Association of high expression in rat gastric mucosal heat shock protein 70 induced by moxibustion pretreatment with protection against stress injury

AIM:To study the effect of moxibustion on Zusanli or Liangmeng point on gastric mucosa injury in stress-induced ulcer rats and its correlation with the expression of heat shock protein 70 (HSP70). METHODS:Sixty healthy SD rats (30 males,30 females) were divided into control group,injury model group,Zushanli point group,Liangmeng point group. Stress gastric ulcer model was induced by binding cold stress method. Gastric mucosa ulcer injury (UI) index was calculated by Guth method. Gastric mucosa blood flow (GMBF) was recorded with a biological signal analyzer. Protein content and gene expression in gastric mucosal HSP70 were detected by immunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR). Thiobarbital method was used to determine malondialdehyde (MDA) content. Gastric mucosal endothelin (ET) and prostaglandin E2 (PGE2) were analyzed by radioimmunoassay. RESULTS:High gastric mucosal UI index,high HSP70 expression,low GMBF and PGF2,elevated MDA and ET were observed in gastric mucosa of rats subjected to cold stress. Moxibustion on Zusanli or Liangmeng point decreased rat gastric mucosal UI index,MDA and ET. Conversely,the expression of HSP70,GMBF,and PGE2 was elevated in gastric mucosa after pretreatment with moxibustion on Zusanli or Liangmeng point. The observed parameters were significantly different between Zusanli and Liangmeng points. CONCLUSION:Pretreatment with moxibustion on Zusanli or Liangmeng point protects gastric mucosa against stress injury. This protection is associated with the higher expression of HSP70 mRNA and protein,leading to release of PGE2 and inhibition of MDA and ET,impairment of gastric mucosal index.

Quantitative ultrastucture analysis of neuroendocrine cells of gastric mucosa on normal and pathological conditions

AIMS To study the quantitative ultrastucture of neu- roendocrine cells of gastric mucosa on normal anc pathological conditions including the duodenal ulcer (DU) and Zollinger-Ellison syndrome (ZES). METHODS The neuroendocrine cells of the gastric mucosa of eight normal subjects,six patients with DU and five patients with ZES were quantitatively investi- gated with electro microscope and ultrastructure image analyzer. RESULTS The volume density of neuroendocrine cells in DU was 1.3% and 0.8% (vs 1.6% and 0.9%,P>0.05) in gastric antrum and corpus respectively. In antrum,G cells was of 65% (P< 0.05),D cells decreased in cell density (3% vs 9.5%) and in number of cell per unit area (P<0.01). In corpus,the cell density of ECL cells increased (49% vs 30%,P<0.05);D cells and EC cells decreasec (2% P<0.01 and 4% P<0.05,respectively),and the number of D cell per unit area markedly decreased. In ZES,D cells in corpus decreased in cell density (4% vs 22%,P<0.01) and P cells also decreased (11% vs 24%,P<0.05). The density of ECL cells increased (65% vs 30%,P<0.01). CONCLUSIONS In DU and ZES,both the number and type of NE cells present some changes. Incresed gastrin in DU and ZES patients may be caused by the decrease of D cells and somatostatin secretion.

Increased susceptibility of aging gastric mucosa to injury:The mechanisms and clinical implications

This review updates the current views on aging gastric mucosa and the mechanisms of its increased susceptibility to injury. Experimental and clinical studies indicate that gastric mucosa of aging individuals-&#x0201c;aging gastropathy&#x0201d;-has prominent structural and functional abnormalities vs young gastric mucosa. Some of these abnormalities include a partial atrophy of gastric glands, impaired mucosal defense (reduced bicarbonate and prostaglandin generation, decreased sensory innervation), increased susceptibility to injury by a variety of damaging agents such as ethanol, aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs), impaired healing of injury and reduced therapeutic efficacy of ulcer-healing drugs. Detailed analysis of the above changes indicates that the following events occur in aging gastric mucosa: reduced mucosal blood flow and impaired oxygen delivery cause hypoxia, which leads to activation of the early growth response-1 (egr-1) transcription factor. Activation of egr-1, in turn, upregulates the dual specificity phosphatase, phosphatase and tensin homologue deleted on chromosome ten (PTEN) resulting in activation of pro-apoptotic caspase-3 and caspase-9 and reduced expression of the anti-apoptosis protein, survivin. The imbalance between pro- and anti-apoptosis mediators results in increased apoptosis and increased susceptibility to injury. This paradigm has human relevance since increased expression of PTEN and reduced expression of survivin were demonstrated in gastric mucosa of aging individuals. Other potential mechanisms operating in aging gastric mucosa include reduced telomerase activity, increase in replicative cellular senescence, and reduced expression of vascular endothelial growth factor and importin-&#x003b1;-a nuclear transport protein essential for transport of transcription factors to nucleus. Aging gastropathy is an important and clinically relevant issue because of: (1) an aging world population due to prolonged life span; (2) older patients have much greater risk of gastroduodenal ulcers and gastrointestinal complications (e.g., NSAIDs-induced gastric injury) than younger patients; and (3) increased susceptibility of aging gastric mucosa to injury can be potentially reduced or reversed pharmacologically.

Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa

AIM: To investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense. METHODS: Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7d sleep deprivation. RT-PCR, immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70. Ethanol (500mL.L(-1), i.g.) was used to induce gastric mucosa damage. RESULTS: RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL.L(-1) ethanol challenge, the ulcer area found in the rats with 7d sleep deprivation (19.15 +/- 4.2)mm(2) was significantly lower (P【0.01) than the corresponding control (53.7 +/- 8.1) mm(2). CONCLUSION: Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection.

Histological changes of gastric mucosa after Helicobacter pylori eradication:a systematic review and meta-analysis

AIM: To systematically review pathological changes of gastric mucosa in gastric atrophy (GA) and intestinal metaplasia (IM) after Helicobacter pylori (H. pylori) eradication.

Endoscopic diagnosis of cervical esophageal heterotopic gastric mucosa with conventional and narrow-band images

AIM: To compare the diagnostic yield of heterotopic gastric mucosa (HGM) in the cervical esophagus with conventional imaging (CI) and narrow-band imaging (NBI).

Effects of bile reflux on gastric mucosal lesions in patients with dyspepsia or chronic gastritis

AIM: To investigate the influences of bile reflux on profiles of gastric mucosal lesions in patients with dyspepsia or chronic gastritis.METHODS: A total of 49 patients diagnosed with dyspepsia and chronic gastritis underwent 24-h ambulatory andsimultaneous monitoring of intragastric bilirubin absorbance and pH values, and then they were divided into bile refluxpositive group and bile reflux negative group. Severity of pathological changes in gastric mucosa including activeinflammation, chronic inflammation, intestinal metaplasia, atrophy and dysplasia as well as Helicobacter pylori (H pylori) infection at the corpus, incisura and antrum were determined respectively according to update Sydney system criteria. The profiles of gastric mucosal lesions in the two groups were compared, and correlations between time-percentage of gastric bilirubin absorbance ＞0.14 and severity of gastric mucosal lesions as well as time-percentage of gastric pH ＞4 were analyzed respectively. RESULTS: Thirty-eight patients (21 men and 17 women, mean age 44.2 years, range 25-61 years) were found existing with bile reflux (gastric bilirubin absorbance ＞0.14) and 11 patients (7 men and 4 women, mean age 46.2 years,range 29-54 years) were bile reflux negative. In dyspepsia patients with bile reflux, the mucosal lesions such as active inflammation, chronic inflammation, intestinal metaplasia, atrophy or H pylori infection in the whole stomach, especially in the corpus and incisura, were significantly more severe than those in dyspepsia patients without bile reflux. Moreover, the bile reflux time was well correlated with the severity of pathological changes of gastric mucosa as well as H pylori colonization in the near-end stomach, especially in the corpus region. No relevance was found between the time of bile reflux and pH ＞4 in gastric cavity. CONCLUSION: Bile reflux contributes a lot to mucosal lesions in the whole stomach, may facilitate H pylori colonization in the corpus region, and has no influence on acid-exposing status of gastric mucosa in patients with dyspepsia or chronic gastritis.

