Ethanol-induced gastric mucosal

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Effects of pithecellobium jiringa ethanol extract against ethanol induced gastric mucosal injuries in Sprague Dawley rats

Effects of pithecellobium jiringa ethanol extract against ethanol induced gastric mucosal injuries in Sprague Dawley rats

The oral administration of absolute ethanol to rats produces linear hemorrhagic lesions, extensive submucosal edema, inflammatory cell infiltration, and epithelial cell loss in the stomach, which are the typical characteristics of alcohol injury [13]. The pathogenesis of ethanol-induced gastric mucosal damage occurs directly and indirectly through various mediators, such as lipoxygenase, cytokines, and oxygen-derived free radicals [14]. Mucus secretion is regarded as a crucial defensive factor in the protection of the gastric mucosa from gastric lesions [15]. The results of the present study showed that P. jiringa extract has an effective anti-ulcer activity against ethanol-induced gastric mucosal injury. The plant extract increased the mucus of the gastric wall, which is consistent with results reported by Thirunavukkarasu et al. [16]. Omeprazole, a proton pump inhibitor (PPI), exhibits an anti-secretory and protective effect [17]. Omeprazole is effective in treating peptic ulcer disease and gastroesophageal reflux in short- and long-term use [18]. The pathogenesis of mucosal damage in the stomach includes the generation of reactive oxygen species (ROS) that appear to play a vital role in the formation of lipid peroxides and is accompanied by the impairment of the activity of antioxidant enzymes in cells [19].
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The gastroprotective effects of hydroalcoholic extract of <em>Monolluma quadrangula</em> against ethanol-induced gastric mucosal injuries in Sprague Dawley rats

The gastroprotective effects of hydroalcoholic extract of <em>Monolluma quadrangula</em> against ethanol-induced gastric mucosal injuries in Sprague Dawley rats

Notes: Mhae effect on the gastric mucosa histology in ethanol-induced gastric mucosal injury in rats. (A) The normal control group. (B) The ulcer control group exhibited a remarkably severe disruption to the gastric mucosa, which deeply penetrated into the mucosa with extensive edema and leukocyte infiltration of the submucosal layer. (C) The omeprazole group shows comparably mild disruption of gastric mucosa with mild edema and leukocytes infiltration of the submucosal layer. (D) rats pretreated with 150 mg/kg showed mild-to-moderate gastric mucosa disruption with edema and leukocyte infiltration of the submucosal layer. (E) rats pretreated with 300 mg/kg displayed mild disruption of the gastric mucosa with edema and leukocyte infiltration of the submucosal layer (H&E stain). The arrows show the H&E evaluation of the gastric mucosa. Abbreviations: h&e, hematoxylin and eosin; Mhae, hydroalcoholic extract of Monolluma quadrangula.
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Protective Effect of Areca Catechu Extract on Ethanol Induced Gastric Mucosal Lesions in Rats

Protective Effect of Areca Catechu Extract on Ethanol Induced Gastric Mucosal Lesions in Rats

Ethanol-induced gastric injury is associated with the significant production of free radicals [31] leading to increased lipid peroxidation, which causes damage to cell and cell membranes [32]. In the present study the level of MDA was significantly increased in ethanol induced gastric mucosal injury. Pretreatment with A. catechu extract attenuated ethanol-induced gastric mucosal injury, and significantly inhibited the gastric mucosal malondialdehyde level, which is an index of lipid peroxidation. The reduced level of MDA suggested the antioxidative activity of A. catechu extract mainly through the presence of flavonoids and procyanidins [11]. Many reports have demonstrated that most injury of gastric mucosa can be reduced by pretreatment with scavengers of reactive oxygen species [32]. Plant flavonoids and procyanidins have been shown to scavenge radicals in a dose dependent manner and therefore are viewed as promising therapeutic drugs for free radical pathologies [33].
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Gastroprotective effect of the traditional herbal medicine, Sipjeondaebo tang water extract, against ethanol induced gastric mucosal injury

