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Stress-induced gastric mucosal lesion (SGML) is one of the most common visceral complications after trauma. Restraint water-immersion stress (RWIS) can induce gastric mucosal lesion within a few hours. It has been confirmed that hyperfunction of parasympathetic nervous system contributes to the gastric dysfunction induced by RWIS. The dorsal motor nucleus of vagus, nucleus of solitary tract, hypothalamic supraoptic nucleus, paraventricular nucleus, mediodorsal thalamic nucleus, central amygdaloid nucleus and medial prefrontal cortex are all involved in the formation of SGML. Neurotransmitter/neuromodulation such as substance P, acetylcholine, oxytocin may be involved in the physiological process. This article reviewed the nervous mechanism of gastric mucosal lesion induced by RWIS in rats.
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Objective To investigate the expression of NADPH oxidase Nox-4 induced by stress in gastric mucosa and its role in inflammation.Methods Twenty male SPF Kunming mice were randomly divided into chronic restraint stress group(stress group) and control group.Stress mice were restrained in selfmade restraint device for 2 hours each day.The rest of the time,the mice in the two groups had free access to food and water normally,experiment lasted 14 days.The histopathological changes of gastric mucosa were assessed by HE staining under light microscope.The expression of Nox-4 in gastric mucosa of mice was carried out by immunohistochemical method.The relative expression levels of Nox-4,antioxidant protein (Mn-SOD,GSH,Catalase) and inflammatory factors(IL-8,IL-1β,TNF-α) in gastric mucosa were detected by real-time quantitative RT-PCR and ELISA.Results Basal cell proliferation,neutrophil,eosinophil and plasma cell infiltration and inflammatory changes were observed in the lamina propria and glandular epithelium of stress mice,while no obvious abnormalities were found in control mice.The expression of Nox-4 in stress group was deeper and more abundant than that in control group,mainly expressed in lamina propria and glandular epithelium.The mRNA expression levels of Nox-4 in gastric mucosa of stress group was(2.42±0.51) times higher than that of control group,and blood concentration of stress group was(2.23±0.67) times higher than that of control group(t=-46.32,P＜0.001).The RT-PCR of antioxidant proteins in gastric mucosa showed that the transcription levels of Mn SOD,GSH and Catalase in stress group were significantly lower than that of control group (Mn-SOD:0.59± 0.10,GSH:0.58± 0.11,Catalase:0.57± 0.09),and there were significant differences between the two groups(t=13.57,11.67,15.01,P＜0.01).RT-PCR results showed that the transcription levels of IL-8,IL-1β,TNF-α in stress group were significantly higher than those in control group (IL-8:1.47±0.34,IL-1β:1.48 ± 0.42,TNF-α:1.51 ± 0.37),and there were significant differences in two groups(t=-18.45,-19.14,-20.85,P＜0.01).ELISA results showed that the serum levels of inflammatory factors in stress group were significantly higher than those in control group(2.25±0.37,3.59±0.45,3.41±0.34),and the differences were statistically significant(t=-47.11,-79.36,-96.32,P＜0.01).Pearson correlation analysis showed that there was a positive correlation between serum concentration of Nox-4 and inflammatory factors(IL-8,IL-1β,TNF-αt) in stress group(r=0.97,0.99,0.98,P＜0.01).Spearman rank correlation analysis showed that the grade of gastric mucosal inflammation was positively correted with serum levels of Nox-4 and inflammatory factors (IL-8,IL-1β,TNF-α) (r =0.96,0.92,0.91,0.94,all P＜ 0.01)Conclusion Stress may lead to gastric mucosal lesion by overexpression of proinflammatory factors through destroying the balance of oxidation/antioxidant system in gastric mucosa.