Molecular cross-talk between Helicobacter pylori and human gastric mucosa

Helicobacter pylori (H.pylori) has co-evolved with humans to be transmitted from person to person and to colonize the stomach persistently.A well-choreographed equilibrium between the bacterial effectors and host responses permits microbial persistence and health of the host,but confers a risk for serious diseases including gastric cancer.During its long coexistence with humans,H.pylori has developed complex strategies to limit the degree and extent of gastric mucosal damage and in? ammation,as well as immune effector activity.The present editorial thus aims to introduce and comment on major advances in the rapidly developing area of H.pylori/human gastric mucosa interaction (and its pathological sequelae),which is the result of millennia of co-evolution of,and thus of reciprocal knowledge between,the pathogen and its human host.

Oxidative stress disturbs energy metabolism of mitochondria in ethanol-induced gastric mucosa injury

AIM: To study the role of mitochondrial energy disorder in the pathogenesis of ethanol-induced gastric mucosa injury. METHODS: Wistar rats were used in this study. A gastric mucosal injury model was established by giving the rats alcohol. Gross and microscopic appearance of gastric mucosa and ultrastructure of mitochondria were evaluated. Malondiadehyde (MDA) in gastric mucosa was measured with thiobarbituric acid. Expression of ATP synthase (ATPase) subunits 6 and 8 in mitochondrial DNA (mtDNA) was determined by reverse transcription polymerase chain reaction (RT- PCR). RESULTS:The gastric mucosal lesion index was correlated with the MDA content in gastric mucosa. As the concentration of ethanol was elevated and theexposure time to ethanol was extended, the content of MDA in gastric mucosa increased and the extent of damage aggravated. The ultrastructure of mitochondria was positively related to the ethanol concentration and exposure time. The expression of mtDNA ATPase subunits 6 and 8 mRNA declined with the increasing MDA content in gastric mucosa after gavage with ethanol. CONCLUSION: Ethanol-induced gastric mucosa injury is related to oxidative stress, which disturbs energy metabolism of mitochondria and plays a critical role in the pathogenesis of ethanol-induced gastric mucosa injury.

Expression of mucosal addressin cell adhesion molecule 1 on vascular endothelium of gastric mucosa in patients with nodular gastritis

AIM:The interaction of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) with integrin α4β7 mediates lymphocyte recruitment into mucosa-associated lymphoid tissue (MALT).Nodular gastritis is characterized by a unique military pattern on endoscopy representing increased numbers of lymphoid follicles with germinal center,strongly associated with H pylori infection.The purpose of this study was to address the implication of the MAdCAM-1/integrin β7 pathway in NG. METHODS:We studied 17 patients with NG and H pylori infection and 19 H pylori-positive and 14 H pylori-negative controls.A biopsy sample was taken from the antrum and snap-frozen for immunohistochemical analysis of MAdCAM- 1 and integrin β7.In simultaneous viewing of serial sections, the percentage of MAdCAM-1-positive to von Willebrand factor-positive vessels was calculated.We also performed immunostaining with anti-CD20,CD4,CD8 and CD68 antibodies to determine the lymphocyte subsets co- expressing integrin β7. RESULTS:Vascular endothelial MAdCAM-1 expression was more enhanced in gastric mucosa with than without H pylori infection.Of note,the percentages of MAdCAM-1-positive vessels were significantly higher in the lamina propria of NG patients than in H pylori-positive controls.Strong expression of MAdCAM-1 was identified adjacent to lymphoid follicles and dense lymphoid aggregates.Integrin β7-expressing mononuclear cells,mainly composed of CD20 and CD4 lymphocytes,were associated with vessels lined with MAdCAM-1-expressing endothelium.CONCLUSION: Our results suggest that the MAdCAM一1/ integrin a4p7 homing system may participate in gastric inflammation in response to H py/o}i-infection and contributes to MALT formation, typically leading to the development of NG.

Helicobacter pylori eradication:Exploring its impacts on the gastric mucosa

Helicobacter pylori(H.pylori)infects approximately 50%of all humans globally.Persistent H.pylori infection causes multiple gastric and extragastric diseases,indicating the importance of early diagnosis and timely treatment.H.pylori eradication produces dramatic changes in the gastric mucosa,resulting in restored function.Consequently,to better understand the importance of H.pylori eradication and clarify the subsequent recovery of gastric mucosal functions after eradication,we summarize histological,endoscopic,and gastric microbiota changes to assess the therapeutic effects on the gastric mucosa.

