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Showing 16 results for Mard

Seyed Ali Mard, Yagoob Farbod, Saeed Khamene,
Volume 7, Issue 2 (Fall and Winter 2003)
Abstract

Memory and learning are considered as the most complicated and important processes of behavioral sciences. On the other hand, considering the wide .and progressively increasing applications of anesthetic agents all over the world, it is of great importance to have a reasonable knowledge regarding their effects on the memory process and its retrieval. The main purpose of this study was to evaluate anterograde and retrograde effects of isoflurane anesthesia on the memory process. For this purpose, male rats were divided into one control and two treatment groups. All of the groups underwent the training program of single trial passive avoidance learning, and the treatment groups (b and c) were exposed to isoflurane anesthesia (1.4% for 60 min) before and after the learning program. After 24 hours, the memory retrieval test was performed. The results showed that the mean retention latency value (which was considered as total in the control groups and measured as 600 sec) significantly decreases to 139 and 179 sec in groups b and c respectively (p<0.05). It can be concluded that that administration of isoflurane both before and after learning program causes disturbances in retrieval process of memory and also results in anterograde and retrograde amnesia in rats.
Mohammad Kazem Gharibnaseri, Seyed Ali Mard,
Volume 10, Issue 4 (Winter 2007)
Abstract

Introduction: Alhagi camelorum belongs to the Leguminosae family is used in Iranian folk medicine to treat some gastric diseases. The present study was undertaken to evaluate the Alhagi camelorum aqueous extract for anti-ulcer activity in rats. Methods: Male Wistar rats were pretreated with the A. camelorum aqueous extract (150, 300 or 450 mg/kg of B.W., P.O.) before induction of gastric ulcer by water immersion restraint-stress at 20-22 °C (5 h) or before induction of the ulcer by ethanol 100% (1 ml/200g of B.W., P.O.). Negative control animals received saline (0.5 ml/100 g of B.W.). Positive control animals received ranitidine (60 mg/kg, P.O.). Results: The A. camelorum aqueous extract (ACE) protected rats against water immersion restraint-stress and ethanol-induced ulcers in a dose-dependent manner. In water immersion restraint induced ulcerated rat, the ACE increased pH and reduced gastric acid content. ACE did not show any signs of toxicity and mortality up to10 g/kg, P.O. in mice. Conclusion: The results suggest that A. camelorum aqueous extract can exert significant mucosal protection and antisecretory effects on gastric mucosa in rats.
Seyyed Ali Mard, Mohamad Kazem Gharibnaseri,
Volume 11, Issue 1 (Spring 2007)
Abstract

Introduction: The effect of esophageal distension (ED) on gastric motility has been well documented, but a few investigations have been carried out on the effect of ED on gastric secretion. The aim of this study was to investigate the effect of ED on gastric acid and pepsin secretion and the mechanism(s) involved. Methods: Male adult Wistar rats (200-240 g) were anesthetized with urethane (1.2 g/kg, i.p.) and underwent tracheostomy and laparotomy. A catheter was inserted in the stomach through duodenum for gastric distension and gastric washout. Esophagus was distended by a balloon (0.3 ml, 10 min). Gastric acid secretion was stimulated by gastric distension (by saline 1.5 ml/100 g of B.W.), pentagastrin (20 μg/kg, i.p.) or insulin (0.6 IU/kg, i.p.). Pepsin secretion was stimulated by carbachol (20 μg/kg, i.p.). Effects of cervical vagotomy and reserpine (1 mg/kg, i.p.) were also investigated. Results: Gastric distension-, pentagastrin- and insulin-stimulated gastric acid secretion were decreased by esophageal distension (P<0.001, P<0.05 and P<0.05, respectively). Carbachol-induced pepsin secretion was also attenuated by esophageal distension (P<0.05). Cervical vagotomy abolished the inhibitory effect of ED on gastric distension-induced acid secretion. In reserpinized rats, ED reduced the basal gastric acid secretion (P<0.05). Conclusion: Results indicated that the ED decreased gastric acid output. The vagus nerve was involved in the inhibitory effect of the ED on gastric acid secretion but the adrenergic system did not play role.
Maryam Anjomshoaa, Khadije Karbalaei, Shahnaz Razavi, Mohammad Mardani, Somayeh Tanhaei, Mohammad Hossien Nasr Esfahani, Hossein Baharvand,
Volume 12, Issue 1 (Spring 2008)
Abstract