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Objective To explore risk factors of influencing operating efficiency of endoscopic submucosal dissection (ESD) for gastric mucosal lesions. Methods The data of 304 cases with gastric mucosal lesion undergoing ESD in Xijing Hospital of Digestive Disease from April 2009 to February 2017 were retrospectively analyzed. The procedure time and complete resection rate ( R0 resection rate ) were regarded as indicators of ESD efficiency. Risk factors influencing procedure time and R0 resection rate were analyzed using Chi-square test and logistic regression. Results Using median procedure time of 45 min as the cutoff value, Chi-square test showed that specimen size ( P=0. 000) , lesion location ( P=0. 001) , and pathological type ( P=0. 003) affected the operation time. Further logistic regression analysis indicated that specimen size (≥40 mm/<40 mm, P<0. 001, OR=3. 748, 95％CI: 2. 247-6. 254) and lesion location (upper or middle 1/3 of stomach/lower 1/3 of stomach, P=0. 001, OR=2. 180, 95％CI: 1. 318-3. 606) were independent risk factors of procedure time. Using R0 resection as outcome measure, neither single nor multiple parameter analysis was statistically significant. Conclusion Specimen size and lesion location are independent risk factors influencing efficiency of gastric mucosal ESD, and could be possibly used to estimate the procedure time of ESD.
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OBJECTIVE:To study the protective effects of Polygonum hydropiper extract on acute gastric mucosal lesion (AGML)in rats. METHODS:48 rats were randomly divided into normal group(normal saline),model group(normal saline), positive group(ranitidine hydrochloride,0.05 g/kg),P. hydropiper extract low-dose,medium-dose and high-dose groups(2.7, 8.1,24.3 g/kg by crude drug),i.g. for consecutive 7 d,once a day. Except for normal group,other groups were given absolute ethyl alcohol to induce AGMI model after 1 h of last administration. 1.5 h after modeling,gastric mucosal lesion index of rats was calculated;the pathological changes of gastric tissue in rats were observed;nuclear factor E2 related factor 2(Nrf2)content and SOD activity in gastric tissue of rats were determined by ELISA. RESULTS:Compared with normal group,the gastric mucosa of model group was damaged obviously,there was blood capillary rupture in submucosa,gastric mucosal lesion index was increased significantly(P<0.01);Nrf2 content and SOD activity were significantly decreased in gastric tissue of rats(P<0.05 or P<0.01). Compared with model group,gastric mucosal lesion of rats was relieved to different extent;in positive group,P. hydropiper extract medium-dose and high-dose groups,gastric mucosal lesion index was decreased significantly(P<0.05),and Nrf2 content and SOD activity were increased significantly(P<0.05 or P<0.01). CONCLUSIONS:P. hydropiper extract has good protective effect on absolute ethyl alcohol-induce AGMI,the mechanism of which may be associated with raising Nrf2 content and enhancing SOD activity in gastric mucosal tissue.
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AIM:To observe the antiulcer effect of butyric acid and hydrogen , the main metabolites of Clos-tridium butyricum (C.butyricum), and to explore the underlying mechanism .METHODS: The mouse model of acute gastric mucosal lesion was prepared by gavage with ethanol .The mice were randomly divided into 4 groups:normal group , model group , butyric acid group and hydrogen group .The mice in butyric acid group and hydrogen group were given buty-rate and hydrogen prior to model establishment , respectively .Macroscopic observation of the pathological changes in gastric tissues was performed to evaluate the effect of the 2 metabolites of C.butyricum.Meanwhile, the mRNA expression levels of inflammatory factors, such as IL-12, RAN1 and MCP-1, were determined by RT-qPCR.The expression levels of apopto-sis-related proteins Bcl-2 and Bax were detected by immunohistochemical staining .RESULTS:The macroscopic observa-tion found that butyrate , not hydrogen , protected gastric mucosa .HE staining also showed that butyrate significantly attenu-ated the pathological damage of the gastric mucosa induced by ethanol .Compared with model group , the mRNA levels of inflammatory factors IL-12, RAN1 and MCP-1 in butyrate group significantly decreased (P<0.01).In butyrate group, the protein level of Bax was obviously decreased compared with model group (P<0.01), while the protein level of Bcl-2 was significantly increased ( P<0.01 ) .CONCLUSION: The gastric mucosa protective metabolite of C.butyricum may be butyric acid , not hydrogen .Butyric acid protects the gastric mucosa against ethanol-induced lesion by inhibiting the inflam- mation and reducing the expression ratio of Bax/Bcl-2.