Low grade gastric mucosa associated lymphoid tissue lymphoma:Treatment strategies based on 10 year follow-up

AIM:To deduce strategic guidelines of gastric mucosa associated lymphoid tissue lymphoma (MALTOMA) by evaluating the long-term outcome of patients in respect to various treatment modalities. METHODS:A total of 55 patients with MALTOMA from May 1992 to August 2002 were retrospectively reviewed. RESULTS:Complete remission was obtained in 24 (82.8%) of 29 patients treated with anti Helicobacter pylori (Hpylori) regimen only.The duration to reach complete remission was 12 months (85 percentile,2-33 months).Five patients showed complete remission with radiation therapy (26-86 months).Two of them were Hpyloritreatment failure cases. CONCLUSION:Hpylorieradication is an effective primary treatment option for low grade MALTOMA and radiation therapy could be considered in patients with no evidence of Hpyloriinfection or who do not respond to Hpylorieradication therapy 12 months after successful eradication.

Microbiome changes in the gastric mucosa and gastric juice in different histological stages of Helicobacter pylori-negative gastric cancers

BACKGROUND The gastric microbiota in patients with gastric cancer(GC)has received increasing attention,but the profiling of the gastric microbiome through the histological stages of gastric tumorigenesis remains poorly understood,especially for patients with Helicobacter pylori-negative GC(HPNGC).AIM To characterize microbial profiles of gastric mucosa and juice for HPNGC carcinogenesis and identify distinct taxa in precancerous lesions.METHODS The 16S rRNA gene analysis was performed on gastric mucosa from 134 Helicobacter pylori-negative cases,including 56 superficial gastritis(SG),9 atrophic gastritis(AG),27 intestinal metaplasia(IM),29 dysplasia(Dys),and 13 GC cases,to investigate differences in gastric microbial diversity and composition across the disease stages.In addition,paired gastric mucosa and juice samples from 18 SG,18 IM,and 18 Dys samples were analyzed.α-Diversity was measured by Shannon and Chao1 indexes,andβ-diversity was calculated using partial least squares discrimination analysis(PLS-DA).Differences in the microbial composition across disease stages in different sample types were assessed using the linear discriminant analysis effect size.RESULTS The diversity and composition of the bacterial microbiota in the gastric mucosa changed progressively across stages of gastric carcinogenesis.The diversity of the gastric mucosa microbiota was found to be significantly lower in the IM and Dys groups than in the SG group,and the patients with GC had the lowest bacterial community richness(P<0.05).Patients with IM and those with Dys had similar gastric mucosa microbiota profiles with Ralstonia and Rhodococcus as the predominant genera.Microbial network analysis showed that there was increasing correlation strength between IM and Dys(|correlation threshold|≥0.5,P<0.05).GC and its precancerous lesions have distinguishable bacterial taxa;our results identified HPNGC-associated bacteria Streptococcaceae and Lactobacillaceae(P<0.05).Additionally,across precancerous lesion stages from AG to Dys in Helicobacter pylori-negative patients,Burkholderiaceae abundance continuously increased,while Streptococcaceae and Prevotellaceae abundance presented a continuous downward trend.Furthermore,the microbial diversity was higher in gastric juice(P<0.001)than in the mucosa,while PLS-DA revealed a statistically significant difference between the two groups(ANOSIM,P=0.001).A significant difference in the microbial structure was identified,with Proteobacteria being more prevalent in the gastric mucosa and Firmicutes being more abundant in gastric juice.CONCLUSION Our results provide insights into potential taxonomic biomarkers for HPNGC and its precancerous stages and assist in predicting the prognosis of IM and Dys based on the mucosal microbiota profile.

