Eradication of Helicobacter pylori significantly reduced gastric damage in nonsteroidal anti-inflammatory drug-treated Mongolian gerbils

AIM: To examine the effect of eradication of Hellcobacter pylori prior to usage of NSAIDs, by investigating gastric inflammatory activity, myeloperoxidase (MPO) activity, prostaglandin (PG) E_2 synthesis in H Pylori-infected, and H pylori-eradicated gerbils followed by administration of indomethacin and rofecoxib. METHODS: Six-week-old male gerbils were orally inoculated with H pylori. Seven weeks later, anti-H pylori triple therapy and vehicle were given to gerbils respectively and followed by oral indomethacin (2 mg/kg·d) or rofecoxib (10 mg/kg·d) for 2 wk. We examined the area of lesions, gastric inflammatory activity, PGE_2 synthesis and MPO activity in the stomach. RESULTS: In indomethacin and rofecoxib-treated gerbils, the following results were obtained in H pylori-infected group vs H pylori-eradicated group respectively: hyperplasia area of the stomach (mm^2): 82.4±9.2 vs 13.9±3.5 (P＜0.05), 30.5±5.1 vs 1.3±0.6 (P＜0.05); erosion and ulcer area (mm^2): 14.4±4.9 vs 0.86±0.5 (P＜0.05), 1.3±0.6 vs0.4±0.3 (P＜0.05); score of gastritis: 7.0±0.0 vs3.6±0.5 (P＜0.05), 7.0±0.0 vs 2.7±0.5 (P＜0.05); MPO activity (μmol H_2O_2/min/g tissue): 104.7±9.2 vs9.0±2.3(P＜0.05), 133.5±15.0 vs2.9±0.7 (P＜0.05); PGE_2 synthesis (pg/mg wet weight/min): 299.2±81.5 vs102.8±26.2 (P＜0.05), 321.4±30.3 vs 11.9±4.8(P＜0.05). CONCLUSION: Eradication of H pylori reduced gastric damage of NSAID-treated Mongolian gerbils. Rofecoxib caused less severe gastric damage than indomethacin in H pylori-eradicated gerbils.

Pathogenesis of NSAID-induced gastric damage:Importance of cyclooxygenase inhibition and gastric hypermotility

This article reviews the pathogenic mechanism of nonsteroidal anti-inflammatory drug(NSAID)-induced gastric damage,focusing on the relation between cyclooxygenase(COX) inhibition and various functional events.NSAIDs,such as indomethacin,at a dose that inhibits prostaglandin(PG) production,enhance gastric motility,resulting in an increase in mucosal permeability,neutrophil infiltration and oxyradical production,and eventually producing gastric lesions.These lesions are prevented by pretreatment with PGE 2 and antisecretory drugs,and also via an atropine-sensitive mechanism,not related to antisecretory action.Although neither rofecoxib(a selective COX-2 inhibitor) nor SC-560(a selective COX-1 inhibitor) alone damages the stomach,the combined administration of these drugs provokes gastric lesions.SC-560,but not rofecoxib,decreases prostaglandin E 2(PGE 2) production and causes gastric hypermotility and an increase in mucosal permeability.COX-2 mRNA is expressed in the stomach after administration of indomethacin and SC-560 but not rofecoxib.The up-regulation of indomethacin-induced COX-2 expression is prevented by atropine at a dose that inhibits gastric hypermotility.In addition,selective COX-2 inhibitors have deleterious influences on the stomach when COX-2 is overexpressed under various conditions,including adrenalectomy,arthritis,and Helicobacter pylori-infection.In summary,gastric hypermotility plays a primary role in the pathogenesis of NSAID-induced gastric damage,and the response,causally related with PG deficiency due to COX-1 inhibition,occurs prior to other pathogenic events such as increased mucosal permeability;and the ulcerogenic properties of NSAIDs require the inhibition of both COX-1 and COX-2,the inhibition of COX-1 upregulates COX-2 expression in association with gastric hypermotility,and PGs produced by COX-2 counteract the deleterious effect of COX-1 inhibition.

