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Showing 14 results for Mohammadi

Mojtaba Salamtian, Vahid Mohammadi, Seyyed Meysam Abtahi Froushani,
Volume 0, Issue 0 (7-2019)
Abstract

This study was designed to evaluate the effects of cinnamon extract on the treatment and control of inflammation in acetic acid-induced ulcerative colitis in Rats. Thirty-two male Wistar rats were divided into four groups: untreated control, positive control group (acetic acid-induced ulcerative colitis), cinnamon extract treated group (150 mg/kg BW; P.O.daily) and treated group with prednisolone (4 mg/kg BW; P.O.daily). After 10 consecutive days, the rats were euthanized and examined for the production of inflammatory mediators and oxidative stress indices in the intestinal tissue. Obtained data showed that both therapies could reduce the cumulative disease score. The results also indicated that treatment with Cinnamon caused a more benefit in restoring the total antioxidant capacity of the colonic specimens of the colitis induced rats compared to treatment with Prednisolone. The levels of MPO and NO were down-regulated in the guts of Cinnamon treated rats more than Prednisolone groups. Prednisolone significantly decreased the levels of TNF- α and IL-6 cytokines more than colitis rats treated with Cinnamon extract. The levels of COX-2 were decreased and conversely, the total protein content of colonic homogenates was increased in the guts of both treatment groups in a non-significant manner, compared to untreated colitis rats. These results demonstrated treatment with Cinnamon as herbal medicine is a promising strategy to improve the inflammation in a rat model of ulcerative colitis. It is logical to consider some of the beneficial effects of cinnamon extract associated with its direct antioxidant benefits, along with its direct anti-inflammatory benefits.
Mohsen Alipour, Davood Sohrabi, Feridoun Hydarpour, Ramazan Falah, Mustafa Mohammadi,
Volume 11, Issue 3 (Fall 2007)
Abstract

Few studies have investigated the effect of exercise on homocysteine and 15-F21-isoprostane in animal models. The present study was designed to examine the effect of long-term exercise and/ or high cholesterol diet on MDA, 15-F21-isoprostane and total homocysteine in the aorta and plasma of rabbits. Methods: 56 male rabbits were divided into four groups: normal diet (control), normal diet with exercise, high-cholesterol diet without exercise and high cholesterol diet with exercise. Animals of exercise groups ran on a treadmill at 0.88 km/h for 7.5 –90 min/day (5 days/week) for 12 weeks. At the end of exercise protocol, blood samples were collected and tHcy, 15-F21-isoprostane were measured using enzyme immunoassay (EIA) kits. MDA levels were determined by the thiobarbituric acid assay. Thoracic aorta was isolated to evaluate atherosclerosis as well as tHcy, 15-F21-isoprostane and MDA levels. Results: Exercise reduced atherogenic diet-induced atherosclerotic lesions in aorta along with positive changes in plasma cholesterol profile. Atherogenic diet significantly increased plasma and aorta concentrations of MDA and tHcy. Exercise significantly reduced diet-increased plasma and aorta concentrations of 15-F21-isoprostane and tHcy in normal animals. MDA levels did not show significant change due to exercise and/or high cholesterol diet feeding. There was a positive correlation among plasma cholesterol, homocysteine and 15-F21-isoprostane in exercised groups compared with control. Conclusion: Our results suggest that elevated homocysteine level can be considered as one of the multiple risk factors in the development of atherosclerosis. In addition, exercise may effectively reduce plasma and aorta homocysteine and 15-F21-isoprostane and may be effective in prevention and attenuation of atherosclerosis.
Marzeieh Hoseini, Sohrab Hajizadeh, Yaghoub Fathollahi, Mojtaba GolMohammadi, Batoul Erfani, Ali Heidarian Pour,
Volume 12, Issue 1 (Spring 2008)
Abstract

