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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Seizures,Pentylenetetrazol,Viola,Electroshock
- چکیده:
- چکیده انگلیسی: Background: Recently, there has been much more interest in the use of medicinal plants in search of novel therapies for human neurodegenerative diseases such as epilepsy. In the present study, we investigated the anticonvulsant effects of Viola tricolor (V. tricolor) on seizure models induced by pentylenetetrazol (PTZ) and maximal electroshock stimulation (MES). Methods: Totally, 260 mice were divided into 26 groups (n=10). Thirty minutes after treatment with the hydroalcoholic extract of V. tricolor (VHE 100, 200, and 400 mg/kg) and its ethyl acetate (EAF 50, 100, and 200 mg/kg) and n-butanol (NBF 50, 100, and 200 mg/kg) fractions as well as diazepam (3 mg/kg), seizure was induced by PTZ (100 mg/kg) or by MES (50 Hz, 1 s and 50 mA). Analysis was performed via ANOVA with the Tukey–Kramer post-hoc test using GraphPad Prism 6.01 (La Jolla, CA). Results: The VHE (400 mg/kg) significantly enhanced latency to the first generalized tonic-clonic seizures (GTCs) induced by PTZ in comparison to the control group (P<0.001). All 3 concentrations of the EAF (50, 100, and 200 mg/kg) significantly prolonged the latency of PTZ-induced seizures compared to the control group. Additionally, all the concentrations of the NBF (50, 100, and 200 mg/kg) made a significant increment in GTCs latency induced by PTZ in comparison to the control group. On the other hand, all the concentrations of the VHE, EAF, and NBF significantly reduced the incidence of hind-limb tonic extension (HLTE) induced by MES, when compared to the control group. Conclusion: The present study showed that V. tricolor and its ethyl acetate and n-butanol fractions possessed anticonvulsant effects as confirmed by the prolongation of latency to the first GTCs induced by PTZ and decrement in the incidence of HLTE induced by MES.
- انتشار مقاله: 02-07-1396
- نویسندگان: Vafa Baradaran Rahimi,Vahid Reza Askari,Mahmoud Hosseini,Bahareh Sadat Yousefsani,Hamid Reza Sadeghnia
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی:
- چکیده:
- چکیده انگلیسی: Gentamicin is an important aminoglycoside antibiotic. However its use is limited to serious and life threatening gram negative infections, because of its high nephrotoxicity potential in patients. There are reports that safranal, the active ingredient of saffron with antioxidant properties, exerts protective effect against ischemic injuries occurred by certain nephrotoxins including gentamicin. Therefore, in the present study, we examined the protective effect of safranal against gentamicin-induced nephrotoxicity in rat. After acclimatization, animals were randomly divided to three groups (8 rats /each group). On day one, each animal was placed separately in a metabolic cage for collecting 24-hour urine samples. On day two, after collecting urine samples for measuring glucose and protein, the rats in group 1 received saline 1 ml/kg for 6 days, those in group 2 received gentamicin 80 mg/kg/day for 6 days, and the remaining rats in group 3 received safranal 0.5 ml/kg followed by gentamicin 80 mg/kg/day for 6 days. Injections were intraperitoneally. All the animals were euthanized 24 hours after the last dose. Blood samples were collected by cardiac puncture, and concentration of blood urea, creatinine, and urinary glucose and protein, as the indicators of nephrotoxicity were measured. Our results showed that in group 2, concentration of blood urea nitrogen p<0.01, creatinine p<0.05, urinary glucose p<0.001, and protein p<0.01 were significantly increased compared with the control and safranal-treated groups. There was no significant difference between the control and safranal-treated groups. Safranal exerts protective effects against gentamicin-induced nephrotoxicity in rat.