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AIM:To observe the antiulcer effect of butyric acid and hydrogen , the main metabolites of Clos-tridium butyricum (C.butyricum), and to explore the underlying mechanism .METHODS: The mouse model of acute gastric mucosal lesion was prepared by gavage with ethanol .The mice were randomly divided into 4 groups:normal group , model group , butyric acid group and hydrogen group .The mice in butyric acid group and hydrogen group were given buty-rate and hydrogen prior to model establishment , respectively .Macroscopic observation of the pathological changes in gastric tissues was performed to evaluate the effect of the 2 metabolites of C.butyricum.Meanwhile, the mRNA expression levels of inflammatory factors, such as IL-12, RAN1 and MCP-1, were determined by RT-qPCR.The expression levels of apopto-sis-related proteins Bcl-2 and Bax were detected by immunohistochemical staining .RESULTS:The macroscopic observa-tion found that butyrate , not hydrogen , protected gastric mucosa .HE staining also showed that butyrate significantly attenu-ated the pathological damage of the gastric mucosa induced by ethanol .Compared with model group , the mRNA levels of inflammatory factors IL-12, RAN1 and MCP-1 in butyrate group significantly decreased (P<0.01).In butyrate group, the protein level of Bax was obviously decreased compared with model group (P<0.01), while the protein level of Bcl-2 was significantly increased ( P<0.01 ) .CONCLUSION: The gastric mucosa protective metabolite of C.butyricum may be butyric acid , not hydrogen .Butyric acid protects the gastric mucosa against ethanol-induced lesion by inhibiting the inflam- mation and reducing the expression ratio of Bax/Bcl-2.
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Objective To investigate the clinical safety and efficacy of endoscopic submucosal dissection (ESD) in the treatment of superficial lesions of gastric mucosa, and to analyze the related factors and management of complications of ESD treatment. Methods We retrospectively analyzed the clinical data of 116 patients with superficial lesions of gastric mucosa undergoing ESD, evaluated the efficacy of ESD, observed the appearance and treatment of complications of ESD, and analyzed the factors influencing intraoperative and postoperative complications. Results The ESD was successfully completed in all cases, with the en bloc resection rate being 99.1% (115/116) and the complete cure rate being 95.7% (111/116). The average tumor size was (25.0 ± 11.6) mm, and the average operation time was (56.6 ± 20.5) min. The incidence rates of acute slight bleeding during operation and delayed bleeding were 3.4% (4/116) and 0.9% (1/116), respectively, without acute hemorrhage; 5 cases of bleeding were successfully treated by coagulation hemostasis and hemoclip. Perforation occured in 3 cases (2.6%) and was closed by hemoclip during operation; all cases of perforation had no pneumoperitoneum and were treated successfully by conservative method. Review at 2 months after ESD showed that the ulcer healing rate was 100%. The average follow-up time was (20.3 ± 5.1) months. Gastric angle χ2 = 7.937, P = 0. 01) and the postoperative pathological results as early carcinoma (χ2= 9.145, P=0. 005) were risk factors influencing the intraoperative bleeding and perforation complications. Conclusion ESD is a safe and effective minimally invasive treatment, and has high operation success rate. The prevention of bleeding should be emphasized during and after ESD operation. Perforation complications also should be discovered during the early stage of operation, which can contribute to complete effective closure of perforation under endoscope inmost cases.