Introduction:Adenosine as a potent vasodilator has physiological role in regulation of regional cerebral blood flow (rCBF). Metod: Laser-Dِoppler flowmetry technique was used to study pial vessels blood flow responses to adenosine receptors agonists and antagonist. Male Sprague Dawley rats (250-350g) that were housed in standard conditions, were anesthetized with Urethane (1.5g/kg). Adenosine (general agonist), NECA (A2Aand A2B receptor agonist) and CGS-21380(A2Aselective agonist), were used in absence and presence of A2A receptors- selective antagonist, ZM-243185, in naive and morphine-dependent rats. Results: Adenosine, NECA and CGS-21680 increased pial vessels blood flow in naive and dependent rats dose dependently. These responses were blocked significantly by ZM-243185. Responses of pial vessels to adenosine (10-4, 10-5, 10-6 M) and NECA (10-4, 10-5, 10-6 M) were increased significantly in morphine- dependent rats in comparison to naive rats. Pial vessels responses to CGS-21680 had not shown any significant deferences between morphine- dependent and naive rats. Conclusion:Based on these results it could be concluded that the role of A2B receptors in regulation of rCBF in morphine-dependent rats is more effective than A2A receptors.
Mojtaba GolMohammadi, Sohrab Hajizadeh, Mohammad Faghihi, Marzeieh Hosein, Kambiz Rohampour,
Volume 13, Issue 2 (Summer 2009)
Abstract

Introduction: In recent study both endothelium-dependent and endothelium-independent mechanisms have been reported for the action of β-adrenoceptor. The aim of this study was to investigate on the role of nitric oxide (NO) and cyclic guanosin monophosphate (cGMP) in vasodilation mechanisms of β2-adrenoceptors (β2-AR) in rat skin vessels. Methods: All drugs were injected subcutaneous into planar skin of hind paw. Injection volume was 10µl (5µl/min). Induction of anesthesia was perform with urethane 1.5 g/kg. Laser Doppler Flowmetery (LDF) technique was used for skin blood flow (SBF) monitoring. Results: The results obtained in this study showed that different doses of salbutamol, selective β2-AR agonist (1µM) caused a significant increase of SBF, but there was not any significant different in the response of different doses. Atenolol, selective β1-adrenoceptor antagonist (10µM) alone and with salbutamol had no significant effect on SBF. Propranolol, non selective β-adrenoceptor antagonist (1µM) by itself did not changed SBF, but significantly reduced the vasodilatory effect of salbutamol. LNNA, NO inhibitor (10µM) and methylen blue, cGMP inhibitor (3µM) caused a significant decrease of SBF 6/95% and 7/91% respectively. Salbutamol injection after LNNA and NO raised the SBF to 24/7% and 22.5% respectively, which shows a significant reduction in comparison to salbutamol’s effect (42.73%). Conclusion: The results indicated that, salbutamol dilate rat skin vessels via β2- ARs. NO and cGMP involved in β2-ARs mediated vasodilation and contribute to regulation of vascular skin tone. To elucidate the exact mechanism of this response more studies are needed.
Moslem Mohammadi, Asghar Ghasemi, Esmaeel Ghani, Ali Khoshbaten, Alireza Asgari,
Volume 13, Issue 2 (Summer 2009)
Abstract

Introduction: Paraoxon (the neurotoxic metabolite of organophosphorus (OP) insecticide, parathion) exerts acute toxicity by inhibition of acetylcholinesterase (AChE), leading to the accumulation of acetylcholine in cholinergic synapses and hence overstimulation of the cholinergic system. Since, reports on changes in the level of γ- amino butyric acid (GABA) during OP-induced convulsion have been controversial, in present study we used cortical and hippocampal synaptosomes from rats after paraoxon poisoning to detect changes in GABA uptake. Methods: Male Wistar rats (200-270 g) were used in this study. Animals were given a single intraperitoneal injection of corn oil (vehicle group) or one of doses of paraoxon (0.1, 0.3, or 0.7 mg/kg) and [3H]GABA uptake by cerebral cortex and hippocampal synaptosomes was measured at 30 min, 4 h, and 18 h after the exposure (n= 7 rats/group). Type of transporter involved in the uptake was also determined using β-alnine, and L-diaminobutyric acid (L-DABA), a glial and a neuronal GABA uptake inhibitor, respectively. Results: GABA uptake was significantly (p<0.001) reduced by both cerebral cortex (18-32%) and hippocampal (16-21%) synaptosomes compared with their respective control groups at all three time points after administering 0.7 of paraoxon (convulsive dose). β-alnine had no inhibitory effect on the uptake, whereas L-DABA abolished most of the transporter mediated GABA uptake. Conclusion: Since GABA uptake did not change in other two paraoxon treated groups, it may be indicating that decrement of GABA uptake is convulsion-related. The decrease in GABA uptake, presumably due to a change in the function of GABA transporters, may represent a compensatory response modulating neuronal overexcitation. Most of synaptosomal GABA uptake was blocked by L-DABA, indicating that the uptake was primarily by a neuronal GABA transporter (GAT), GAT-1.
Mohammad Taghi Mohammadi, Seyed Mostafa Shid Moosavi, Gholam Abbas Dehghani,
Volume 14, Issue 1 (Spring 2010)
Abstract