Gastric mucosal injury due to hemorrhagic reperfusion and efficacy of Salvia miltiorrhizae extract F and cimetidine

AIM: To observe the gastric mucosal injury caused by hemorrhagic shock and reperfusion and to compare the effect between Salvia miltiorrhizae extract F (SEF) and cimetidine (CI) on it. METHODS: A model of hemorrhage/reperfusion injury was produced by Itoh method. Wistar rats were randomly divided into three groups: 0.9% sodium chloride treatment group (NS group), SEF treatment group (SEF group), and CI treatment group (CI group). Saline, SEF and CI were injected respectively. The index of gastric mucosal lesions (IGML) was expressed as the percentage of lesion area in the gastric mucosa. The degree of gastric mucosal lesions was categorized into grades 0, 1, 2, 3. Atom absorption method was used to measure the intracellular calcium content. Radioimmunoassay was used to measure the concentrations of prostaglandins. RESULTS: IGML (%) and grade 3 (%) were 23.18±6.82, 58.44±9.07 in NS group, 4.42±1.39, 20.32±6.95 in SEF group and 3.74±1.56, 23.12±5.09 in CI group, and the above parameters in SEF group and CI group decreased significantly (IGML: SEF vs NS, t=6.712, P=0.000<0.01; CI vs NS, t=6.943, P=0.000<0.01; grade 3: SEF vs HS, t=8.386, P=0.000; CI vs HS, t=8.411, P= 0.000), but the grade 0 and grade 1 damage in SEF group (22.05±5.96, 34.12±8.12) and CI group (18.54±4.82, 30.15±7.12) were markedly higher than those in NS group (3.01±1.01, 8.35±1.95; grade 0: SEF vs HS, t=8.434, P=0.000<0.01; CI vs NS, t=7.950, P=0.000<0.01; grade 1: SEF vs NS, t =8.422, P=0.000<0.01; CI vs NS, t=8.448, P=0.000<0.01). The intracellular calcium content (μg/mg) in SEF group (0.104±0.015) and CI group (0.102±0.010) was markedly lower than that in NS group (0.131±0.019, SEF vs NS, t=2.463, P=0.038<0.05; CI vs HS, t=3.056, P=0.017<0.05). The levels (pg/mg) of PGE_2, 6-keto-PGF_(1α) and 6-keto-PGF_(1α)/TXB_2 were 540±183, 714±124,17.38±5.93 in NS group and 581±168, 737±102, 19.04±8.03 in CI group, 760±192,1 248±158, 33.42±9.24 in SEF group, and the above parameters in SEF group markedly raised (PGE_2: SEF vs NS, t=2.282, P=0.046<0.05; SEF vs CI, t=2.265, P=0.047<0.05; 6-keto-PGF_(1α): SEF vs NS, t=6.583, P=0.000<0.000; SEF vs CI, t=6.708, P=0.000<0.01; 6-keto-PGF_(1α)/TXB_2: SEF vs NS, t=3.963, P=0.003<0.001; SEF vs Cl, t=3.243, P=0.009<0.01), whereas TXB_2 level in SEF group (45.37±7.54) was obviously lower than that in NS group (58.28±6.74, t=3.086, P=0.014<0.05) and CI group (54.32±6.89, t=2.265, P=0.047<0.05). No significant difference was shown between NS group and CI group (PGE_2: t=0.414, P=0.688>0.05; 6-keto-PGF_(1α): t=0.310, P=0.763>0.05; TXB_2: t=1.099, P=0.298>0.05; 6-keto-PGF_(1α)/TXB_2: t=0.372, P=0.718>0.05). CONCLUSION: Both SEF and CI could inhibit reperfusioninduced injury in gastric mucosa, but with different mechanisms. SEF could not only enhance the protective effect of gastric mucosa, but also abate the injury factors, while CI can only abate the injury factors.

Possibility of non-invasive diagnosis of gastric mucosal precancerous changes

AIM: To assess the possibility of non-invasive screening of atrophic chronic gastritis for preventing further development of gastric cancer.METHODS: One hundred and seventy-eight consecutive Helicobacter pylori ( H pylori)-positive dyspeptic patients after detection of serum levels of pepsinogen-1 (PG-1) and gastrin-17 (G-17) by enzyme immunoassay were proposed for endoscopy and histology. The serologic and morphologic results were compared with estimating the sensitivity, specificity and prognostic values of the tests.RESULTS: There was statistically significant reverse dependence between the grade of stomach mucosal antral or corpus atrophy and the proper decreasing of serum G17 or PG1 levels. The serologic method was quite sensitive in the diagnosis of non-atrophic and severe antral and corpus gastritis. Also, it was characterized by the high positive and negative prognostic values.CONCLUSION: Detection of serum G-17 and PG1 levels can be offered as the screening tool for atrophic gastritis. The positive serologic results require further chromoendoscopy with mucosal biopsy, for revealing probable progressing of atrophic process with development of intestinal metaplasia, dysplasia or gastric cancer.