Mechanistic evaluation of gastro-protective effects of KangFuXinYe on indomethacin-induced gastric damage in rats

KangFuXinYe(KFX),the ethanol extract of the dried whole body of Periplaneta americana,is a well-known important Chinese medicine preparation that has been used to treat digestive diseases such as gastric ulcers for many years in China.However,its therapeutic effect and mechanism are not yet well understood.Thus,the aim of this study was to investigate the gastroprotective effects of KangFuXinYe(KFX)in indomethacin-induced gastric damage.Rats were randomly divided into six groups as follows:control,treated with indomethacin(35 mg·kg^-1),different dosages of KFX(2.57,5.14 and 10.28 mL·kg^-1,respectively)plus indomethacin,and sucralfate(1.71 mL·kg^-1)plus indomethacin.After treatment,rat serum,stomach and gastric homogenates were collected for biochemical tests and examination of histopathology firstly.Rat serum was further used for metabolomics analysis to research possible mechanisms.Our results showed that KFX treatment alleviated indomethacin-induced histopathologic damage in rat gastric mucosa.Meanwhile,its treatment significantly increased cyclooxygenase-1(COX-1),prostaglandin E2(PGE2)and epidermal growth factor(EGF)levels in rat serum and gastric mucosa.Moreover,KFX decreased cyclooxygenase-2(COX-2)and interleukin-6(IL-6)levels.Nine metabolites were identified which intensities significantly changed in gastric damage rats,including 5-hydroxyindoleacetic acid,indoxylsulfuric acid,indolelactic acid,4-hydroxyindole,pantothenic acid,isobutyryl carnitine,3-methyl-2-oxovaleric acid,sphingosine 1-phosphate,and indometacin.These metabolic deviations came to closer to normal levels after KFX intervention.The results indicate that KFX(10.28 mL·kg^-1)exerts protective effects on indomethacin-induced gastric damage by possible mechanisms of action(regulating tryptophan metabolism,protecting the mitochondria,and adjusting lipid metabolism,and reducing excessive indomethacin).

Increased susceptibility of ethanol-treated gastric mucosa to naproxen and its inhibition by DA-9601, an Artemisia asiatica extract

AIM： To examine the effect of DA-9601, a new gastroprotective agent, on the vulnerability of ethanoltreated rat＇s stomach to naproxen （NAP）. METHODS： Male Sprague-Dawley rats were pretreated with 1 mL of 50% ethanol twice a day for 5 d and then NAP （50 mg/kg） was administered. DA-9601 was admin- istered 1 h before NAP. Four hours after NAP, the rats were killed to examine gross injury index （mm2）, histologic change and to determine mucosal levels of malondialdehyde （MDA）, prostaglandin E2 （PGE2）, glutathione （GSH） and myeloperoxidase （MPO）. RESULTS： Pretreatment of ethanol significantly increased NAP-induced gastric lesions, as well as an increase in NDA and MPO. On the contrary, mucosal PGE2 and GSH contents were decreased dramatically by ethanol pretreatment, which were aggravated by NAR DA-9601 significantly reduced NAP-induced gastric injury grossly and microscopically, regardless of pretreatment with ethanol. DA-9601 preserved, or rather, increased mucosal PGE2 and GSH in NAP-treated rats （P〈0.05）, with reduction in mucosal MDA and MPO levels. CONCLUSION： These results suggest that repeated alcohol consumption renders gastric mucosa more susceptible to NSAIDs though, at least in part, reduction of endogenous cytoprotectants including PGE2 and GSH, and increase in MPO activation, and that DA-9601, a new gastroprotectant, can reduce the increased vulnerability of ethanol consumers to NSAIDs-induced gastric damage via the mechanism in which PGE2 and GSH are involved.