Introduction: Nitric oxide seems to play a dual role in ischemia/reperfusion injury. Few studies have investigated whether it exacerbates or improves brain edema. In the present study, we inhibited the activity of nitric oxide synthase by L-NAME and evaluated the cerebral infarct volume, tissue swelling and brain edema, alongside the measurement of blood flow of the ischemic region. Methods: Transient focal cerebral ischemia was induced by 60 min middle cerebral artery occlusion followed by 12 hours reperfusion in rat. Experiments were performed in three groups of rats (n=12 each) Sham, control ischemic, and L-NAME pretreated (1 mg/kg IP). Laser Doppler flowmetry was used to measure the regional blood flow. After neurological deficit score (NDS) testing, the brains were prepared for TTC staining or brain water content technique to measure the infarct volume and brain edema. Results: Pretreatment with L-NAME significantly reduced NDS (3.66 ± 0.33 to 1.5 ± 0.34), infarct volume of cortex (374 ± 34 to 160 ± 41 mm3) and striatum (158 ± 15 to 87 ± 16 mm3), tissue swelling (7.35 ± 1.27% to 4.05 ± 0.91%) and brain edema (3.5 ± 0.48% to 1.6 ± 0.6%) without significant alteration of blood flow of the ischemic region. Conclusion: The findings of this study indicate that inhibition of nitric oxide synthase activity reduces infarct volume and brain edema of the ischemic region induced during 60 min middle cerebral artery occlusion. This effect is not accompanied with any alteration in the blood flow of the ischemic region.
Hamid-Reza Mohammadi-Motlagh, Kamran Mansouri, Ali Mostafaie,
Volume 14, Issue 3 (Fall 2010)
Abstract

Introduction: Angiogenesis, the process of new blood vessel formation from pre-existing vessels, has important physiological roles in embryonic development, female reproduction cycle, and wound healing. It is also crucial for pathological processes in several diseases especially tumor growth and metastasis. Thereby, inhibition of angiogenesis as an addition to the conventional therapies such as chemotherapy and radiotherapy has attracted the attention of scientists. Results: Different studies have shown that botanical derivatives specifically antagonize new vessel formation in tumors without significant toxicity to normal tissues and without major adverse reactions. Furthermore, many studies have revealed that the active ingredients of these natural products inhibit tumor cell proliferation through interference with other physiological pathways such as intracellular signaling pathways. A number of studies have also demonstrated that many traditional foods especially plant derived foods have preventive potential against around one third of cancers. Therefore, plant rich diet can inhibit the progression of many chronic diseases such as malignant solid tumors which are related to angiogenesis.
Zahra Jahanbakhsh, Mohammad Taghi Mohammadi, Mahvash Jafari, Ali Khoshbaten, Maryam Salehi,
Volume 16, Issue 2 (Summer 2012)
Abstract

Introduction:Severe abdominal aortic constriction above the renal arteries induces arterial hypertension above the stenotic site that is the cause of cardiac hypertrophy. Previous studies have shown that high blood pressure induces myocardial oxidative stress with conflicting results. In the present study, we assessed the effects of acute hypertension on the myocardial oxidative stress and its relation with cardiac hypertrophy. Methods:Experiments were performed on two groups of rats, sham and hypertensive (n=5 each group). Rats were made acutely hypertensive by aortic constriction above the renal arteries. After 10 days, the carotid artery pressure of rats was recorded and hearts were removed. Following tissue homogenization, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods in heart tissues. Results:Arterial pressure and cardiac hypertrophy index (heart weight/body weight, g/kg) were increased in hypertensive rats 66% and 74%, respectively. SOD and CAT activity were significantly higher in hypertensive rats (34.42±2.51 and 38.63±4.03 U/mg protein, respectively) compared to sham animals (28.58±0.28 and 23.27±2.13 U/mg protein, respectively). Aortic-banding significantly increased GSH content of myocardium by 47%, and there was not any significant difference in the myocardial MDA between the two groups. Conclusion:The findings of this study indicate that acutely elevated arterial blood pressure induces cardiac hypertrophy concomitant with oxidative stress in rat myocardium. This study also reconfirms that oxidative stress may play an important role in the development of cardiac hypertrophy during hypertension.
Simin Riahy, Mohammad Taghi Mohammadi, Vahid Sobhani,
Volume 18, Issue 1 (Spring 2014)
Abstract