Protective Action of Acupuncture and Moxibustion on Gastric Mucosa in Model Rats with Chronic Atrophic Gastritis

Objective: To probe the mechanism of acupuncture and moxibustion in atrophic gastritis so as to provide a basis for clinical treatment. Method: Observe the effects of acupuncture and moxibustion at the points of Zusanli, Zhongwan and Tianshu on gastric mucosa in model rats with chronic atrophic gastritis. Results:Acupuncture and moxibustion can increase the contents of PGE2α, PGF2α and cAMP, and decrease the content of cGMP in the tissue of gastric mucosa. Conclusion: Acupuncture and moxibustion shows cytoprotection on gastric mucosa, so it is an effective method for treating chronic atrophic gastritis.

Relationship between trefoil factor 1 expression and gastric mucosa injuries and gastric cancer

AIM:To determine whether trefoil factor 1 (TFF1) is associated with mucosa healing and carcinoma suppression, we assess the expression of trefoil factor 1 in normal and pathologic gastric mucosa. METHODS: TFF1 in normal and pathologic gastric mucosa was assessed by immunohistochemical method, and the average positive A was estimated by Motic Images Advanced 3.0 software. RESULTS: Increased TFF1 was detected in gastritis, gastric ulcer and duodenal ulcer compared with normal mucosa. The same result could be seen in multiple and compound ulcer compared with simple ulcer. There was no significant difference between gastric ulcer and duodenal ulcer, gastritis and simple ulcer respectively. Increased TFF1 was detected in the peripheral mucosa of the gastric adenocarcinoma compared with normal mucosa. The expression of TFF1 in gastric adenocarcinoma was related to the differentiation of adenocarcinoma. The lower the differentiation of adenocarcinoma, the weaker the expression of TFF1. There was no TFF1 expressed in low-differentiated adenocarcinoma. The expression of TFF1 in middle and highly differentiated adenocarcinoma was a little lower than that in normal mucosa. But there was no significant difference. No TFF1 was assessed in esophageal squamous carcinoma and peripheral tissue. There was no significant difference between male and female. CONCLUSION: The expression of TFF1 was higher in gastritis and peptic ulcer than that in normal mucosa, and was also higher in multiple and compound ulcer than in simple ulcer. It seems that TFF1 plays a role in gastric mucosa protection and epithelial restitution. Increased expression of TFF1 in peripheral tissue suggests that TFF1 is associated with mechanism of carcinoma suppression and differentiation. Decreased expression of TFF1 in carcinoma and its relativity to the differentiation suggests that TFF1 is related to gland and cell destruction of carcinoma.

Protective effect of Weikang decoction and partial ingredients on model rat with gastric mucosa ulcer