Effect of electroacupunture on gastric mucosal intestinal trefoil factor gene expression of stress-induced gastric mucosal injury in rats

AIM： To investigate electroacupunture（EA） at the acupoints of Stomach Meridian of Foot-Yangming（SMFY）, Gallbladder Meridian of Foot-Yangming（SMFY） on gastric mucosal intestinal trefoil factor （ITF） gene expression detection in stress-induced rats with gastric mucosal lesion, and to explore the regulatory mechanism and significance of EA-related gastric mucosal protective effect. METHODS： Forty rats were randomly divided into 4 groups： Blank group, Model group, Model group＋EA at acupoints of SMFY group（＂SMFY group＂）, and Model group＋EA at acupoints of GMFY group（GMFY group）. All rats （except blank group） were made model by water immersion and restraint stress （WRS）. Then the gastric mucosa tissue in each rat was taken off alter assessment of gastric mucosal lesion index（GUI）, and the expression of ITF mRNA of the tissues was detected by reverse transcdption-polymerase chain reaction（RT-PCR） method. RESULTS： Compared with Model group（S4.3± 1.34）, the GUI value in SMFY group （31±2.211 decreased significantly（P〈0.01）, so did that in GMFY group （39.8± 1.62, P〈0.05）, meanwhile GUI value in SMFY group was significantly lower than in GMFY group（P〈0.01）. Compared with Model group （0.65±0.01）, EA had a tendency to improve the expression of gastric mucosal ITFmRNA gene： such tendency existed in GMFY group （0.66±0.01） but with no signficant difference（P〉 0.05）, in SMFY group（0.76±0.01） with an extremely obvious difference （P〈0.01）, furthermore the expression in SMFY group was significantly higher than in GMFY group （P〈 0.01）.CONCLUSION： The gastric mucosal protective effect by EA at the acupoints of SMFY and GMFY was related to the expression variance of ITF, indicating certain meridian specificity exists, It could be one proof for the TCM theory ＂Relative pardcularity between SMFY and stomach＂.

Curcumin prevents indomethacin-induced gastropathy in rats

AIM： To investigate the effects of curcumin on gastric microcirculation and inflammation in rats with indo- methacin-induced gastric damage. METHODS： Male Sprague-Dawley rats were randomly divided into three groups. Group 1 （control group, n = 5） was fed with olive oil and 5% NaHCOf （vehicle）. Group 2 [indomethacin （IMN） group, n = 5] was fed with olive oil 30 min prior to indomethacin 150 mg/kg body weight （BW） dissolved in 5% NaHCO3- at time 0th and 4th h. Group 3 （INN ± Cur group, n = 4） was fed with curcumin 200 mg/kg BW dissolved in olive oil 0.5 mL, 30 min prior to indomethacin at 0th and 4th h. Leukocyte-endothelium interactions at postcapillary venules were recorded after acridine orange injection. Blood samples were determined for intercellular ad- hesion molecule （ICAM）-1 and tumor necrosis factor （TNF）-a levels using enzyme linked immunosorbent assay method. Finally, the stomach was removed for histopathological examination for gastric lesions and grading for neutrophil infiltration. RESULTS： In group 2, the leukocyte adherence in postcapillary venules was significantly increased com- pared to the control group （6.40±2.30 cells/frame vs 1.20 ± 0.83 cells/frame, P = 0.001）. Pretreatment with curcumin caused leukocyte adherence to postcapil- lary venule to decline （3.00±0.81 cells/frame vs 6.40 ± 2.30 cells/frame, P = 0.027）. The levels of ICAM-1 and TNF-aincreased significantly in the indomethacin- treated group compared with the control group （1106.50 ± 504.22 pg/mL vs 336.93 a= 224.82 pg/mL, P = 0.011 and 230.92±114.47 pg/mL vs 47.13±65.59 pg/mL, P = 0.009 respectively）. Pretreatment with curcumin sig- nificantly decreased the elevation of ICAM-1 and TNF-a levels compared to treatment with indomethacin alone （413.66 ± 147.74 pg/mL vs 1106.50 ± 504.22 pg/mL, P = 0.019 and 58.27 ± 67.74 pg/mL vs 230.92 ± 114.47 pg/mL, P = 0.013 respectively）. The histological appear- ance of the stomach in the control group was normal. In the indomethacin-treated group, the stomachs showed a mild to moderate neutrophil infiltration score. Gastric lesions were erosive and ulcerative. In rats treated with indomethacin and curcumin, stomach histopathology improved and showed only a mild neutrophil infiltration score and fewer erosive lesions in the gastric mucosa. CONCLUSION： The results indicate that curcumin pre- vents indomethacin-induced gastropathy through the improvement of gastric microcirculation by attenuating the level of ICAM-1 and TNF-a,