Introduction: The aim of this study was evaluate the ability of notochord to induce neural induction and/or differentiation of mouse embryonic stem cell to neuron and motor neuron, respectively. Methods: In order to produce embryoid bodies, ES cells line Royan B1 were grown in suspension in the absence of LIF for 4 days. EBs were divided into 4 groups. EBs in group 1 & 2 were further cultured in suspension for 4 days in presence of retinoic acid (RA) while EBs in group 3 and 4 were cultured in absence of RA. Unlike group 2 and 4, EBs in the group 1 and 3 were also co-cultured with notochord for further 4 days. Numbers and type of neurons were assessed for each group. Results: EBs in group 3 and 4 lead to 6 to 5 % neuron production while EBs in the group 1 and 2 lead to 55 and 42% neuron production, respectively. There were only significant difference at P <0.05 between groups 3 and 4 with groups 1 and 2. Assessment of percentage of motor neuron (Hb9 positive) reveals a significant increase in the group 1 compared to group 2. Conclusion: Apparently, co-culture of mouse embryonic stem cells in presence of notochord did not induce neural differentiation of mouse embryonic stem cells, while notochord may direct neural differentiation of mouse embryonic stem cells toward motor neurons
Ali Nasimi, Ali Mohammad Moradi, Mardomak Ravari, Fatemeh Kharazmi, Masoumeh Hatam,
Volume 12, Issue 4 (Winter 2009)
Abstract

Introduction: The bed nucleus of the stria terminalis (BST) is a limbic structure which is involved in cardiovascular regulation and baroreflex modulation. The presence of cholinergic synaptic terminalis with high level of muscarinic receptors in the BST has been demonstrated. This study was performed to find the role of the cholinergic muscarinic receptor in cardiovascular response and baroreflex activity in urethane anesthetized rat. Methods: Acetylcholine (Ach, 3, 6 nmol in 50 nl) was microinjected unilaterally into the BST of 53 urethane anesthetized male rats. Femoral artery and vein were cannulated to record the blood pressure (AP) and heart rate (HR), respectively. The maximum average changes in the mean arterial pressure (MAP) and (HR), were compared with control group and before injection using t-test and paired t-test, respectively. To evaluate baroreflex activity, bradycardia values corresponding to progressive 20 mmHg increases in MAP were determined. The slope of the linear regression curves was calculated and compared to before injection using ANOVA repeated measure. Results: Microinjection of Ach into the dorsal, lateral and ventral portion of the BST resulted in an increase of AP (20.69 ± 1.8 mmHg, p<0.01) with no significant changes of the HR. The pressor response evoked by Ach was blocked by microinjection of atropine into the BST. However, atropine did not affect the bradycardia reflex evoked by increased blood pressure caused by intravenous phenylephrine injection. Microinjection of cobalt chloride into the BST did not affect the baseline AP and HR but significantly increased bradycardic response to lower pressure changes (less than 40 mm Hg) and decreased bradycardic response to higher pressure changes (more than 40 mm Hg) (p>0.05) indicating that neuronal circuitry of BST is an essential part of the baroreflex.. Conclusion: The present study indicated that the BST muscarinic receptors are involved in the cardiovascular regulation but are not involved in the modulation of baroreflex activity, although synapses within the BST have influence on the bradycardia baroreflex component.
Ali Mard, Mohammad Kazem Gharib Naseri, Mhamad Badavi,
Volume 13, Issue 1 (Spring 2009)
Abstract