Gastroprotective effect of the traditional herbal medicine, Sipjeondaebo tang water extract, against ethanol induced gastric mucosal injury

Sipjeondaebo-tang (Shi-Quan-Da-Bu-Tang in Chinese, Juzen-taiho-to in Japanese) comprises 10 different crude components obtained from natural herbs. It is commonly prescribed for the treatment of a depressed or weakened state including fatigue, anemia and anorexia associated with various diseases [5,6]. Previous experimental reports have shown that Sipjeondaebo-tang exerts various bio- logical activities such as the enhancement of phagocytosis [6], anti-tumor [7], anti-inflammatory [8], and immuno- modulatory [9] properties. However, its antioxidant effect has not been studied sufficiently, and there are no reports about whether Sipjeondaebo-tang water extract (SDTW) can prevent ethanol-induced gastric injury. The present study was done to evaluate the antioxidant activities of SDTW against ethanol-induced gastric injury in rats.
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Evaluation of acute toxicity and gastroprotective activity of curcuma purpurascens BI  rhizome against ethanol induced gastric mucosal injury in rats

Evaluation of acute toxicity and gastroprotective activity of curcuma purpurascens BI rhizome against ethanol induced gastric mucosal injury in rats

Our findings in this study showed that CPRHE can ef- fectively suppress gastric acidity and also suppress the de- struction of gastric wall mucus. It was reported earlier that herbal products could elevate the gastro-defensive system, especially gastric wall mucus secretion in patients with gastric ulcer [33]. The depletion of mucus secretion is one of the pathogenic mechanisms accountable for gastric mucosal erosions [34]. Previous studies have explained the close correlation between suppression of gastric acidity and effectiveness of treatment. The ability to attenuate the gastric acid secretion is considered to be the mainstay of treatment for gastric ulceration [35,36]. One of the stand- ard drug, omeprazole, has shown remarkable healing rates among patients with peptic ulcer because of its ability to minimize the degree of gastric acidity through inhibition of the proton pump [37].
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Mechanisms of gastroprotective effects of ethanolic
leaf extract of jasminum sambac against HCl/ethanol induced
gastric mucosal injury in rats

Mechanisms of gastroprotective effects of ethanolic leaf extract of jasminum sambac against HCl/ethanol induced gastric mucosal injury in rats

in the gastric motility may play a role in the development and prevention of experimental gastric lesions [8]. Relaxation of circular muscles may protect the gastric mucosa through flattening of the folds. This will increase the mucosal area exposed to necrotizing agents and reduce the volume of the gastric irritants on rugal crest [8, 10]. Ethanol produces a marked contraction of the circular muscles of rat fundic strip. Such a contraction can lead to mucosal compression at the site of the greatest mechanical stress, at the crests of mucosal folds leading to necrosis and ulceration [17]. Gastric tissue homogenate from animals pretreated with omeprazole or plant extract showed significant antioxidant activity by decreasing the levels of MDA and by elevating the levels of PGE 2 and SOD in response to oxidative stress due to absolute
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Dynamic observation and analysis of metabolic response to moxibustion stimulation on ethanol-induced gastric mucosal lesions (GML) rats

Dynamic observation and analysis of metabolic response to moxibustion stimulation on ethanol-induced gastric mucosal lesions (GML) rats