Suicidal ingestion of potassium permanganate

BACKGROUND:Potassium permanganate is used clinically as an antiseptic and antifungal agent.Ingestion of potassium permanganate may result in damage to the upper gastrointestinal tract.Burns and ulceration of the mouth,esophagus and stomach occur due to its action.Emergency endoscopy is useful to assess the severity of damage and also to guide management.METHODS:We reported a patient presenting to the emergency department after suicidal ingestion of potassium permanganate.RESULTS:After treatment,the patient was discharged home on the 7th day after admission.CONCLUSION:Early emergency endoscopy should be considered to determine the extent of upper gastrointestinal damage in the emergency department.

Helicobacter pylori gamma-glutamyl transpeptidase and its pathogenic role

Helicobacter pylori(H.pylori)gamma-glutamyl transpeptidase(GGT)is a bacterial virulence factor that converts glutamine into glutamate and ammonia,and converts glutathione into glutamate and cysteinylglycine.H.pylori GGT causes glutamine and glutathione consumption in the host cells,ammonia production and reactive oxygen species generation.These products induce cell-cycle arrest,apoptosis,and necrosis in gastric epithelial cells.H.pylori GGT may also inhibit apoptosis and induce gastric epithelial cell proliferation through the induction of cyclooxygenase-2,epidermal growth factor-related peptides,inducible nitric oxide synthase and interleukin-8.H.pylori GGT induces immune tolerance through the inhibition of T cell-mediated immunity and dendritic cell differentiation.The effect of GGT on H.pylori colonization and gastric persistence are also discussed.

Effects of moxibustion pretreatment on extracellular signal-regulated kinase signaling transduction pathway in the gastric tissues of rats with gastric mucosal damage

Objective： To observe the effects of moxibustion pretreatment on the protein expressions of epidermal growth factor receptor （EGFR）, phosphorylation extracellular signal-regulated kinase I/2 （p-ERKI/2） and activated protein-1 （AP-2）, the key factors of extracellular signal-regulated kinase signaling transduction pathway in gastric tissue of rats with stress-induced gastric mucosal damage, and to discuss the mechanisms of moxibustion therapy in promoting the restoration of damaged gastric mucosa. Methods： Thirty Sprague-Dawley （SD） rats were randomly divided into a normal group, a model group, and a moxibustion group using the random digits table, 10 in each group. Except the rats in the normal group, rats in the other two groups were used to make stress-induced gastric mucosal damage model using restraint and cold stress. Before modeling, rats in the moxibustion group were alternately treated with moxibustion a/t Zusanli （ST 36） and Zhongwan （CV 12）, or Pishu （BL 20） and Weishu （BL 22）, once a day, for a total of 8 d. Histolo^cal changes of gastric mucosa were observed under the light microscopy, the expression of gastric tissue p-ERKI/2 was detected by immunohistochemistry assay, and the protein levels of EGFR and AP-I were measured by Western blots. Results： Compared with rats in the normal group, gastric mucosal damage was more serious, and protein expressions of gastric tissue EGFR, p-ERK1/2 and AP-1 increased in the model group （P〈0.01, P〈O.05, P〈0.05）. Compared with rats in the model group, gastric mucosal damage was milder, and protein expressions of gastric tissue EGFR, p-ERK1/2 and AP-1 increased in the moxibustion group （all P〈0.01）. Conclusion： Moxibustion at Zusanli （ST 36）, Zhongwan （CV 12）, Pishu （BL 20） and Weishu （BL 21） could increase EGFR, p-ERK1/2 and AP-1 expression levels in gastric tissue of stress-induced gastric mucosal damage rats, maintain the information transfer function of ERK signaling transduction pathway, and promote restoration of gastric mucosal damage.