AIM: To investigate the protective mechanisms of Weikang (WK) decoction on gastric mucosae. METHODS: Ninety rats were randomly divided into nine groups of 10 each, namely group, model group, group with large WK dosage, group with medium WK dosage, group with small WK dosage, group with herbs of jianpiyiqi (strengthening the spleen and replenishing qi), group with herbs of yangxuehuoxue (invigorating the circulation of and nourishing the blood), group with herbs of qingrejiedu (clearing away the heat-evils and toxic materials), group with colloidal bismuth pectin (CBP) capsules. According to the method adopted by Yang Xuesong, except normal control group, chronic gastric ulcer was induced with 100% acetic acid. On the sixth day after moldmaking, WK decoction was administered, respectively at doses of 20, 10 and 5 g/kg to rats of the WK groups, or the groups with herbs of jianpiyiqi, yangxuehuoxue and qingrejiedu, 10 ml/kg was separately administered to each group every day. For the group with CBP capsules, medicine was dissolved with water and doses 15 times of human therapeutic dose were administered (10 mL/kg solution containing 0.35% CBP). Rats of other groups were fed with physiological saline (10 ml/kg every day). Administration lasted for 16 d. Rats were killed on d 22 after mold making to observe changes of gastric mucosa. The mucus thickness of gastric mucosa surface was measured. Levels of epidermal growth factor (EGF) in gastric juice, nitric oxide (NO) in gastric tissue, endothelin (ET) in plasma, superoxide dismutase (SOD) in plasma, malondialdehyde (MDA) in plasma and prostaglandin I2 (PGI2) were examined. RESULTS: Compared with control group, ulceration was found in gastric mucosa of model group rats. The mucus thickness of gastric mucosa surface, the levels of EGF, NO, 6-K-PGF1α and SOD decreased significantly in the model group (EGF: 0.818±0.18 vs 2.168±0.375, NO: 0.213±0.049 vs 0.601±0.081, 6-K-PGF1α 59.7±6.3 vs 96.6±8.30, SOD: 128.6±15.0 vs 196.6±35.3, P<0.01),the levels of ET (179.96±37.40 vs 46.64±21.20, P<0.01) and MDA (48.2±4.5 vs 15.7±4.8, P<0.01) increased. Compared with model group, the thickness of regenerative mucosa increased, glandular arrangement was in order, and cystic dilative glands decreased, while the mucus thickness of gastric mucosa surface increased (20 g/kg WK: 51.3±2.9 vs 23.2±8.4,10 g/kg WK: 43.3±2.9 vs23.2±8.4,, 5 g/kg WK: 36.1±7.2 vs 23.2±8.4, jianpiyiqi: 35.4±5.6 vs 23.2±8.4, yangxuehuoxue: 33.1±8.9 vs 23.2±8.4, qingrejiedu: 31.0±8.0 vs 23.2±8.4 and CBP: 38.2±3.5 vs23.2±8.4, P<0.05-0.01). The levels of EGF (20 g/kg WK: 1.364±0.12 vs 0.818±0.18, 10 g/kg WK: 1.359±0.24 vs 0.818±0.18, 5 g/kg WK: 1.245±0.31 vs 0.818±0.18, jianpiyiqi: 1.025± 0.45 vs 0.818±0.18, yangxuehuoxue: 1.03±0.29 vs 0.818±0.18, qingrejiedu: 1.02±0.47 vs 0.818±0.18 and CBP: 1.237±0.20 VS 0.818±0.18, p<0.05-0.01), NO (20 g/kg WK: 0.480±0.026 vs 0.213±0.049, 10 g/kg WK: 0.390±0.055 vs 0.213±0.049, 5 g/kg WK: 0.394±0.026 vs 0.213±0.049, jianpiyiqi: 0.393±0.123 vs 0.213±0.049, yangxuehuoxue: 0.463±0.077 vs 0.213±0.049, qingrejiedu: 0.382±0.082 vs 50.213±0.049 and CBP: 0.395±0.053 vs 0.213±0.049, P<0.05-0.01), 6-K-PGF1α (20 g/kg WK: 86.8±7.6 vs 59.7±6.3,10 g/kg WK: 77.9±7.0 vs 59.7±6.3, 5 g/kg WK: 70.0±5.4 vs 59.7±6.3, jianpiyiqi: 73.5±12.2 vs 59.7±6.3, yangxuehuoxue: 65.1±5,3 vs 59.7±6.3, qingrejiedu: 76.9±14.6 vs 59.7±6.3,and CBP: 93.7±10.7 vs 59.7±6.3, P<0.05-0.01) and SOD (20 g/kg WK: 186.4±19.9 vs 128.6±15.0,10 g/kg WK: 168.2±21.7 vs 128.6±15.0, 5 g/kg WK: 155.6±21.6 vs 128.6±15.0, jianpiyiqi: 168.0±85.3 vs 128.6±15.0, yangxuehuoxue: 165.0±34.0 vs 128.6±15.0, qingrejiedu: 168.2±24.9 vs 128.6±15.0, and CBP: 156.3±18.1 vs 128.6±15.0, P<0.05-0.01) significantly increased. The levels of ET (20 g/kg WK: 81.30± 17.20 vs 179.96±37.40, 10 g/kg WK: 83.40±25.90 vs 179.96±37.40, 5 g/kg WK: 93.87±20.70 vs 179.96±37.40, jianpiyiqi: 130.67±43.66 vs 179.96±37.40, yangxuehuoxue: 115.88±34.09 vs 179.96±37.40, qingrejiedu: 108.22±36.97 vs 179.96±37.40, and CBP: 91.96±19.0 vs 179.96±37.40, P<0.01) and MDA (20 g/kg WK: 21.6±7.4 vs 48.2±4.5, 10 g/kg WK: 32.2±7.3 vs 48.2±4.5, 5 g/kg WK: 34.2±6.2 vs 48.2±4.5, jianpiyiqi: 34.9±13.8 vs 48.2±4.5, yangxuehuoxue: 35.5±16.7 vs 48.2±4.5, qingrejiedu: 42.2±17.6 vs 48.2±4.5, and CBP: 30.1±6.1 vs 48.2±4.5, P<0.05-0.01) obviously decreased. The 20 g/kg WK group was better than 10 g/kg (the mucus thickness: 51.3±2.9 vs 43.3±2.9, NO: 0.480±0.026 vs 0.390±0.055, SOD: 186.4±19.9 vs 168,2±21.7, P<0.01) and 5 g/kg (the mucus thickness: 51.3±2.9 vs36.1±7.2, NO: 0.480±0.026 vs0.394±0.026, SOD: 186.4±19.9 vs155.6±21.6, P<0.01) groups and CBP group (the mucus thickness: 51.3±2.9 vs 38.2±3.5, NO: 0.480±0.026 vs 0.395±0.053, SOD: 186.4±19.9 vs 156.3±18.1, P<0.01) in the mucus thickness, NO and SOD levels and better than 10 g/kg (86.8±7.6 vs 77.9±7.0, P<0.05) and 5 g/kg (86.8±7.6 vs 70.0±5.4,P<0.05) groups in 6-K-PGF1α level, 10 g/kg WK group was better than 5 g/kg WK (the mucus thickness: 43.3±2.9 vs 36.1±7.2, P<0.01, SOD: 168.2±21.7 vs 155.6±21.6, P<0.05) and CBP groups (the mucus thickness: 43.3±2.9 vs 38.2±3.5, P<0.01, SOD: 168.2±21.7 vs 156.3±18.1, P<0.05) in the mucus thickness and SOD level. In compound group, jianpiyiqi group, yangxuehuoxue group, qingrejiedu group, the level of ET was decreased, NO contents were increased in gastric tissue of ulcers in rats. CONCLUSION: WK decoction and separated recipes have significantly protective effect on ethanol-induced gastric mucosal injury. They can increase the content of EGF in gastric juice, PGI2 SOD in plasma and NO in gastric tissues, thicken the mucus on the gastric mucosa, and decrease the impairing factor MDA, ET in plasma.