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<p><b>OBJECTIVE</b>To observe the influence of electroacupuncture (EA) at lower-sea points of stomach, large intestine, small intestine and gallbladder on interleukin-1β (IL-1β), high mobility group protein 1 (HMGB 1) and alpha 7 nicotinic acetylcholine receptor (nAchR α7) in rats with acute gastric mucosal lesion (AGML), so as to explore whether there is relative specificity in treating gastric viscera disease by stimulating Zusanli (ST 36).</p><p><b>METHODS</b>Sixty healthy SD rats were randomly assigned into a blank group, a model group, a Zusanli group, a Shangjuxu group, a Xiajuxu group and a Yanglingquan group, ten rats in each one (half male and half female). The WRS method was applied to induce the AGML model except the rats in the blank group. The rats in the blank group were treated with routine diet; the rats in the model group were treated with immobilization at rat platform, 30 min per time; the rats in the Zusanli group, Shangjuxu group, Xiajuxu group and Yanglingquan group were treated with acupuncture and connected with EA device (dilatational wave 10 Hz/50 Hz, positive electrode on the left side and negative electrode on the right side, intensity was appropriate when rat hind leg slightly shook), 30 min per time. The treatment was given once a day. After consecutive 10-day treatment, the gastric tissue was collected and the damage of gastric mucosa was evaluated; ELISA method was applied to measure the content of serum IL-1β and tissue HMGB 1; the Western blot method was applied to measure the expression of nAchR α7 receptor.</p><p><b>RESULTS</b>(1) Compared with the model group, the ulcer index (UI) of gastric mucosa, serum IL-1β and tissue HMGB 1 were lower, and the expression of nAchR α7 was increased in the remaining groups (<0.05,<0.01). (2) Compared with the Zusanli group, the UI of gastric tissue, serum IL-1β and tissue HMGB 1 were higher in the Shangjuxu group, Xiajuxu group and Yanglingquan group (<0.05,<0.01), and the expression of nAchRα7 was reduced in the Yanglingquan group (<0.01).</p><p><b>CONCLUSIONS</b>(1) EA at digestive system-related lower-sea points, through IL-1β, HMGB 1 and nAchR α7, could regulate immune response, lighten inflammatory reaction and reduce mucosal injury, which could realize the intervention effect on AGML rats. (2) From the comparison, it is concluded the intervention effect of Zusanli group is superior to the other groups, partly indicating the relative specificity between Zusanli and stomach.</p>
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Objective To investigate the role of TRPV1 in exacerbation of gastric mucosal injury in a rat water immersion restraint stress (WIRS) model by acute postoperative pain. Methods Thirty Wistar rats were randomly divided into normal controlled group (N group, n=10), WIRS model group (WIRS group, n=10) and surgery after WIRS group (WS group, n = 10). The general extent of gastric mucosal injury was observed and assessed for gastric mucosal ulcer index (UI), intragastric pH and serum SOD/MDA ratio were measured and the expression of TRPV1 mRNA in gastric mocusal was accessed by Real-time Quantitative PCR. Immunohistochemistry was performed to detect the mean density of TRPV1. Results Compared with NC group, WIRS group showed obvious gastric mocusal injure with higher UI , lower values of intragastric pH serum SOD/MDA ratio and TRPV1 (P<0.05). The treatment with surgery after onset of WIRS significantly aggravated the gastric mucusal erosion and hemorrhage, with UI increased (P < 0.05), the value of intragastric pH, serum SOD/MDA ratio and TRPV1 further reduced (P < 0.05). Meanwhile, TRPV1 was inversely correlated with UI, and positively associated with intragastric pH and serum SOD/MDA ratio. Conclusion TRPV1 expression in gastric mocusal of AMGL model is inhibited by acute postoperative pain. TRPV1 may involve in the exacerbation of gastric mucosal injury in WIRS model by acute postoperative pain.
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Objective to investigate the protective effect of omega-3 fish oil fat emulsion on cyclophosphamide-induced gastric mucosal injury in mice. Methods Forty-five kunming mice were randomly divided into three groups as control,model,and omega-3 fish oil fat emulsion group(with 15 mice in each group). Mice of the two experiment groups were administrated with cyclophosphamide i.p. for 2 days to establish the damage model. then mice in omega-3 fish oil fat emulsion group received omega-3 fish oil fat emulsion at a dose of 15 mL/kg daily for 14 days. Meanwhile,the ani-mals in control group and model group were intravenously administered with the same volume of saline. the weight and food intake of the mice in each group were assessed daily. Five mice in each group were respectively sacrificed at day 1,day 7,day 14 after intravenous injection. Morphology of gastric mucosa was observed by HE staining and the activities of SOD and MAO in gastric mucosa were measured respectively by xanthine oxida-tion and ultraviolet spectrophotometry methods. Results Compared with the model group,the general status,nutritional status and the injury in stomach mucosa in omega-3 fish oil fat emulsion group were significantly improved. After 14 day′s treatment,the activities of SOD and MAO in gas-tric mucosa of mice in omega-3 fish oil fat emulsion group were significantly increased(P < 0.05)compared with model group. Conclusion omega-3 fish oil fat emulsion has a significant protective effect on the cyclophosphamide induced injury in gastric mucosa of mice,which may be related to the upregulation of MAO and SOD.