Abstract Introduction: There are many studies about the inhibitory effect of the esophageal distention (ED) on gastric motility. Recently, it has been shown that ED decreases the gastric secretions. It is well established that the inhibitory effect of ED is mediated by activation of vago-vagal inhibitory reflex. However, there is not any investigation about the effect of the reflex on the gastric blood flow and release of gastric hormones. The aim of this study was to investigate the effect of esophageal distention (ED) on gastric blood flow and release of gastrin and somatostatin hormones. Methods: In this study 79 male Wistar rats (175-230 g) were used. deprived of food but not water 24 h before the experiments. Under urethane anesthesia (1.2 g/kg, i.p.), animals underwent tracheostomy and laparotomy. A catheter was inserted in the stomach through duodenum for gastric distension. The esophagus was cannulated with a balloon orally to distend distal portion of esophagus (0.3 ml, 10 min). Saline was used for gastric distension (1.5 ml/100 g, b.w., pH 7 and 37 °C). Gastric blood flow was measured by a Laser Doppler flowmeter. Gastrin serum and somatostatin plasma levels were assessed by RIA method. Vagotomy was carried out in a group to reveal the role of vagus nerve in this action. Results: ED reduced the blood flow of gastric proximal portion (P<0.001) but the antrum blood flow was unaffected by ED. Cervical vagotomy abolished the inhibitory effect of the ED on the proximal area blood flow. Gastrin serum level and somatostatin plasma level were unaffected by ED. Conclusion: Removal of the inhibitory effect of ED after vagotomy shows that the vagus nerve was involved in the inhibitory effect on gastric blood flow. Keywords: Esophageal distension, Gastric blood flow, Vagus nerve, Rat, Gastrin, Somatostatin
Narges HoseinMardi, Leila Azimi, Mohammad Javan, Naser Naghdi, Yaghoub Fathollahi,
Volume 13, Issue 2 (Summer 2009)
Abstract

Abstract* Introduction: Chronic morphine exposure can cause addiction and affect synaptic plasticity, but the underlying neural mechanisms of this phenomenon remain unknown. Herein we used electrophysiologic approaches in hippocampal CA1 area to examine the effect of chronic morphine administration on short-term plasticity. Methods: Experiments were carried out on hippocampal slices taken from either control animals or animals made dependent via oral chronic morphine administration. Population spikes (PSs) were recorded from stratum pyramidale of CA1 following stimulation the Schaffer collateral afferents. For examining the short-term synaptic plasticity, paired pulse stimulations with inter pulse interval (IPI) of 10, 20, 80, and 200 ms were applied and paired pulse index (PPI) was calculated. Results: Chronic morphine exposure had no effect on the baseline response. A significant increase in PPI was observed in dependent slices at 80 ms IPI as compared to the control ones. There was no significant difference in baseline response between control and dependent slices when we used long term morphine, naloxone, and both. However, long term morphine administration caused significant difference in PPI at IPI of 20 ms. This effect was eliminated in the presence of naloxone. Conclusion: These findings suggest that morphine dependence could affect short-term plasticity in hippocampal CA1 area and increase the hippocampus network excitability. Keywords: Addiction, CA1 neural networks, short-term synaptic plasticity.
Seyyed Ali Mard, Maryam Maleki, Mohammad Kazem Gharib Naseri, Alihosein Saberi,
Volume 15, Issue 4 (Winter 2012)
Abstract

Introduction: Recently, hydrogen sulfide has been introduced as the third gas that acts as a transmitter. It has many physiological and pharmacological roles in the human body. The aim of the present study was to investigate the effect of exogenously administered and endogenously produced H2S on the basal and distention-induced gastric acid secretion in rats. Methods: Forty-nine male Wistar rats (150-200 g) were randomly assigned into 7 groups (7 rats per group). To evaluate the effect of H2S on the basal acid secretion, three groups of animals received an IV bolus of NaHS, a H2S donor, at the doses of 20, 40 or 80 μg/Kg. The effects of IV NaHS 20, 40 or 80 μg/Kg were also investigated on distention-induced gastric acid secretion in other three groups. In order to evaluate the effect of endogenously produced H2S on distention-induced gastric acid secretion, one group of animals received IV propargylglycine (PAG), a cystathionine-γ-lyase inhibitor, 100 mg/kg. Results: NaHS decreased the basal and distention-induced gastric acid secretion in a dose-dependent manner (P<0.01). PAG increased the gastric output in response to distention compared to the control group (P<0.001). Conclusion: Our results showed that both exogenous administration and endogenous production of H2S decrease the gastric acid output. Also, the findings of the present study suggest that endogenously produced H2S has a modulatory effect on stimulated gastric acid output similar to nitric oxide (NO).
Jafar Doost Mohammad Pour, Narges HosseinMardi, Mahyar Janahmadi, Yaghoub Fathollahi, Fereshteh Motamedi, Mehdi Hooshmandi,
Volume 17, Issue 3 (Fall 2013)
Abstract

