧(ROS)、丙二醛(MDA)水平,高迁移率族蛋白B1(HMGB1)、核因子κB(NF-κB)m RNA相对表达量,一氧化氮合酶(iNOS)、HMGB1蛋白相对表达量以及NF-κB p65磷酸化水平。结果与正常对照组比较,模型组大鼠DOB值,胃黏膜组织病理评分,IL-8、IL-1β、TNF-α、ROS、MDA水平,HMGB1、NF-κB mRNA相对表达量,iNOS、HMGB1蛋白相对表达量和NF-κB p65磷酸化水平均显著升高(P<0.05);大鼠胃黏膜上皮细胞结构不完整且数量减少,细胞碎片及空泡增多,细胞固缩明显。与模型组比较,GL各剂量组和阳性对照组上述指标变化均显著逆转(P<0.05),且GL高剂量组上述指标变化均较GL低、中剂量组更显著(P<0.05);大鼠胃黏膜细胞病理变化均改善。结论GL可能通过抑制HMGB1/NF-κB信号通路的激活,抑制炎症和氧化应激反应,从而减轻HP引起的胃黏膜损伤。

Study of Clinical and Genetic Risk Factors for Aspirin-inducec Gastric Mucosal Injury

Background： Current knowledge about clinical and genetic risk factors for aspirin-induced gastric mucosal injury is not sufficient to prevent these gastric mucosal lesions. Methods： We recruited aspirin takers as the exposed group and healthy volunteers as the control group. The exposed group was categorized into two subgroups such as subgroup A as gastric mucosal injury diagnosed by gastroscopy, including erosion, ulcer or bleeding of the esophagus, stomach, or duodenum; subgroup B as no injury of the gastric mucosa was detected by gastroscopy. Clinical information was collected, and 53 single nucleotide polymorphisms were evaluated. Results： Among 385 participants, 234 were in the aspirin-exposed group. According to gastroscopy, 82 belonged to subgroup A, 91 belonged to subgroup B, and gastroscopic results of 61 participants were not available. Using the Chi-square test and logistic regression, we found that peptic ulcer history （odds ratio [OR] = 5.924, 95% confidence intervals [C/]： 2.115-16.592）, dual anti-platelet medication （OR = 3.443, 95% CI： 1.154-10.271 ）, current Helicobacterpylori infection （OR = 2.242, 95% CI： 1.032-4.870）, male gender （OR = 2.211, 95% CI： 1.027-4.760）, GG genotype ofrs2243086 （OR = 4.516, 95% CI： I. 180-17.278）, and AA genotype ofrs 1330344 （OR = 2.178, 95% CI： 1.016-4.669） were more frequent in subgroup A than subgroup B. In aspirin users who suffered from upper gastrointestinal bleeding, the frequency of the TT genotype ofrs2238631 and TT genotype ofrs2243100 was higher than in those without upper gastrointestinal bleeding. Conclusions： Peptic ulcer history, dual anti-platelet medication, tt. pylori current infection, and male gender were possible clinical risk factors for aspirin-induced gastric mucosal injury. GG genotype of rs2243086 and AA genotype of rs 1330344 were possible genetic risk factors. TT genotype ofrs2238631 and TT genotype ofrs2243100 may be risk factors for upper gastrointestinal bleeding in aspirin users.