Effects of San Qi on Gastric Secretion and Protective Factors of Gastric Mucosa in the Rat with Precancerous Lesion of Stomach

In the model rat with precancerous lesion of stomach induced by the combined method of insertion of a spring into the pylorus and high salt hot paste,effects of San Qi (三七 Radix Notoginseng) on gastric secretion and protective factors of stomach were investigated.The results indicated that gastric secretion,gastric mucosal blood flow (GMBF) and aminohexose content lowered significantly,and malondialdehyde (MDA) increased significantly (P<0.01) in the model group as compared with the normal group;after treatment with San Qi Powder for 12 weeks,both gastric secresion and GMBF increased,and MDA content decreased as compared with the negative control group (P<0.01),with no significant increase of aminohexose content.It is suggested that San Qi (三七 Radix Notoginseng) may improve gastric secretion,and that increase of GMBF and antagonism against the lesion of oxygen free radicals are possibly one of its mechanisms.

Role of Injury of Gastric Parietal Vessels by Immunocomplexes in the Mechanism of Gastric Mucosal Lesion in Portal Hypertension with Cirrhosis

The present experiment employed the immunohistochemical technique and morphological observation to investigate the expression and distribution of C3, C4, IgG, IgE and 5-HT in portal hypertensive pigs with pathological change of gastric mucosa and gastric parietal vessels. The wall of gastric mucosal microvessels in portal hypertensive pigs had a positive or strong positive reaction of C3,C4, IgG, IgE and 5-HT with obvious injury of gastric mucosa normal pigs imparted negative or feeble positive reaction, suggesting that during portal hypertension, the gastric mucosal micr0-vessels has deposit of immunocomplexes resulting in the injury of the micro-vessels. It might be a factor inv01ved in the pathogenesis of the gastric mucosal lesion during portal hypertension with cirrhosis.