در هنگام جستجو کلمه در قسمت عنوان میتوانید کلمات مورد جستجو را با کاراکتر (-) جدا کنید.
کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Journal of Kerman University of Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Trehalose,Spinal cord injury,Chondroitin sulfate proteoglycans
- چکیده:
- چکیده انگلیسی: Background: Chondroitin sulfate proteoglycans (CSPGs) are the major cause of axonal regeneration failure at the site of lesion in spinal cord injury (SCI). Inflammation is believed to stimulate the upregulation of CSPGs expression. Recent evidence showed that trehalose reduces the development of inflammation in SCI. The aim of this study was to investigate the effect of trehalose on neurocan and Neural-Glial Antigen 2 (NG2) mRNA levels in SCI in rats.
Methods: In this experimental study, male rats were divided into six groups (n=15). Sham (laminectomy), SCI (laminectomy and SCI), vehicle (laminectomy and SCI, treated with phosphate buffer saline), and T10, T100 and T1000 (laminectomy and SCI, treated with 10, 100 and 1000 mM trehalose). Five rats in each group were sacrificed at 1, 3 and 7 days post-injury to measure neurocan and NG2 mRNA levels in lesion. Statistical analysis was performed using Kruskal-Wallis methods followed by the Mann-Whitney test.
Results: Findings indicated that SCI upregulated neurocan and NG2 mRNA levels at all times. No significant difference was observed in neurocan and NG2 gene transcripts between SCI and vehicle groups (p>0.05). However, 10 mM trehalose downregulated the mRNA level of both neurocan (0.76 and 0.65 fold) and NG2 (0.75 and 0.70 fold) at 3 and 7 days post-SCI compared to vehicle group (p p<0.01, respectively).
Conclusion: Collectively, treatment with low dose trehalose showed a decrease in neurocan and NG2 mRNA levels in spinal cord injured rats.- انتشار مقاله: 05-10-1397
- نویسندگان: Mehrnaz Karimi,Masoumeh Mirzaie,Mohammad Khaksari,Mahboobeh Akbari,Mahdieh Nazari
- مشاهده
- جایگاه : پژوهشی
- مجله: Journal of Kerman University of Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: oxidative stress,Liver,Acetaminophen,Mumijo
- چکیده:
- چکیده انگلیسی: Background: A majority of people widely use acetaminophen as a sedative. Overusing the drug for prolonged periods of time can lead to acute liver damage. Mumijo, as a strong antioxidant and anti-inflammatory drug, could possibly reduce some of the acetaminophen-induced side effects on the liver. Thus, the aim of this study is to evaluate the effect of Mumijo on the liver damage caused by the use of acetaminophen. Methods: 40 male Wistar rats were randomly divided into five groups: sham, acetaminophen, low and high doses of mumijo, and vehicle. All groups except the sham group received a single dose of 500 mg/kg acetaminophen via ip injection. Then the groups that were under treatment received 150 mg/kg (low dose) and 250 mg/kg (high dose) of mumijo, and the vehicle group received distilled water as vehicle. After 24 hours, blood samples were taken for biochemical tests, and a part of the liver was extracted for histopathological examination. Results: acetaminophen increases the activities of functional liver enzymes including alanine amino transferase (ALT), aspartate aminotransferase (AST), and gamma glutamine transferase (GGT). In groups under treatment, values of the mentioned enzymes were significantly reduced in comparison with the acetaminophen and vehicle groups (P <0.05), and on the other hand, malondialdehyde (MDA), nitric oxide (NO), and protein carbonyl (PC) increase caused by acetaminophen were reduced by mumijo. Furthermore, the amount of glutathione (GPX) was increased by mumijo (P <0.05). From a histopathological point of view, necrosis and liver damage caused by acetaminophen was decreased by mumijo. Conclusion:The findings showed that mumijo is salient in preventing liver damage caused by consumption of high doses of acetaminophen probably through reducing oxidant activities and also through increasing anti-inflammatory and antioxidant activities.
- انتشار مقاله: 13-04-1396
- نویسندگان: Jabber Atashbar,Nader Shahrokhi,Mohammad Khaksari Haddad,Gholamreza Asadi Karam,Nava Shahrokhi,Farhood Ghazi
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Immunology
- نوع مقاله: Journal Article
- کلمات کلیدی: Vitamin D,Experimental autoimmune encephalomyelitis,IL-33,IL-27
- چکیده:
- چکیده انگلیسی: Background: It has been reported that vitamin D has broad anti-inflammatory and immunomodulatory effects.
Objective: To evaluate the effects of vitamin D on the expression of IL-27 and IL-33 in a model of experimental autoimmune encephalomyelitis (EAE).