Metabolomics is an emerging system biological approach after genomics and proteomics. NMR-based metabolomics can be used to identify metabolic reac- tions and potential biomarkers, it can analyse hun- dreds or even thousands of samples in a relatively short period of time with the help of an auto sample [13]. Meanwhile, metabolomics is a powerful approach for studying pathophysiological processes, and metab- olomic analysis of human samples may shed light on the mechanisms of gastric mucosal and help iden- tify potential therapeutic targets [14]. It can analysis changes of metabolic profiles caused by disease and other stimuli from a holistic view, which coincides exactly with the TCM theory [15]. Nuclear magnetic resonance (NMR) is one of the most commonly used platform in metabolomics studies for its advantages including low per-sample cost, non-invasive and non- selective analysis [16]. Many studies have revealed that the metabolism of amino acids, sugars and lipids in the body is disordered after gastric mucosal injury. Meta- bolic abnormalities are one of the key pathological aspects of gastric mucosal injury [17, 18]. Therefore, the overall regulation characteristics of acupuncture and moxibustion are in line with the technical advan- tages of metabolomics. The use of metabolomics to study acupuncture theory and its mechanism of action may become the common language for Chinese tra- ditional medicine to become international. Currently, metabolomics was increasingly applied for therapeu- tic mechanisms of TCM including moxibustion [19, 20]. In this study, to a better understanding for thera- peutic mechanism of moxibustion on GML rats, the time-related metabolic profiles of samples (stomach, cerebral cortex and medulla) in GML rats were ana- lyzed by 1 H NMR-based metabolomics.
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Cytoprotective effect of benzyl n' (5 chloro indol 3 ylmethylidene)  hydrazinecarbodithioate against ethanol induced gastric mucosal injury in rats

Cytoprotective effect of benzyl n' (5 chloro indol 3 ylmethylidene) hydrazinecarbodithioate against ethanol induced gastric mucosal injury in rats

Rats pre-treated with either omeprazole or various concentrations of BClHC before being given absolute alcohol had significantly reduced areas of gastric ulcer formation compared to rats pre-treated with vehicle, 10% Tween 20 solution (ulcer group) (Table 3 and Figure 2). Moreover, BClHC administration significantly suppressed the formation of the ulcers and it was interesting to note the flattening of gastric mucosal folds in rats pretreated with this compound. It was also observed that protection of gastric mucosa was more prominent in rats pre-treated with 400 mg/kg BClHC (Table 3). In addition, ethanol-induced mucosal damage was significantly and dose-dependently reduced in size and severity by pre-treating the animals with BClHC (the significant inhibition of gastric ulcers in pretreatment with BClHC was compared with omeprazole, which is a standard drug used for curing gastric ulcers).
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<p>Selenium Nanoparticles-Embedded Chitosan Microspheres and Their Effects Upon Alcohol-Induced Gastric Mucosal Injury in Rats: Rapid Preparation, Oral Delivery, and Gastroprotective Potential of Selenium Nanoparticles</p>

<p>Selenium Nanoparticles-Embedded Chitosan Microspheres and Their Effects Upon Alcohol-Induced Gastric Mucosal Injury in Rats: Rapid Preparation, Oral Delivery, and Gastroprotective Potential of Selenium Nanoparticles</p>

Selenium (Se) is an indispensable trace element required for most of the living organisms including ani- mals and human beings. 9 Se-de fi ciency might condone the development of acute gastric mucosal injury induced by alcohol, especially for those living in Se-de fi cient area. 7,10–12 Low-Se diet affects both in fl ammatory cyto- kine production and histological characteristics, especially in the digestive system. 11 As reported, selenium inhibits the formation of ethanol-induced gastric mucosal lesions in rats through prevention of lipid peroxidation and activa- tion of enzymatic radical scavenging. 7 As well, selenium either alone or in combination with N-acetylcysteine and vitamin E has a protective effect against ethanol-caused gastric mucosal injury in rats, by increasing gastric glu- tathione (GSH) and lowering gastric lipid peroxide (LPO) levels. 12 Besides, Se-supplement can be gastroprotective against the gastric mucosal damage induced by water- immersion restraint stress in rats. 13 Apart from its gastro- protective effects, Se can accelerate the healing of gastric mucosal injury caused by chemicals. For instance, this element has a curative effect on gastric ulcer induced by indomethacin. 14 As well, it can accelerate the healing of acetic acid-induced gastric ulcer by facilitating mucosal regeneration, reducing LPO, increasing antioxidant activ- ity and altering mucus secretion response. 15 Collectively, the aforementioned studies indicate that Se-supplement has protective and curative effects upon acute gastric injury, involving the antioxidant activity of this element.
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Banhabaekchulchunma tang, a traditional herbal formula attenuates absolute ethanol induced gastric injury by enhancing the antioxidant status