Free radical can be defined as a molecule or molecular fragments containing unpaired electron in the outer orbital, which react with nearby molecules to get stability. There are two types of them in the body: oxygen free radicals and nitrogen free radicals. Our body has an antioxidant defense system which prevents accumulation of these radicals. There is a balance between free radical production and antioxidant defense system. Excessive free radical production or weak antioxidant system leads to oxidative or nitrosative stress. Diabetes mellitus is one of most important diseases that show cell injury due to oxidative and nitrosative stress in many tissues especially arteries. It causes atherosclerotic plaques in arteries by induction of inflammation, increasing the adhesive molecule expression, extravasation of circulating inflammatory cells, over-expression of some transcription factors, and fat deposition in the wall of arteries. Exercise is one of the main factors that influence production of free radicals and performance of antioxidant defense system. Although strenuous and acute exercise induces oxidative stress by increasing production of free radicals, but regular moderate exercise causes resistance against oxidative and nitrosative stress by potentiating antioxidant defense/repair systems. It appears that regular exercise accompanied by changes in life style is effective in reducing complications of diabetes, especially in prevention of atherosclerosis.
Mohammad Taghi Mohammadi, Gholam Abbas Dehghani,
Volume 18, Issue 1 (Spring 2014)
Abstract

Introduction: Arterial hypertension is one of the causes of stroke, and as one of the vasculotoxic conditions intensifies ischemic stroke complications. The aim of the present study was to analyze the effects of short-term cerebral hypertension on ischemia/reperfusion injury and pathogenesis of ischemic stroke. Methods: The experiments were performed on three groups of rats (N=36) Sham, control ischemia and hypertensive ischemia. Rats were made acutely hypertensive by abdominal aortic coarctation, and after 8 days, were randomly selected for cerebral ischemia induced by middle cerebral artery occlusion (MCAO) for 60 min followed by 12 h reperfusion. The rats were slaughtered under deep anesthesia for measurement of cerebral injury area by triphenyltetrazolium chloride staining method or blood-brain barrier (BBB) integrity disruption by Evans blue extravasation technique. Results: Arterial pressure was increased >36% in hypertensive rats, and blood flow of the ischemic region was reduced by 80% in the ischemic groups compared with the sham. MCAO induced infarction in large areas of the right hemisphere in hypertensive rats compared with control ischemic rats, and subcortical infarct volume was significantly more in ischemic groups (236±43 vs. 139±25 mm3). MCAO also increased Evans blue extravasations in hypertensive rats (9.48±2.03 μg/g) more than non-hypertensive rats (5.09±1.41 μg/g). Conclusion: The findings of present study indicate that the short-term hypertension intensifies the ischemia/reperfusion-induced brain injuries. This type of hypertension also causes severe damage in BBB function and enhanced cerebrovascular permeability after brain ischemia.
Negar Kayedi Bakhtiari, Hooman Eshagh Harooni, Ahmad Ali Moazedi, Mohammad Mohammadi,
Volume 18, Issue 2 ( Summer 2014)
Abstract

Introduction: Previous studies have shown that zinc deficiency and castration could increase anxiety, while administration of zinc or testosterone has anxiolytic effects. This study examined the effect of zinc chloride administration on anxiety in gonadectomized male rats. Methods: For this purpose, adult male Wistar rats (weighing 200-250 g) were castrated. One month after surgery, different doses of zinc chloride (0, 5, 7.5 and 10 mg/kg IP) were administered 30 min before the elevated plus maze test. Time spent and the number of entries in open arms was recorded as measures of anxiety and the number of closed arm entries recorded as locomotor activity. Results: 1) Zinc chloride significantly decreased the time spent and the number of entries in the open arms in gonadectomized rats compared to the control group. 2) Zinc chloride administration could not decrease anxiety, even in the testosterone pretreated gonadectomized male rats. Conclusion: Our findings showed that zinc significantly increased anxiety in gonadectomized rats. Since our previous findings showed that zinc chloride decreased the anxiety level in intact male rats, it seems that zinc chloride effects on anxiety would change in relation to the presence or absence of the gonads and it might interact with androgenic system through an effect on the testis.
Ekram Mohammadi, Mohammad Reza Bigdeli,
Volume 19, Issue 2 (June 2015 2015)
Abstract