- انتشار مقاله: 23-02-1394
- نویسندگان: Mohammad Taher Boroushaki,Hamid Reza Sadeghnia
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Phytochemicals,Glutamate,Neurodegenerative disorders,Excitotoxicity,Neurotransmitter
- چکیده:
- چکیده انگلیسی: Glutamate, as an essential neurotransmitter, has been thought to have different roles in the central nervous system (CNS), including nerve regeneration, synaptogenesis, and neurogenesis. Excessive glutamate causes an up-regulation of the multiple signaling pathways, including phosphoinositide-3 kinase/protein kinase B (PI3K/Akt), Akt/mammalian target of rapamycin (mTOR) protein, mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK)1/2, and autophagy that are involved in neurodegenerative diseases pathophysiology. There are numerous findings on curcumin, astaxanthin, thymoquinone, and berberine, as natural products, which have outstanding effects in cell signaling far beyond their anti-oxidant activity, considering as a potential therapeutic target for glutamate excitotoxicity. Herein, we address the role of glutamate as a potential target in neurodegenerative diseases and discuss the protective effects of certain phytochemicals on glutamate-induced neurotoxicity.
- انتشار مقاله: 16-07-1398
- نویسندگان: Amir R. Afshari,Sahar Fanoudi,Arezoo Rajabian,Hamid Reza Sadeghnia,Hamid Mollazadeh,Azar Hosseini
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: oxidative stress,Apoptosis,DNA,PC12,Rutin
- چکیده:
- چکیده انگلیسی: Objective(s): Rutin is a flavonoid with potent antioxidant property, which exhibited cytoprotective effects in several models of neuronal injury. This work aimed to examine whether rutin can protect neurons against oxidative DNA damage caused by serum/glucose deprivation (SGD) as an in vitro model of neurodegeneration and ischemia.
Materials and Methods: The PC12 cells were cultured for 2 hr in normal culture medium containing different concentrations of rutin or α-tocopherol (positive control) and then further incubated for 12 hr in SGD condition. Then, cell viability, DNA fragmentation, lipid peroxidation, generation of reactive oxygen species (ROS), and the expression of proteins involved in apoptosis were determined.
Results: The SGD condition significantly decreased viability of the cells, which was accompanied by a significant rise in the generation of ROS and lipid peroxidation. Rutin enhanced the viability of PC12 cells in SGD condition and reduced the production of ROS and lipid peroxidation. In addition, rutin decreased DNA damage and inhibited apoptotic cell death by decreasing the levels of proapoptotic proteins (Bax, caspase-3, caspase-9) and increasing the level of anti-apoptotic protein Bcl-2.
Conclusion: This study demonstrated that rutin inhibits oxidative DNA damage and neuronal death induced by nutrients deprivation condition. Further studies may warrant the use of rutin as an appropriate neuroprotective agent for ischemic attacks and other neurodegenerative disorders.- انتشار مقاله: 23-02-1397
- نویسندگان: Marjan Nassiri-Asl,Ahmad Ghorbani,Sahar Salehisar,Elham Asadpour,Hamid Reza Sadeghnia
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: cognitive,Neuroprotection,Neurodegenerative diseases,Alzheimer’s diseases,Boswellia
- چکیده:
- چکیده انگلیسی: Neurodegenerative diseases, characterized by progressive loss of neurons, share common mechanisms such as apoptotic cell death, mitochondrial dysfunction, inflammation, and oxidative stress. Genus Boswellia is a genus in the Burseraceae family. It comprises several species traditionally used for treatment of chronic inflammatory diseases, cerebral edema, chronic pain syndrome, gastrointestinal diseases, tumors, as well as enhancing intelligence. Many studies have been carried out to discover therapeutic approaches for neurodegenerative diseases such as Alzheimer’s diseases, Parkinson’s disease, Huntington’s disease, multiple sclerosis and amyotrophic lateral sclerosis, stroke, and concomitant cognitive deficits. However, no curative treatment has been developed. This paper provides an overview of evidence about the potential of the Boswellia species and their main constituents, boswellic acids, as modulators of several mechanisms involved in the pathology of the neurodegenerative diseases. In vitro, animal, and clinical studies have confirmed that Boswellia species contain bioactive components that may enhance cognitive activity and protect against neurodegeneration. They exert the beneficial effects via targeting multiple pathological causes by antioxidative, anti-inflammatory, antiamyloidogenic, and anti-apoptotic properties. The Boswellia species, having neuroprotective potential, makes them a promising candidate to cure or prevent the neurodegenerative disorders.