Banhabaekchulchunma tang, a traditional herbal formula attenuates absolute ethanol induced gastric injury by enhancing the antioxidant status

of gastric mucosa [2]. To protect tissues from the damage induced by oxidative stress, cells contain antioxidant defense systems including catalase, glutathione (GSH), glutathione- S-transferase (GST), glutathione peroxidase (GPx), glutathi- one reductase (GR) and superoxide dismutase (SOD) [3]. The antioxidant defense system protects against the oxida- tive stress induced by ethanol intake by scavenging oxygen- derived free radicals directly or increasing levels of radical scavengers, such as sulfhydryl compounds [4]. Several re- searchers have investigated the effects of many herbal medi- cines in protection against ethanol-induced gastric mucosal injuries by focusing on increases in the antioxidant defense system. Indeed, previous studies have demonstrated such increases with several herbal medicines, such as Argyreia
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Effects of ethanol and arachidonic acid pathway inhibitors on the effectiveness of gastric mucosa cytoprotection

Effects of ethanol and arachidonic acid pathway inhibitors on the effectiveness of gastric mucosa cytoprotection

vestigating the details of ethanol-induced gastric mucosal damage, showed that ethanol administra- tion induced intracellular oxidative stress and pro- duced mitochondrial permeability transition and mitochondrial depolarisation, which resulted in cell death in the mucosa. They also noticed that glu- tathione — an intracellular antioxidant had a pro- tective action against ethanol. Suzuki et al. [36] no- ticed in their investigations that oral administration of ethanol caused an increase in the content of thiobarbituric acid-reactive substances of the injured mucosa in rats. The pretreatment with compounds scavenging both superoxide anions and hydroxyl rad- icals (querticin, alpha-tocopherol, nifedipine and tet- racycline) markedly prevented the ethanol gastric mucosal injury and an increase in the MDA level. Cho et al. [3] and Moghadasian et al. [23] showed that ethanol-induced injury of an antioxidant status in the gastric mucosa was dependent on the concentration of alcohol. Cho showed that oral administration of absolute ethanol caused an increase in the CAT-activ- ity and did not influence the SOD activity. Moghada- sian noticed that 8% ethanol increased the activity of glutathione peroxide dismutase in the gastrointesti- nal tract but undiluted alcohol only increased the glu- tathione peroxide activity in the gastric mucosa.
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 ANTI-ULCER AND ANTIOXIDANT ACTIVITIES OF THE LEAF AQUEOUS EXTRACT OF CORCHORUS OLITORIUS (TILIACEAE) IN RATS