Introduction: The prostaglandin E2 (PGE2), a cyclooxygenase (COX) product, play critical roles in the synaptic plasticity. Therefore, long term use of COX inhibitors may impair the synaptic plasticity. Considering the wide clinical administration of aspirin and its unknown effects on information processing in the brain, the effect of aspirin and sodium salicylate on the short term synaptic plasticity was investigated. Methods: Field excitatory post synaptic potential (fEPSP) from stratum radiatum of CA1 neurons were recorded following Schaffer collateral stimulation in rats receiving aspirin in drinking water (2 mg/ml) for 6 weeks or sodium salicylate (six injection of 300 mg/kg, IP, twice daily) for 3 days. In order to examine the short-term synaptic plasticity, paired pulse stimulations with inter pulse intervals (IPI) of 20, 80, and 200 ms were applied and paired pulse index (PPI) was calculated. Results: The data showed that both sodium salicylate and aspirin decreased basal synaptic responses, although this change was significant in the sodium salicylate group, but not in aspirin treated rats (ANOVA P<0.001). Sodium salicylate significantly increased PPI at 20 ms IPI (%90.7±1.6, n=5Vs. control: %76.1±1.5, n=5). Also significant increase in PPI was observed in aspirin treated rats (%125.9±6.6, n=5) at 20 ms IPI compared to control ones (%76.3±2.4, n=5, P<0.05, unpaired t-test). Conclusion: In summary, our study suggests that aspirin and sodium salicylate may affect synaptic transmission and short term synaptic plasticity in the rat hippocampus.
Seyyed Ali Mard, Hajar Godarzinejad, Mahin Dianat,
Volume 20, Issue 1 (March 2016)
Abstract

Introduction: It has been reported the alkaline response of pancreas to duodenal acidification is partly mediated through duodenal release of H2S, but till now the effect of duodenal acidification on gastric H2S release has not been investigated. Therefore, the present study designed to evaluate the effects of duodenal acidification on gastric H2S release and level of mRNA expression of cystathionine gamma lyase (CSE).
Methods: Twenty four rats were randomly assigned into 3 groups (8 in each). They were control, pH2-, and pH3-treated groups. Under anesthesia, animals underwent midline laparotomy. Neutral isotonic saline or acidic isotonic solutions (pH=2 or 3) were injected in the duodenum 1 cm just below the pyloric sphincter. Ninety minutes after beginning the experiment, animals were sacrificed, stomachs ligated at lower esophageal sphincter and 2 ml saline infused in the stomach through pylorus and then gastric content was drained for measuring the pH. Two samples of gastric mucosal tissue were quickly snap-frozen and stored in liquid nitrogen for measuring the mucosal H2S concentration using ELISA kit and quantifying the mRNA expression of CSE by quantitative real-time PCR.
Results: Duodenal acidification with acidic solution (pH=2) increased the gastric release of H2S and upregulated mRNA expression of CSE in gastric mucosa. The gastric mucous content was significantly increased in response to duodenal application of acidic solutions with pH2 and 3.
Conclusion: Our findings indicated the stimulatory effect of duodenal acidification on gastric H2S release and mucous content is mediated through upregulation of CSE mRNA expression.


Sharareh Daryani, Alireza Farzaei, Narges HosseinMardi, Farideh Bahrami, Mahyar Janahmadi,
Volume 20, Issue 2 (June 2016)
Abstract

Introduction: Although aging is the most important risk factor for Alzheimer's disease (AD), there is evidence indicating that neuroinflammation may contribute to the development and progression of the disease. Several studies indicated that minocycline may exert neuroprotective effects in rodent models of neurodegenerative diseases. Nevertheless, there are also other studies implying that minocycline has no positive beneficial effects. Thus, the aim of the present study was to assess the preventive effect of minocycline against Aβ-induced changes in intrinsic electrophysiological properties in a rat model of AD. Methods: The present study extended this line of research by examining whether inhibition of microglial activation may alter the intrinsic electrophysiological properties of CA1 pyramidal neurons in a rat model of Aβ neurotoxicity, using whole cell patch clamp. Results: Findings showed that bilateral injection of the Aβ (1-42) into the prefrontal cortex caused membrane hyperpolarization, action potential (AP) narrowing and after hyperpolarization (AHP) amplitude enhancement. It was also resulted in a faster decay time of AP, higher rheobase current, lower firing frequency and smaller post stimulus AHP amplitude. Administration of minocycline (45mg/kg, i.p) not only failed to prevent Aβ-induced alterations in the intrinsic electrophysiological properties, but also enhanced the effects of Aβ on neuronal firing behavior. Conclusion: It can be concluded that minocycline, as a microglial inhibitor, may enhance the disruption of electrophysiological properties of CA1 pyramidal neurons induced by Aβ neurotoxin, including AP parameters and intrinsic neuronal excitability.