Methods: EAE was induced in C57BL/6 mice by immunization with myelin oligodendroglial glycoprotein mixed with complete Freund's adjuvant. The mice were administered with PBS or olive oil, intraperitoneally, in the control groups and vitamin D (200 ng every two days) in the treatment group, from day +3 to +30. At day 31, the mice were scarified and their spinal cords and brains were harvested. The expression of the IL-27 and IL-33 mRNA in the spinal cord was measured using real time-PCR.
Results: In PBS- or olive oil-treated EAE mice the expression of IL-27 P28 mRNA was significantly lower than that in the healthy control group (p<0.002). In both PBS- and olive o il-treated EAE groups, the expression of IL-27 EBI3 mRNA was also lower than that observed in the healthy group, but the differences were not significant. In vitamin D-treated EAE group, the expression of IL-27 P28 and IL-27 EBI3 were significantly higher compared with the olive oil-treated EAE groups (p<0.002 and p<0.04, respectively). The expression of IL-33 was significantly higher in PBS-or olive oil-treated EAE groups compared with healthy mice (p<0.05 and p<0.02, respectively). Vitamin D significantly decreased the expression of IL-33 compared with PBSor olive oil-treated EAE mice (p<0.04, p<0.02, respectively). The PBS- or oliv -treated e oil EAE mice showed the clinical symptoms of EAE at days 9 and 10, respectively. The vitamin D-treated EAE group exhibited the symptoms at day 12 post immunization. The maximum mean clinical score and mean pathological scores were also significantly lower in vitamin Dtreated EAE group, in comparison with PBS- or olive oil treated EAE mice (p<0.001).
Conclusion: Vitamin D may modulate the expression of IL-27 and IL-33 in the spinal cord of EAE mice and also ameliorate the clinical symptoms of the disease.- انتشار مقاله: 14-05-1395
- نویسندگان: Marziyeh Mohammadi-Kordkhayli,Rayhane Ahangar-Parvin,Sayed Vahab Azizi,Maryam Nemati,Ali Shamsizadeh,Mohammad Khaksari,Sayed Mohammad Moazzeni,Abdollah Jafarzadeh
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Lipid Peroxidation,candesartan,Intracranial pressure,Brain injury,Brain edema,Blood-brain barrier,Angiotensin II receptor
- چکیده:
- چکیده انگلیسی: Objective(s): Neuroprotection is created following the inhibition of angiotensin II type 1 receptor (AT1R). Therefore, the purpose of this research was examining AT1R blockage by candesartan in diffuse traumatic brain injury (TBI).
Materials and Methods: Male rats were assigned into sham, TBI, vehicle, and candesartan groups. Candesartan (0.3 mg/kg) or vehicle was administered IP, 30 min post-TBI. Brain water and Evans blue contents were determined, 24 and 5 hr after TBI, respectively. Intracranial pressure (ICP) and neurologic outcome were evaluated at -1, 1, 4 and 24 hr after TBI. Oxidant index [malondialdehyde (MDA)] was determined 24 hr after TBI.
Results: Brain water and Evans blue contents, and MDA and ICP levels increased in TBI and vehicle groups in comparison with the sham group. Candesartan attenuated the TBI-induced brain water and Evans blue contents, and ICP and MDA enhancement. The neurologic score enhanced following candesartan administration, 24 hr after TBI.
Conclusion: The blockage of AT1R may be neuroprotective by decreasing ICP associated with the reduction of lipid peroxidation, brain edema, and blood-brain barrier (BBB) permeability, which led to the improvement of neurologic outcome.- انتشار مقاله: 05-07-1396
- نویسندگان: Mohammad Khaksari,Mohammad Amin Rajizadeh,Mohammad Abbas Bejeshk,Zahra Soltani,Sina Motamedi,Fatemeh Moramdi,Masoud Islami,Shahriyar Shafa,Sepehr Khosravi
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Melatonin,Intracranial pressure,Estrogen,TBI,Brain edema,Aquaporin 4
- چکیده:
- چکیده انگلیسی: Objective(s): Traumatic brain injury (TBI) is one of the most common causes of death and disability in modern societies. The role of steroids and melatonin is recognized as a neuroprotective factor in traumatic injuries. This study examined the role of melatonin receptors in the neuroprotective effects of estrogen.
Materials and Methods: Seventy female ovariectomized Wistar rats were divided into five groups and two subgroups. All animals underwent brain trauma. The groups were as follow: 1) trauma, 2) melatonin receptor antagonist vehicle + estrogen, 3) MT1 melatonin receptor antagonist + estrogen, 4) MT2 melatonin receptor antagonist+ estrogen, 5) MT3 melatonin receptor antagonist+ estrogen. Brain edema (24 hr), intracranial pressure (ICP) (-1, 0, 1, 4 and 24 hr) and blood–brain barrier (BBB) permeability (5 hr) and aquaporin (AQP4) expression (24 hr) were evaluated after TBI.