 ANTI-ULCER AND ANTIOXIDANT ACTIVITIES OF THE LEAF AQUEOUS EXTRACT OF CORCHORUS OLITORIUS (TILIACEAE) IN RATS

The present study was carried out to find the possible antiulcer mechanism of action of C. olitorius. Several models of gastric ulcers were induced in rats to evaluate the prophylactic (HCl/ethanol, indomethacin/HCl-ethanol, indomethacin and pylorus ligature) and the healing (Acetic acid and ethanol/aspirin) potential of the leaf queous extract of Corchorus olitorius (ECO). The gastric ulcerations, mucus production, pH, volume and acidity of the gastric juice were measured. Some parameters of oxidative stress (SOD and MDA) were measured in stomach simples obtained from the animals in the indomethacin model. Oral administration of ECO (100, 200 and 400 mg/kg) dose-dependently prevented ulcer formation by HCl/ethanol (4.65%, 39.70% and 46.17% of inhibition), indomethacin/HCl-ethanol (7.97, 34.95 and 45.85%), indomethacin (24.94, 48.83 and 58.44%) and pylorus ligature (36.93, 54.95 and 77.47%). The inhibitory effect of the extract against HCl/ethanol induced ulcer was not suppressed by the pre-treatment with indomethacin (20 mg/kg, i.p.). ECO reduced Shay- ligated gastric acid secretion from 81.20 mEq/l in the controls to 56.57, 53.96 and 49.421 mEq/l for the extract doses 100, 200 and 400 mg/kg, respectively. The ulcer-healing test showed a dose-dependent reduction of ulceration induced by acetic acid and ethanol/aspirin. The highest dose of extract (400 mg/kg) showed a highly significant (p<0.001) reduction of ulcer with corresponding healing rate of 94.08 and 33.75, respectively, for acetic acid and ethanol/aspirin induced ulcers. The prophylactic and healing actions of ECO were associated with significant increases in gastric mucus production. The levels of SOD were improved in rats treated with the extract. The antiulcer activity of ECO in rats was attributed to its ability to reduce acid secretion, to enhance mucosal defense and in vivo antioxidant status.
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BIOCHEMICAL STUDIES ON THE ANTI ULCEROGENIC POTENTIAL OF CARDIOSPERMUM HALICACABUM L  SEEDS

BIOCHEMICAL STUDIES ON THE ANTI ULCEROGENIC POTENTIAL OF CARDIOSPERMUM HALICACABUM L SEEDS

DISCUSSION: Seed oils of C. halicacabum varieties significantly reduced the formation of gastric ulcer in ethanol induced ulcer rat model. A dose dependent response on the intensity of gastric ulceration was noted. However, statistically more effect was noted in var. microcarpum. The increase in potassium content is significant because it alters the hydrogen ion content there by increasing the mucosal protective action. The mucosal defense mechanism may be due to the epithelial cells of the gastric mucosa which are impermeable to hydrogen ions thereby forming a physical barrier 26 . Carbohydrate and protein ratio also supports the above observation. Difference between the two seed oils may be due to the quantitative variation of the biological compounds.
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The antiulcer effect of <em>Cibotium barometz</em> leaves in rats with experimentally induced acute gastric ulcer

The antiulcer effect of <em>Cibotium barometz</em> leaves in rats with experimentally induced acute gastric ulcer

Figure 6 The effect of Cibotium barometz on the histology (hematoxylin and eosin staining) of ethanol-induced gastric mucosa damage in male sprague Dawley rats. Notes: g1 (normal control group) had intact surface mucosal epithelium, no lesion; g2 (ulcerated control group) had a severe disruption of the surface epithelium and necrotic lesions; G3 (omeprazole) had a mild disruption of the surface epithelium and reduction in submucosal edema with leucocyte infiltration. The animals pretreated with C. barometz extract in the g4 (62.5 mg/kg), g5 (125 mg/kg), g6 (250 mg/kg), and g7 (500 mg/kg) groups revealed a moderate-to-mild disruption of the surface epithelium, reduction in submucosal edema, and leucocyte infiltration in a dose-dependent manner as shown by the reduction in or absence of the ulcer area in the treated groups (white arrows), submucosal edema and leucocyte infiltration (blue arrows).
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EVALUATION OF GASTROPROTECTIVE EFFECTS OF  THE ETHANOLIC EXTRACT OF PEPEROMIA  PELLUCIDA (L) KUNTH