- انتشار مقاله: 14-07-1397
- نویسندگان: Arezoo Rajabian,Hamid Reza Sadeghnia,Sahar Fanoudi,Azar Hosseini
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Phytochemicals,Glutamate,Neurodegenerative disorders,Excitotoxicity,Neurotransmitter
- چکیده:
- چکیده انگلیسی: Glutamate, as an essential neurotransmitter, has been thought to have different roles in the central nervous system (CNS), including nerve regeneration, synaptogenesis, and neurogenesis. Excessive glutamate causes an up-regulation of the multiple signaling pathways, including phosphoinositide-3 kinase/protein kinase B (PI3K/Akt), Akt/mammalian target of rapamycin (mTOR) protein, mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK)1/2, and autophagy that are involved in neurodegenerative diseases pathophysiology. There are numerous findings on curcumin, astaxanthin, thymoquinone, and berberine, as natural products, which have outstanding effects in cell signaling far beyond their anti-oxidant activity, considering as a potential therapeutic target for glutamate excitotoxicity. Herein, we address the role of glutamate as a potential target in neurodegenerative diseases and discuss the protective effects of certain phytochemicals on glutamate-induced neurotoxicity.
- انتشار مقاله: 16-07-1398
- نویسندگان: Amir R. Afshari,Sahar Fanoudi,Arezoo Rajabian,Hamid Reza Sadeghnia,Hamid Mollazadeh,Azar Hosseini
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: oxidative stress,Apoptosis,DNA,PC12,Rutin
- چکیده:
- چکیده انگلیسی: Objective(s): Rutin is a flavonoid with potent antioxidant property, which exhibited cytoprotective effects in several models of neuronal injury. This work aimed to examine whether rutin can protect neurons against oxidative DNA damage caused by serum/glucose deprivation (SGD) as an in vitro model of neurodegeneration and ischemia.
Materials and Methods: The PC12 cells were cultured for 2 hr in normal culture medium containing different concentrations of rutin or α-tocopherol (positive control) and then further incubated for 12 hr in SGD condition. Then, cell viability, DNA fragmentation, lipid peroxidation, generation of reactive oxygen species (ROS), and the expression of proteins involved in apoptosis were determined.
Results: The SGD condition significantly decreased viability of the cells, which was accompanied by a significant rise in the generation of ROS and lipid peroxidation. Rutin enhanced the viability of PC12 cells in SGD condition and reduced the production of ROS and lipid peroxidation. In addition, rutin decreased DNA damage and inhibited apoptotic cell death by decreasing the levels of proapoptotic proteins (Bax, caspase-3, caspase-9) and increasing the level of anti-apoptotic protein Bcl-2.
Conclusion: This study demonstrated that rutin inhibits oxidative DNA damage and neuronal death induced by nutrients deprivation condition. Further studies may warrant the use of rutin as an appropriate neuroprotective agent for ischemic attacks and other neurodegenerative disorders.- انتشار مقاله: 23-02-1397
- نویسندگان: Marjan Nassiri-Asl,Ahmad Ghorbani,Sahar Salehisar,Elham Asadpour,Hamid Reza Sadeghnia
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: cognitive,Neuroprotection,Neurodegenerative diseases,Alzheimer’s diseases,Boswellia
- چکیده:
- چکیده انگلیسی: Neurodegenerative diseases, characterized by progressive loss of neurons, share common mechanisms such as apoptotic cell death, mitochondrial dysfunction, inflammation, and oxidative stress. Genus Boswellia is a genus in the Burseraceae family. It comprises several species traditionally used for treatment of chronic inflammatory diseases, cerebral edema, chronic pain syndrome, gastrointestinal diseases, tumors, as well as enhancing intelligence. Many studies have been carried out to discover therapeutic approaches for neurodegenerative diseases such as Alzheimer’s diseases, Parkinson’s disease, Huntington’s disease, multiple sclerosis and amyotrophic lateral sclerosis, stroke, and concomitant cognitive deficits. However, no curative treatment has been developed. This paper provides an overview of evidence about the potential of the Boswellia species and their main constituents, boswellic acids, as modulators of several mechanisms involved in the pathology of the neurodegenerative diseases. In vitro, animal, and clinical studies have confirmed that Boswellia species contain bioactive components that may enhance cognitive activity and protect against neurodegeneration. They exert the beneficial effects via targeting multiple pathological causes by antioxidative, anti-inflammatory, antiamyloidogenic, and anti-apoptotic properties. The Boswellia species, having neuroprotective potential, makes them a promising candidate to cure or prevent the neurodegenerative disorders.