Results: MT1, MT2 and MT3 melatonin receptors had anti-edema effects while MT1 and MT2 have a role in protecting BBB by estrogen. Furthermore, the activity of MT3 and MT2 melatonin receptors weakened the effect of estrogen on ICP. However, melatonin receptors had no role in the effect of estrogen on AQP4 protein.
Conclusion: Based on the above results, it seems that melatonin receptors appear to influence the effect of estrogen in TBI without altering AQP4 expression. The role of the receptors is different in this interaction.- انتشار مقاله: 06-06-1396
- نویسندگان: Nader Shahrokhi,Mohammad Khaksari,Gholamreza Asadikaram,Zahra Soltani,Nava Shahrokhi
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Estradiol,Progesterone,Traumatic brain injury,Neuromedin U,NMS,NMUR2
- چکیده:
- چکیده انگلیسی: Objective(s): Neuroprotective effects of female gonadal steroids are mediated through several pathways involving multiple peptides and receptors after traumatic brain injury (TBI). Two of these peptides are including the regulatory peptides neuromedin U (NMU) and neuromedin S (NMS), and their common receptor neuromedin U2 receptor (NMUR2). This study investigates the effects of physiological doses of estradiol and progesterone on brain edema, NMS and NMU as well as NMUR2 expression following TBI.
Materials and Methods: Ovariectomized female rats were given high-and low-dose of female sex steroid hormones through implantation of capsules for a week before trauma. The brain NMUR2 expression, prepro-NMS expression, NMU content, and water content (brain edema) were evaluated 24 hr after TBI induced by Marmarou’s method.
Results: Percentage of brain water content in high- and low-dose estradiol, and in high- and low- dose progesterone was less than vehicle (P<0.01). Results show high expression of prepro-NMS in high dose progesterone (TBI-HP) rats compared to the high dose estrogen (TBI-HE), as well as vehicle (P<0.01). NMU content in low-dose progesterone (TBI-LP) group was more than that of vehicle group (P<0.001). Furthermore a difference in NMU content observed between TBI-HP compared to TBI-HE, and vehicle (P<0.05). The NMUR2 mRNA expression revealed an upregulation in TBI-HP rats compared to the TBI-HE group (P<0.001).
Conclusion: Findings indicate that progesterone attenuates brain edema and induces an increase in NMS and its receptor which may mediate the anti-edematous effect of progesterone after TBI.- انتشار مقاله: 02-08-1395
- نویسندگان: Mohammad Khaksari,Fatemeh Maghool,Gholamreza Asadikaram,Zahra Hajializadeh
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: oxidative stress,Vagus nerve,Melatonin Ischemia/reperfusion
- چکیده:
- چکیده انگلیسی: Objectives:Vagal pathways in gastrointestinal tract are the most important pathways that regulate ischemia/reperfusion (I/R). Gastrointestinal tract is one of the important sources of melatonin production. The aim of this study was to investigate probable protective effect of the interaction between vagus nerve and melatonin after I/R.
Materials and methods:This study was performed in male rats that were divided into six groups. Cervical vagus nerve was cut bilaterally after induction of I/R and the right one was stimulated by stimulator. Melatonin or vehicle was injected intraperitoneally. The stomach was removed for histopathological and biochemical investigations.
Results: A significant decrease in infiltration of gastric neutrophils and malondialdehyde (MDA) level after I/R was induced by melatonin and was disappeared after vagotomy. The stimulation of vagus nerve significantly enhanced these effects of melatonin. However, a stimulation of vagus nerve alone increased neutrophils infiltration and MDA level. Melatonin significantly increased the activities of catalase, glutathione peroxidase (GPx), superoxide dismutases (SOD). Unlike stimulation of vagus nerve, vagotomy decreased these effects of melatonin.
Conclusion:According to these results, it is probable that protective effects of melatonin after I/R may be mediated by vagus nerve. Therefore, there is an interaction between melatonin and vagus nerve in their protective effects.- انتشار مقاله: 10-11-1394
- نویسندگان: Nader Shahrokhi,Mohammad Khaksari,Shahla Nourizad,Nava Shahrokhi Shahrokhi,Zahra Soltani,Ahmad Gholamhosseinian
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Traumatic brain injury,Blood-brain-barrier,Brain edema,ERα antagonist,ERβ antagonist,ICI182780
- چکیده:
- چکیده انگلیسی: Objective(s):Estrogen (E2) has neuroprotective effects on blood-brain-barrier (BBB) after traumatic brain injury (TBI). In order to investigate the roles of estrogen receptors (ERs) in these effects, ER-α antagonist (MPP) and, ER-β antagonist (PHTPP), or non-selective estrogen receptors antagonist (ICI 182780) were administered.