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Objective To discuss the therapy for acute gastric mucosal lesion(AGML)after pericardial devascularization of advanced schistosomiasis. Methods Fifteen advanced schistosomiasis patients with AGML after pericardial devascularization re-ceived supporting therapy,reducing stomach acid and protecting gastric mucosa therapy,reducing gastric blood flow therapy,en-doscopic spraying topical hemostatic agents or electric coagulation therapy,etc. Results After pericardial devascularization of ad-vanced schistosomiasis,15 patients occurred AGML,and among which,10 cases occurred from 8 to 14 days,and the shortest pe-riod was 5 days and the longest was 23 days. Among the 15 patients,13 patients were cured(86.7%),and 2 died. Conclusion The comprehensive therapy including supporting therapy,reducing gastric acid and protecting gastric mucosa,and endoscopic he-mostasis is effective in the treatment of AGML.
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Objective To observe the coexistence expression of TRPV1 and μ-opoid receptorin spinal dorsal root ganglion (DRG) projected to stomach , and to investigate the relationship between TRPV1 andμ-opoid receptorand its clinical significance in rats with acute gastric mucosal lesion induced by water immersion and restraint stress. Methods FortyWistar rats were randomly assigned to 3 groups, including normal control group(group NC, n = 10), WIRS group (group WIRS, n = 20), and sufentanil pretreatment group (group SP, n = 10). A rat model of gsatric mucosal lesion was induced by WIRS. 6 hours after WIRS treatment, gastric tissues were excised and microscopically observed; ulcer index (GI) was noted. The coexistence expression of TRPV1 and μ-opioid receptor in DRG neurons was detected by immunofluorescence assay, and the levels of CGRP was measured by ELASA. Results As compared withgroup WIRS, the degree of gastric injury was obviously relieved in group SF. Coexistence of TRPV1 and μ-opioid receptor was detected in thoracic DRG neurons projected to stomach; the CGRP level was higher in group WIRS than in group NC. ConclusionsTRPV1 isinvolved in protection of acute gastric mucosal lesion. Activation of μ-opioid receptor can induce TRPV1 to release CGRP, resulting in protection of gastric mucosa.
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Objective To discuss the effect of growth hormone(GH) on acute gastric mucosal lesion(AGML) in rats.Methods 120 Wistar rats were divided into four groups randomly: blank control group(n=8),simple model group(n=32),model+rhGH group(n=40) and model+cimetidine group(n=40).Animal models of AGML were set up through soak and tie of rats.GH was injected to the rats in experimental groups,while cimetidine was used in the positive control group.Morphologic changes of rat gastric mucosa in each group were observed and compared on different days(0,4,8,12 d) after stress through gross looking,light microscope,and electron microscope.Ulcer index(UI),secretion amount of gastric acid,pH value and gastric mucosal were compared.Results Compared with blank control and model+cimetidine groups,the histomorphologic changes of gastric mucosa were obviously alleviated in model+rhGH group: only part of epithelial cells swelled,red blood cells were seldom seen,neutrophils infiltration reduced obviously,no remarkable changes were observed in the submucosal tissue.Mucosal cells were in good state and degeneration were seen in only a few cells under the electronic microscope.In addition,UI and the degree of gastric mucosal atrophy in model+rhGH group were lower than that in control group significantly(P
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Objective The aim of this study was to investigate the relationship of gastric mucosal lesions and the parietal oxyntic function in rats under stress as a result of seawater-immersion after open abdominal injury. Methods Thirty-two SD rats were subjected to open abdominal injury followed by seawater immersion. The animals were randomly divided into four groups: control, 1h, 2h, 3h stress for 1h, 2h, and 3h groups. The pH value of gastric juice and gastric mucosal ulcer index (UI) were measured. The gastric mucosal lesions were observed with light microscopy, and the ultrastructural changes in parietal cells were observed by transmission electron microscopy. Results There was a significantly negative relationship between UI and pH value (r=-0.70,P