Organic carbon monoxide prodrug, BW-CO-111, in protection against chemically-induced gastric mucosal damage

Metal-based carbon monoxide(CO)-releasing molecules have been shown to exert antiinflammatory and anti-oxidative properties maintaining gastric mucosal integrity.We are interested in further development of metal-free CO-based therapeutics for oral administration.Thus,we examine the protective effect of representative CO prodrug,BW-CO-111.in rat models of gastric damage induced by necrotic ethanol or aspirin,a representative non-steroidal anti-inflammatory drug.Treatment effectiveness was assessed by measuring the microscopic/macroscopic gastric damage area and gastric blood flow by laser flowmetry.Gastric mucosal mRNA and/or protein expressions of HMOX1,HMOX2,nuclear factor erythroid 2-related factor 2,COX1,COX2,iNos,Anxa1 and serum contents of TGFB1,TGFB2,IL1 B,IL2,IL4,IL5,IL6,IL10,IL12,tumor necrosis factorα,interferonγ,and GM-CSF were determined.CO content in gastric mucosa was assessed by gas chromatography.Pretreatment with BW-CO-111(0.1 mg/kg,i.g.)increased gastric mucosal content of CO and reduced gastric lesions area in both models followed by increased GBF.These protective effects of the CO prodrug were supported by changes in expressions of molecular biomarkers.However,because the pathomechanisms of gastric damage differ between topical administration of ethanol and aspirin,the possible protective and anti-inflammatory mechanisms of BW-CO-111 may be somewhat different in these models.

Effect of moxibustion stimulation on repair of injured gastric mucosa after common peroneal nerve transection

Objective： To investigate the protective effect of moxibustion in initiating the endogenous protection information on gastric mucosa, and its relationship with the pathway of common peroneal nerve. Methods： Forty-eight Sprague-Dawley（SD） rats were randomly divided into a normal group（group A）, a model group（group B）, a moxibustion model group（group C） and a moxibustion model plus surgery group（group D）, 12 in each group. Except for group A, rats in the other groups were treated with dehydrated ethanol and aspirin to prepare gastric mucosal damage model. The rats in group B were not treated with any interventions; rats in group C received moxibustion at Zusanli（ST 36）, twice a day for continuous 3 d. The rats in group D were subjected to preparing the gastric mucosal damage model after the common peroneal nerve transection, followed by moxibustion at Zusanli（ST 36）. After a 3-day intervention, ulcer index（UI） in each group was observed, and the levels of gastric mucosa-related repair cytokines of tumor necrosis factor-α（TNF-α）, interleukin-4（IL-4） and heat shock protein 70（HSP70） were detected. Results： Compared with group A, the pathological changes and UI of group B were worse（P=0.000）, but TNF-α in serum and tissue was changed significantly（P=0.000, P=0.002）, IL-4 in serum and tissue was improved significantly（P=0.000, P=0.000）. Compared with group B, TNF-α and IL-4 in group C and group D were significantly improved（TNF-α： P=0.003, P=0.016; IL-4： P=0.000, P=0.002）. Compared with group C, the changes of UI in group B and group D were poor（both P=0.000）; the levels of TNF-α and IL-4 in serum were significantly decreased（TNF-α： P=0.000, P=0.025; IL-4： P=0.000, P=0.034）; and tissue HSP70 levels were decreased significantly（P=0.000, P=0.033）. Conclusion： Zusanli（ST 36） can transmit information through the pathway of common peroneal nerve, regulate the release of gastric mucosal protective factors, and up-regulate the expression of cytothesis-related proteins, so as to achieve the effect in repairing gastric mucosa.