Materials and Methods: Ovariectomized rats were divided into 10 groups, as follows: Sham, TBI, E2, oil, MPP+E2, PHTPP+E2, MPP+PHTPP+E2, ICI+E2, MPP, and DMSO. E2 (33.3 µg/Kg) or oil were administered 30 min after TBI. 1 dose (150 µg/Kg) of each of MPP, PHTPP, and (4 mg/kg) ICI182780 was injected two times, 24 hr apart, before TBI and estrogen treatment. BBB disruption (Evans blue content) and brain edema (brain water content) evaluated 5 hr and 24 hr after the TBI were evaluated, respectively.
Results: The results showed that E2 reduced brain edema after TBI compared to vehicle (P<0.01). The brain edema in the MPP+E2 and PHTPP+E2 groups decreased compared to the vehicle (P<0.001). There was no significant difference in MPP+PHTPP+E2 and ICI+E2 compared to TBI. This parameter in MPP was similar to vehicle. Evans blue content in E2 group was lower than vehicle (P<0.05).The inhibitory effect of E2 on Evans blue was not reduced by MPP+E2 and PHTPP+E2 groups, but decreased by treatment with MPP+PHTPP or ICI. MPP had no effect on Evans blue content.
Conclusion: A combined administration of MPP and PHTPP or ICI inhibited the E2-induced decrease in brain edema and BBB disruption; this may suggest that these effects were mediated via both receptors.- انتشار مقاله: 06-12-1393
- نویسندگان: Vida Naderi,Mohammad Khaksari,Reza Abbasi,Fatemeh Maghool
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Celecoxib,Ibuprofen,Brain injury,Gastric Emptying
- چکیده:
- چکیده انگلیسی: Objective(s):This study was carried out to investigate the effects of COX-2 selective inhibitor (Celecoxib) or non-selective COX inhibitor (Ibuprofen) on gastrointestinal motility.
Materials and Methods: The rats were randomly divided into five groups including: intact, sham, traumatic brain injury (TBI) group (intact rats under TBI), Celecoxib group (10 mg/kg), Ibuprofen group (10 mg/kg). Rats of the treatment groups received gavages at 1 hr before the TBI induction. The TBI was moderate and diffused using the Marmarou method. The gastric emptying and small intestine transit were measured by phenol red method.
Results: The gastric emptying didn’t change following TBI induction compared to intact group. The consumption of ibuprofen or celecoxib didn’t have any effect on gastric emptying compared to sham group. TBI induction didn’t have any effect on the intestinal transit. Also, there was no significant difference between ibuprofen or celecoxib consumption vs. sham group (P>0.05).
Conclusion: The COX-2 selective inhibitor (celecoxib) or non-selective COX inhibitor (ibuprofen) have no effects on gastric or small bowel transit. Further work is necessary to investigate the effects of non-selective COX inhibitors and their impact on gastrointestinal motility disorders.- انتشار مقاله: 03-04-1393
- نویسندگان: Zakieh Keshavarzi,Mohammad Khaksari,Nader Shahrokhi
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Interleukin-10,Celecoxib,Ibuprofen,Brain injury
- چکیده:
- چکیده انگلیسی: Objective(s) Cytokines such as IL-1β are involved in inflammatory responses. This study evaluated the role of two different kinds of drugs (ibuprofen and celecoxib) on brain IL-10 and IL-1β after traumatic brain injury (TBI) in male rats. Materials and Methods Rats were assigned into 6 groups: intact, sham, TBI, and treated rats with vehicle, celecoxib or iboprophen. Cytokine concentrations were quantified by ELISA kits. Results Groups showed no significant difference in brain IL-10 either after TBI induction or after treatment with ibuprofen or celecoxib. Serum IL-10 in vehicle or ibuprofen treated animals was lower than in sham groups (P< 0.01). Brain IL-1β decreased after treatment by ibuprofen or celecoxib (P< 0.001). There was no statistical difference in serum IL-1β in TBI and intact. Serum IL-1β significantly decreased in rats that received celecoxib compared to TBI group (P< 0.01). Conclusion Based on our study IL-1β can decrease through both cyclooxygenase 1 (COX-1) and COX-2 pathway but serum IL-1β can decrease only by COX-2 pathway.
- انتشار مقاله: 28-06-1394
- نویسندگان: Zakieh Keshavarzi,Mohammad Khaksari,Zohre Razmi,Ava Soltani Hekmat,Vida Naderi,Sima Rostami
- مشاهده