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To investigate the role of ET 1 in the pathogenesis of SU, a model was established by cold restraint stress(CRS) inducing rat ulcer, immunohistochemistry(IHC)ABC method and radioimmunoassay(RIA) methods were used to determine ET 1 content and to study the expression and location of ET 1 in stomach of normal and CRS rats,and to evaluate the ulcer index(UI). IHC showed that ET 1 was stained as brownish grains,localized in the cytoplasm of vascular endothelial cells, stomach smooth muscle cells, gastric epithelial and vascular smooth muscule cells around lamina muscularis mucosae in stomach. The proportion of ET 1 positive cells was significantly higher in 3h poststress gastric mucosa than in normal gastric mucosa in rats by IHC( P
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To observe the protective effect of takepron(lansoprazole)on the gastric mucosal lesion in rats and its mechanisms . Before gastric mucosal lesion was produced in rats with pure alcohol,takepron was administered into the gastric lumen, and N? nitro L arginine methyl ester(L NAME) and L arginine were injected intravenously. Gastric mucosal blood flow(GMBF)was assessed with laser Doppler flowmetry,gastric mucosal and serum NO - 2 /NO - 3 were measured by cadmium granulation reduction and colorimetric method,and the gastric mucosal ulcer index(UI),the degree of tissue necrosis and neutrophil infiltration were observed . The results showed that UI of the takepron group was much lower than that of the control group( P
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Granulocyte elastase released from activated leukocytes plays an important role in leukocyte infiltration. Since activated leukocytes have been shown to be involved in the pathogenesis of gastric mucosal lesion formation induced by indomethacin, inhibition of granulocyte elastase release from activated leukocytes may be useful in the prevention of these lesions. Rikkunsi-to and ONO-5046, a granulocyte elastase inhibitor, markedly inhibited gastric mucosal lesion formation in rats. Gastric myeloperoxidase activity was significantly increased 3 hours after indomethacin administration. This increase was significantly inhibited by Rikkunsi-to and ONO-5046. Rikkunsi-to inhibited granulocyte elastase release from activated neutrophils in vitro while cimetidine did not. Although cimetidine markedly prevented the indomethacin-induced gastric mucosal lesion formation, it did not reduce gastric myeloperoxidase activity. Therefore, unlike cimetidine, Rikkunsi-to may prevent indomethacin-induced gastric mucosal lesion formation by inhibiting neutrophil activation.
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AIM: To investigate the protective effects and its mechanism of Jinkui Gastric Drug(JK). METHODS: The model of gastric mucosal lesion in rats induced by hydrochloride acid-aspirin was used.The indexes of gastric mucosal lesion in JK and control groups were observed.The contents of nitric oxide(NO) and the activity of nitric oxide synthase(NOS) in blood serum and gastric tissue in rats,the levels of 6-keto-PGF_(1?),thromboxane B_2(TXB_2) in blood plasma and epidermal growth factor(EGF) in blood serum were examined. RESULTS: The index of gastric mucosal lesion after administration of JK reduced obviously.The contents of NO and the activity of NOS in serum and gastric tissue increased markedly.The levels of 6-keto-PGF_(1?),TXB_2 and EGF increased significantly. CONCLUSION: JK can protect experimental gastric mucosal lesion and its mechanism may be related to increasing the protective factors.
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To explore the significance of endothelin-1 converting enzyme (ECE-1)mRNA expression in the development and progression of stress ulcer in cold-restraint-stress(CRS) rats, a model was established by CRS-induced ulcers in rats. ET-1 contents in plasma and gastric mucosa of rats were measured by using radioimmunoassay(RIA)method, gastric mucosa blood flow(GMBF) in rats were determined by using laser-doppler flowmetry, ulcer index(UI) in rats was estimated according to"Guth standard", and the expression levels of ECE-1mRNA in gastric mucosa of normal and CRS rats were measured by using dot blot and reverse transcription-polymerase chain reaction(RT-PCR). The results indicated that compared with control values,the ET-1 contents in both plasma and gastric mucosa of CRS rats were increased significantly after stress (P