Effect of herbal cake-partitioned moxibustion on MEK1/2 and ERK1/2 expressions of gastric tissues in rats with spleen deficiency syndrome

Objective： To observe the effect of herbal cake-partitioned moxibustion on the expressions of mitogen-activated protein kinase （MEK：1/2） and extracellular regulatory protein kinase （ERK：1/2） in gastric tissues of rats with spleen deficiency syndrome, and to explore the possible mechanisms of herbal cake-partitioned moxibustion in treating spleen deficiency syndrome. Methods： Sixty Sprague-Dawley （SD） rats were randomly divided into a blank control group （group A）, a model group （group B）, a ranitidine group （group C）, and a herbal cake-partitioned moxibustion group （group D） by random digit, 15 rats in each group. Rat models of spleen deficiency syndrome were made by intragastric administration of 4℃ 200% concentrated Da Huang （Radix et Rhizoma Rhei）. After successful modeling, the rats in group C were treated with 25 mg/（kg.bw） ranitidine by intragastric adminstration and rats in group D were treated with herbal cake-partitioned moxibustion at Zusanli （ST 36） and Zhongwan （CV 12）, for 8 d. Excepted for rats in group A, all the other rats were treated with indomethacin at 5 mg/（kg.bw） at 8：00 a.m. on the second day after finishing all the intervention and sacrificed 7 h later to isolate the stomach. Histopathological changes of the gastric tissues were observed under light microscope after hematoxylin-eosin （HE） staining. The protein expressions of MEK：1/2 and ERK：1/2 in the gastric tissues were detected by immunohistochemistry. Results： After intervention, the gastric mucosal injury in group B was significantly severer than that in group A, with large breakage and ablating; the damage of gastric mucosa was decreased in group C compared with group B; the gastric mucosal surface remained relatively complete, and the status of breakage and ablating was significantly improved. After intervention, compared with group A, the protein expressions of MEK：1/2 and ERK：12 in gastric tissues of the other groups were significantly higher （P〈0.01）. Compared with group B, the protein expressions of MEK：1/2 and ERK：1/2 in group C and D were significantly higher （all P〈0.01）. Compared with group C, the protein expressions of MEK：1/2 and ERK：1/2 in group D were significantly higher （P〈0.01）. Conclusion： Herbal cake-partitioned moxibustion promotes the repair of gastric mucosa in rats with spleen deficiency syndrome, via improving protein expressions of MEK：1/2 and ERK：1/2 in gastric tissues, as well as activating MEK/ERK signaling pathway.