EVALUATION OF GASTROPROTECTIVE EFFECTS OF THE ETHANOLIC EXTRACT OF PEPEROMIA PELLUCIDA (L) KUNTH

PPE is effective orally against gastric damage in various experimental models. The result of this study showed that PPE inhibits the formation of gastric ulcer induced by different ulcerogenic drugs by cytodestructive agents. PPE exerts a dose dependent inhibitory action on gastric mucosal lesions caused by various necrotizing agents. A key feature of (gastric) cytoprotection is that a variety of gastric mucosal damage produced by different nectrotizing agents (e. g. 0.6 M HCl, 0.2 M NaOH, 96 % ethanol, 25 % NaCl or thermal stress) without affecting gastric acid secretion (17). Such cytoprotection has commonly been referred to as the ability of prostaglandins to reduce the severe of injury of the gastrointestinal tract induced by an array of noxious agents. Cytoprotection may occur as result of the capacity that some compounds have to induce prostaglandin production, fundamental for mucus protection because they stimulate mucus and bicarbonate synthesis (19). Therefore we can postulate that PPE may have cytoprotective factors based due to the reduction of total lesion area when induced with necrotizing agents .
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Effect of melatonin in oxidant induced gastric mucosal lesions in rat

Effect of melatonin in oxidant induced gastric mucosal lesions in rat

lesions (Fig. 2). The selected antacid drugs were able to significantly decrease the total acidity of the rat gastric content, when compared to the control group (Table 2). There are conflicting results in the literature regarding the antacid drugs in necrotizing agent-induced gastric mucosal damage and protection. Tarnawski et al. (1985) reported that neither ranitidine nor cimetidine was able to protect the gastric mucosa from ethanol-induced lesions. On the contrary, Sener- Muratoglu et al. (2001) reported that both omeprazole and famotidine have a protective effect against gastric mucosal damage induced by acetylsalicylic acid and other non-steroidal anti-inflammatory drugs. These findings suggest that inhibition of acid secretion cannot protect the gastric mucosa from H 2 O 2 -
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Lagerstroemia speciosa L  tannins reduces the gastric mucosal damage caused
by ethanol and cold restraint stress

Lagerstroemia speciosa L tannins reduces the gastric mucosal damage caused by ethanol and cold restraint stress

Gastric hyperacidity and gastro-duodenal ulcers are illnesses that affect a considerable number of people in the world and are considered a very common global problem today. They are induced by several factors for example stress, smoking, nutritional deficiencies and ingestion of non-steroidal anti-inflammatory drugs [7].The etiology of gastro-duodenal ulcers are influenced by various aggressive and defensive factors, such as acid-pepsin secretion, parietals cell, mucosal barrier, mucus secretion, blood flow, cellular regeneration, endogenous protective agents (prostaglandins and epidermic growth factor etc [8]. The modern approach to control gastric ulceration is to inhibit gastric acid secretion, to stimulate epithelial cell proliferation for effective healing. Antioxidant activity has also been studied as the role of the ROS in ulcers in definite [9]. Reactive oxygen species (ROS) have been shown to be to be involved in the etiology of many inflammatory disorders of the gastrointestinal system [10]. This is evidenced by the increased oxidative stress by pro-ulcerative factors in the gut such as H. pylori, [11] use of non-steroidal anti- inflammatory drugs [12], psychological stress etc [13]. The aim of the current study was to examine the effects of tannins in ethanol and cold stress induced ulcer models on rats, and to evaluate its effects on oxidant and antioxidant parameters in rat stomach tissue.
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Evidence of the gastroprotective and anti-<em>Helicobacter pylori</em> activities of &beta;-mangostin isolated from <em>Cratoxylum arborescens</em> (vahl) blume

Evidence of the gastroprotective and anti-<em>Helicobacter pylori</em> activities of &beta;-mangostin isolated from <em>Cratoxylum arborescens</em> (vahl) blume