Mohsen Fathi, Narges HosseinMardi, Kambiz Rohampour, Mahyar Janahmadi, Ali Sonboli, Jalal Zaringhalam,
Volume 20, Issue 3 (September 2016)
Abstract

Introduction: The management of pain and inflammation related problem is a real challenge that people face daily. Although several drugs are available for these conditions, medicinal plants are believed to be an important source of new chemical substances with potential therapeutic effects. The objective of current study was to investigate the anti-nociceptive effect of Tanacetum Fisherae which has been traditionally used for treatment of pain. Methods: In this experimental study, formalin test was performed with drug (Tanacetum Fisherae) or DMSO pretreatment 30 min prior to formalin injection in 40 male Wistar rats. Fifty microliters of 2.5% formalin was injected into the plantar surface of the right hind paw. Immediately after injection, licking and flinching number and paw-shaking responses were observed at 5-min intervals for 1 h. Animals were divided into five experimental groups. There were 8 animals in each group. Each group received vehicle (7% DMSO) or Tanacetum Fisherae essential oil (25, 50 or 100 μg) or morphine (5 mg/kg). Two-way and one-way ANOVA were used for data analysis. Differences were considered significant at the level of P<0.05 (with 95% confidence interval). Results: Results showed that Tanacetum Fisherae essential oil dose dependently reduced licking and flinching number and also pain score in the late (15-35 min) and recovery phase (35-60 min) of formalin test (p<0.05, p<0.01, and p<0.001). It had no anti-nociceptive effect (p>0.05) in early (0-5 min) phase and interphase (5-15 min). Conclusion: Results demonstrate the effectiveness of Tanacetum Fisherae to mitigate the inflammatory pain.


Jamileh Mardookhi, Mohammad Reza Bigdeli, Sepideh Khaksar,
Volume 20, Issue 4 (December 2016)
Abstract

Introduction: Ischemic stroke is a serious neurological disease and a leading cause of death and severe disability in the world. A key component of the Mediterranean diet is olive oil, which contains compounds with antioxidant and anti-inflammatory effects. In this regard, the aim of the present study was to investigate the effect of olive oil on the ischemic damages and the inflammatory pathway of TNFR1/NF-кB in various regions of the rat brain. Methods: In this experimental research 58 male Wistar rats were totally divided into six groups including sham, control (intact), control (middle cerebral artery occlusion, MCAO), and treatments. The intact group received distilled water, while the treatment groups received different doses (0.25, 0.50, and 0.75 ml/kg) of olive oil by gastric gavage for 30 days. Two hours after the last gavage, the rats were subjected to 60 min MCAO surgery. Twenty four hours later, the neurologic defects scores, infarct volume (in total, cortex and striatum of hemisphere) and the inflammatory factors protein expression were evaluated separately. Data were analyzed by kruskal-wallis and two-way ANOVA tests. Results: The olive oil 0.75 ml/kg-received group displayed a significant reduction in the infarct volume, the neurological scores and the inflammatory factors protein level in comparison to the control group. Moreover, this significant difference was observed in the cortex and striatum. Conclusion: The present results demonstrated that the neuroprotective effects of the olive oil could improve ischemic injuries. It seems that its positive impacts are partly attributed to anti-inflammatory effects of the olive oil.


Parham Reisi, Fatemeh Sepahvand, Ghasem Zarei, Leila Kamali Dolatabadi, Shaghayegh Haghjooye JavanMard, Hojjatallah Alaei,
Volume 21, Issue 2 (June 2017)
Abstract