Effect of oxytocin on gastric ischemia-reperfusion injury in rats

The effect of peripherally administered oxytocin(OT)on gastric ischemia-reperfusion injury(GI-RI)and its possible mechanism were investigated.The Sprague-Dawley(SD)rats were randomly divided into different treatment groups(n=6).The animal GI-RI model was established by clamping the celiac artery for 30 min to induce ischemia and then released to allow reperfusion for 1 h,and the degree of GI-RI was assessed by scoring the gastric mucosal damage index(GMDI),the gastric fluid output,gastric fluid output,gastric acidity were measured and the surgical preparations of vagotomy and sympathectomy were used to investigate the possible mechanism of OT on GI-RI.The results were as follows.Compared with the control group(NS plus GI-R only,GMDI 121.33P10.40,n=6),the intra peritoneal(ip)administration of oxytocin(20,100μg/0.5 mL)obviously attenuated GI-RI(P<0.05),GMDI were 82.33P14.26,53.5P5.58 respectively(n=6);the gastric fluid output and the gastric acidity(evaluated by pH)of the control group were(430.17P87.36)μL,1.55P0.25(n=6),and those of the OT group were(102.45P48.00)μL,2.65P0.40(n=6)res pectively;differences had statistical significance(P<0.01).The effect of oxytocin was reversed by atosiban,a selective oxytocin receptor antagonist.The GMDI of the group given atosiban 10 min before OT was 138.17P24.06(n=6),which had no significant difference with the control group.Oxytocin further attenuated GI-RI after vagotomy and sympathectomy(GMDI 6.83P8.89,29.67P5.54,n=6),compared with the GI-R group and the oxytocin group(P<0.01).These results indicated that the oxytocin could significantly protect gastric mucosal against injury induced by ischemia-reperfusion,and the oxytocin receptor was involved.This effect of oxytocin may be mediated through the vagus and sympathetic nerve,and then lead to the reduction of gastric juice output and the depression of gastric acidity.

Effects of different doses of ginger-partitioned moxibustion on trefoil factor 1,mucin 5AC and epidermal growth factor receptor in rats with spleen deficiency syndrome

To observe the effects of different doses of ginger-partitioned moxibustion on serum trefoil factor 1 （TFF1） and mucin 5AC （MUCSAC） levels, as well as the expression of epidermal growth factor receptor （EGFR） in gastric mucosa of rats with spleen deficiency syndrome, therefore, to explore the possible mechanism and the dose-effect characteristics of ginger-partitioned moxibustion in spleen deficiency syndrome. Methods： Seventy-five SPF grade Sprague-Dawley （SO） rats were randomly divided into a blank control group （group A）, a model group （group B）, a 3 moxa-cone ginger-partitioned moxibustion group （group C1）, a 6 moxa-cone ginger-partitioned moxibustion group （group C2） and a 9 moxa-cone ginger-partitioned moxibustion group （group C3） using random number table method, 15 rats in each group. Except group A, rats in the other groups received intragastric administration of 4 ~C 200% concentrated Da Huang （Radix et RhizomaRhei） to prepare spleen deficiency syndrome model. After successful modeling, rats in group B received no treatment; rats in group C1, C2 and C3 were treated with 3, 6 and 9 moxa-cone ginger-partitioned moxibustion at Zusanli （ST 36）and Zhongwan （CV 12） respectively for 8 continuous days. The general symptom score of rats was observed. The serum levels of TFF1 and MUC5AC were detected by enzyme-linked immunosorbent assay （ELISA）. The expression of EGFR protein in gastric mucosa was detected by immunohistochemistry. Results： After the treatment, compared with group A, the spleen deficiency symptom score was increased in group B, the levels of serum TFF1 and MUC5AC, the EGFR protein expression in gastric tissues of group C1, C2 and C3 were significantly increased （all P〈0.01）; compared with group B, the spleen deficiency scores were decreased in group C1, C2 and C3, and the serum levels of TFF1 and MUC5AC, as well as EGFR protein expression in gastric tissues were increased （all P〈0.01）. Compared with group C1, the spleen deficiency scores were decreased in group C2 and C3, the serum levels of TFF1 and MUC5AC, and the expression of EGFR protein in gastric tissues were increased （all P〈0.01）, however, there was no significant difference between group C2 and C3 （all P〉0.05）. The mechanism may be related to the increase of serum TFF2 and MUC5AC levels and activation of EGFR protein. Conclusion： Ginger-partitioned moxibustion can improve the symptoms, as well as promote the proliferation and repair of gastric mucosa in rats with spleen deficiency. The therapeutic efficacy of 6 or 9 moxa-cone ginger-partitioned moxibustion is better than that of 3 moxa-cone ginger-partitioned moxibustion, while the efficacies are equivalent between 6 and 9 moxa-cone Ringer-Dartitioned moxibustion groups.