Notes: The microscopic appearance of gastric mucosa of the rats of the normal control (A) showed the positive Pas stain noted as a bright-magenta color to the mucus cells lining the gastric pits (black arrow). The gastric mucosa of the rats of the ulcer control pretreated with only Tween 80 (B) showed that the ethanol-induced complete depletion to the mucous layer as seen by the absence of the Pas stain. however, the pretreatment with omeprazole at 20 mg/kg (C) showed intense Pas stain noted as a bright-magenta to the mucus cells lining the gastric pits due to the carbohydrate-rich, viscous mucus they secrete (black arrow). The pretreatment with BM at 5 mg/kg (D) showed moderate expansion of a substantial continuous Pas-positive mucous gel layer that lining the entire gastric mucosal surface observed histologically as a bright- magenta-stained area lining the mucosa (black arrow). The pretreatment with BM at 10 mg/kg (E) showed intense Pas stain and increased expansion of a substantial continuous Pas-positive mucous gel layer that lining the entire gastric mucosal surface observed histologically as a bright-magenta-stained area lining the mucosa (black arrow). The pretreatment with BM at 20 mg/kg (F) showed increased expansion of a substantial continuous Pas-positive mucous gel layer that lining the entire gastric mucosal surface observed histologically as a bright-magenta-stained area lining the mucosa (black arrow) (Pas stain: ×20).
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Cytosolic phospholipase A2 S nitrosylation in ghrelin protection against detrimental effect of ethanol cytotoxicity on gastric mucin synthesis ——Ghrelin in gastric mucosal protection

Cytosolic phospholipase A2 S nitrosylation in ghrelin protection against detrimental effect of ethanol cytotoxicity on gastric mucin synthesis ——Ghrelin in gastric mucosal protection

To assess the influence of ghrelin on the disturbances in gastric mucin synthesis caused by alcohol cytotoxicity, we employed rat gastric mucosal cells exposed to etha- nol at the dose range (3%) that impairs the mucosal ca- pacity for mucin synthesis and prostaglandin generation [1-3]. We determined that preincubation of the mucosal cells with ghrelin led to a concentration-dependent pre- vention of ethanol cytotoxicity, and afforded nearly com- plete protection at 0.8 µg/ml of ghrelin (Figure 1). Fur- ther, our results revealed that cytotoxicity induced in gastric mucosal cells by 3% ethanol was reflected in a 32.6% decrease in mucin synthesis (Figure 1), as well as a 29.8% reduction in PGE2 generation and a 51.7% drop in NO production (Figure 2). Ghrelin at its optimal con- centration (0.8 µg/ml) for the protection against ethanol
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ANTIULCER EVALUATION OF MUSSAENDA GLABRATA LEAVES ON EXPERIMENTALLY INDUCED ULCER MODELS OF RAT

ANTIULCER EVALUATION OF MUSSAENDA GLABRATA LEAVES ON EXPERIMENTALLY INDUCED ULCER MODELS OF RAT

results obtained simply the activity of extract either by inhibiting or scavenging the ABTS + radicals. The present study was undertaken to determine the anti-ulcer potential of the EEMG by employing indomethacin, ethanol and pylorus ligation ulcer models. The antiulcer activity of EEMG in pylorus ligation model is evident from its significant reduction in gastric volume, total acidity, free acidity, ulcer index and increase in pH of gastric juice. Because of animals treated with EEMG significantly inhibited the formation of pylorus ulcer in the stomach and also decreased both acid concentration, gastric volume and increased the pH values. It is suggested that EEMG can suppress gastric damage induced by aggressive factors. In order to explore the effects of antioxidant defenses on the process of ulceration, in all stomach tissues, the antioxidant levels (SOD, CAT, and GSH) were evaluated. In the present study the levels of SOD, CAT and GSH were reduced by the ulcer induction. The administration of EEMG resulted in a significant increase in the SOD, CAT and GSH levels. Similarly, the results showed that there was a significant increase in the LPO level in rat stomach tissues-administrated with indomethacin, ethanol and pylorus ligation. Preventive antioxidants such as SOD, CAT and GSH are the first line of defense against ROS. The result shows that the different dose of EEMG reduces the MPO levels, thus exhibiting their gastro- protective effect on the gastric mucosa against the excess of oxygen radicals generated by the neutrophils. And it was observed that the total protein level was significantly lower in the ulcer control groups and the level was found significantly higher in standard and extract treated groups. These observations were further substantiated by the histo-pathological findings wherein, decreased mucosal ulceration, inflammatory infiltration in mucosa and edema in sub mucosa were observed in the EEMG treated groups compared with ulcer control group.
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