Introduction: Studies have indicated that diabetes mellitus impairs hippocampus. Diabetes increases the risk of depression and treatment with antidepressants may affect learning and memory. The aim of this study was to evaluate the effects of amitriptyline and fluoxetine on synaptic plasticity and TNF-α level in the hippocampus of streptozotocin-induced diabetic rats. Methods: Experimental groups were control, diabetes, diabetes-amitriptyline and diabetes-fluoxetine (n=8 for each experimental group). Three weeks after the induction of diabetes, the rats received treatment with amitriptyline (5 mg/kg) or fluoxetine (5 mg/kg) for 21 days. Long-term potentiation (LTP) in perforant path-dentate gyrus synapses was assessed (by 400 Hz tetanization) for investigating the effect of treatments on synaptic plasticity. Field excitatory post-synaptic potential indices were measured. Finally, TNF-α levels were measured in hippocampus by enzyme-linked immunosorbant assay. Results: Six weeks after the diabetes induction, LTP wasn’t different between the control and the diabetes groups and also no significant differences were observed between the diabetes and the diabetes-treated groups; however, amitriptyline and fluoxetine impaired LTP in diabetic rats and there was a significant difference between the control and the diabetes-treated groups. Comparing to the controls, TNF-α level was increased significantly (P<0.05) only in the diabetes-amitriptyline group. Conclusion: Results suggest that amitriptyline and fluoxetine intensify the destructive effects of diabetes on hippocampus and that TNF-α may act as a mediator for these changes; however, other factors may also be involved. Hence, treatment of diabetic patients with antidepressants must be done with extra care.


Seyyed Ali Mard, Iraj Ahmadi, Mohammad Kazem Gharib-Naseri, Feryal Savary,
Volume 21, Issue 3 (September 2017)
Abstract

Introduction: Sodium hydrosulfide (NaHS) has shown to enhance the gastric emptying rate in normal rats but till now its effect on gastric emptying of food stuffs in diabetic rats was not investigated. Therefore, this study designed to determine the role of an oral administration of NaHS on gastric emptying rate (GER) of glucose, albumin and olive oil in gastroparetic and normal rats. Methods: To evaluate the effect of NaHS on the gastric emptying of glucose, albumin and olive oil in normal rats, thirty-six normal rats randomly assigned in six experimental groups (6 per group). Three groups of rats considered as control. They received albumin, glucose or olive oil orally. Three other normal groups considered as NaHS-treated animals. These groups received NaHS (320 μg/kg, orally) 30 min prior to food stuffs. To investigate the effect of NaHS on the gastric emptying of food stuffs in diabetic rats, the same protocols carried out. Thirty min after intragastric administration of food stuffs, animals received acetaminophen (as a marker for gastric emptying rate). Results: The results showed that in normal and gastroparetic rats, an oral administration of NaHS accelerated gastric emptying of glucose, albumin and olive oil. The increased gastric emptying of glucose, albumin and olive oil in NaHS-pretreated gastroparetic rats was 89.9, 92.3 and 60% respectively more than in corresponding’s controls.


Nasim Nazariani, Seyyed Ali Mard, Sima Nasri, Ali Veisi,
Volume 22, Issue 1 (Winter 2018)
Abstract

Introduction: The incidence rate of gastric erosions and ulcers in diabetic patients are higher due to failure of mucosal antioxidant defense and maintain enough blood flow. The present study evaluated the gastro-protective effect of sodium hydrosulfide (NaHS) against indomethacin-induced gastric lesions in diabetic rats. Methods: In order to test anti-ulcer activity of NaHS against indomethacin, four diabetic groups of rats including diabetic control and 3 NaHS-treated groups received a single dose of physiologic saline or NaHS at 320, 640 and 1280 μg/kg respectively, 30 min before ulcer induction by indomethacin. Five hours later, the animals were killed and their stomachs were removed for macroscopically and microscopically evaluations. In order to evaluate the antacid effect of NaHS, 4 groups of diabetic rats received physiologic saline or NaHS at 320, 640 and 1280 μg/kg and 30 min later anesthetized, underwent a midline laparotomy and then their pylorus ligated. Five hours later, the animals were killed, their stomachs were removed and pH of gastric effluents were measured. Results: Indomethacin induced gastric lesions in glandular part of the stomach. NaHS at 640 and 1280 μg/kg significantly decreased the indomethacin-induced gastric lesions in diabetic rats. The pH of gastric effluents and mucus content increased by NaHS at doses of 640 and 1280 μg/kg. Macroscopic and microscopic observations showed that mucosal erosions induced by indomethacin were significantly inhibited by NaHS. Conclusion: results suggest NaHS through decreasing the rate of gastric acid output and increasing the mucus production, protected the gastric mucosa against indomethacin-induced gastric lesions in diabetic rats.



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