Introduction: The purpose of this study was to determine Na-Ca exchanger 2, 3 (NCX2, 3) protein level changes during 2, 5, 10, 15 days after induction of normobaric hyperoxia (HO) preconditioning. Materials and Methods: Rats were divided in two experimental groups. The first group was exposed to 95% inspired HO for 4 h/day for 6 consecutive days (HO). The second group acted as control, and was exposed to 21% oxygen in the same chamber. Each main group was subdivided to middle cerebral artery occlusion (MCAO-operated) and intact (without any surgery) subgroups. After 2, 5, 10 and 15 days from pretreatment, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 hours reperfusion, neurologic deficit score (NDS) and infarct volume (IV) were measured in MCAO-operated subgroups. The NCX 2, 3 expression levels of core, penumbra and subcortex regions were assessed in sham-operated and intact subgroups. Results: Expression of NCX 2, 3 proteins were increased in penumbra (P=0.000, P=0.002), core (P=0.001, P=0.033) and just NCX3 was increased in subcortex (P=0.033) during preconditioning with HO. Neurologic deficit score and infarct volume were decreased with HO preconditioning. These effects of hyperoxia disappeared gradually during 15 days after pretreatment. Conclusion: Although further studies are needed to clarify the mechanisms of time course of neuroprotection, HO durable effects on NCX2, 3 expression, IV and NDS are consistent with an active role in the genesis of ischemic neuroprotection.
Samira Yazdanimehr, Mohammad Taghi Mohammadi,
Volume 22, Issue 1 (Winter 2018)
Abstract

Introduction: According to the powerful antioxidant effects of rosuvastatin, the present study aimed to examine the protective effects of rosuvastatin against oxidative damage of diabetic pancreas by potentiation of the antioxidant capacity in streptozotocin-induced diabetic rats. Methods: Experiment was performed in four groups of male Wistar rats (n=6 in each group): normal, diabetic and two treatment groups (normal and diabetic rats treated with rosuvastatin). Rats were made diabetic by a single intravenous injection of streptozotocin (40 mg/kg) at the beginning of study. Treatment groups received orally rosuvastatin at dose of 10 mg/kg/day. After eight weeks, the pancreas tissues were removed under deep anesthesia. After tissue homogenization, the contents of glutathione and malondialdehyde (MDA) as well as superoxide dismutase (SOD) activity were assessed by biochemical methods. Results: Blood glucose of diabetic rats was above 350 mg/dl. The MDA content of the homogenized pancreas significantly increased in diabetic rats by 92%. Diabetes also decreased the content of glutathione (32%) as well as SOD activity (68%) of pancreas tissues. Treatment with rosuvastatin noticeably decreased the MDA levels of diabetic pancreas (90%). Moreover, rosuvastatin significantly increased the glutathione content (21%) and SOD activity (67%) of pancreas tissues in treated diabetic rats. Conclusion: Our findings reveal that rosuvastatin is able to attenuate the uncontrolled hyperglycemia-induced oxidative damage of pancreas through potentiation of the antioxidant defense system.


Zakieh Keshavarzi, Fatemeh NurMohammadi, Saba Majlesi, Fatemeh Maghool,
Volume 23, Issue 1 (March 2019)
Abstract

Introduction: Walnuts (Juglans regia), has been shown to exert anti-inflammatory and antioxidant effects. The present study was designed to evaluate the anti-inflammatory and antioxidant effects of walnut extract (WE) on an experimental model of ulcerative colitis caused by intracolonic administration of acetic acid in rats. Methods: A total number of 30 rats were used, randomly assigned to five groups of 6 rats each. Group I: colitis without treatment (colitis control), group II: normal animals (normal control), in groups III and IV colitis induced rats were treated with WE (10 and 20mg/kg) for 8 consecutive days, and group V were treated with sulfasalazine (SLS, 200mg/kg) as a standard drug. Several parameters, including macroscopic and histopathological scores and malondialdehyde (MDA), total sulfhydryl (SH) groups, colonic superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured using standard assay procedures. Results: Results revealed that treatment with 10mg/kg WE for 8 days attenuated the macroscopic and histopathological colonic damage scores as well as colonic levels of MDA, while increased the levels of total SH, SOD and GPx compared with colitis untreated group. The 20mg/kg dose had no protective effects. Conclusion: These findings suggest that protective effect of WE in the experimental model of colitis could be through an antioxidant mechanism.


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