- انتشار مقاله: 14-07-1397
- نویسندگان: Arezoo Rajabian,Hamid Reza Sadeghnia,Sahar Fanoudi,Azar Hosseini
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Apoptosis,Berberine,Neuroprotection,Glutamate cytotoxicity,Oxidative injury
- چکیده:
- چکیده انگلیسی: Objective(s): Neurodegenerative diseases have been associated with glutamatergic dysfunction. Berberine, an isoquinoline alkaloid broadly present in different medicinal herbs, has been reported to have neuroprotective effect. In the present study, the effects of berberine against glutamate-induced oxidative damage and apoptosis were investigated.
Materials and Methods: The cultured PC12 and N2a cells were pretreated (2 hr) with varying concentrations of berberine (50-1000 µM), followed by exposure to glutamate (10 mM) for 24 hr. The cells viability, intracellular reactive oxygen species (ROS), lipid peroxidation, glutathione (GSH) content, superoxide dismutase (SOD) activity, DNA fragmentation and the expressions of pro-apoptotic (cleaved caspase-3 and bax) and anti-apoptotic (bcl-2) proteins were then measured.
Results: In both cell lines, pretreatment with berberine (especially at low concentrations) significantly decreased ROS generation, lipid peroxidation, and DNA fragmentation, while improving glutathione content and SOD activity in glutamate-injured cells. Moreover, berberine showed anti-apoptotic effects by reducing the glutamate-evoked caspase-3 and bax/bcl-2 overexpression.
Conclusion: The results of present study suggest that berberine protects against glutamate-induced PC12 and N2a cells injury by decreasing oxidative stress and subsequently inhibiting apoptosis. This is relevant to berberine treatment in neurodegenerative disorders, such as dementia (Alzheimer’s disease), seizures, and stroke.- انتشار مقاله: 16-03-1396
- نویسندگان: Hamid Reza Sadeghnia,Monireh Kolangikhah,Elham Asadpour,Fatemeh Forouzanfar,Hossein Hosseinzadeh
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Seizure,Berberine,Berberis vulgaris,Barberry,Excitatory amino acids,4-Aminopyridine (4-AP)
- چکیده:
- چکیده انگلیسی: Objective(s): K+ channel blocker 4-aminopyridine (4-AP) stimulates the release of glutamate from nerve terminals and induces seizures. Berberine as a potential herbal drug exerts several pharmacological actions on the central nervous system including anxiolytic, anticonvulsant, and neuroprotective properties. The present study aimed to investigate the effect of berberine on seizure onset and time course of the extracellular levels of excitatory amino acids (EAA), glutamate and aspartate, changes produced by 4-AP in rat hippocampus.
Materials and Methods: The rats were given either saline or berberine (50, 100 and 200 mg/kg, IP) 40 min before administration of 4-AP (15 mg/kg, IP) and the onset of seizure was recorded. A group of rats also received diazepam (DZP, 15 mg/kg, IP) 20 min prior to 4-AP administration. Hippocampal extracellular levels of EAA were also measured using microdialysis assay. Analysis of the dialysate samples was performed by reversed-phase high performance liquid chromatography (HPLC) with precolumn derivatization with o-phthaldialdehyde and fluorescence detection.
Results: Our findings suggest that berberine significantly delayed the seizure onset following 4-AP injection. There was a considerable increase in the extracellular glutamate and aspartate levels in 4-AP treated rats and 4-AP-evoked release of EAA was sharply reduced (about 4-5 fold especially at 20 min after 4-AP administration) in berberine treatment groups.
Conclusion: The results of present study show that berberine attenuates 4-AP induced seizures by decreasing hippocampal aspartate and glutamate release in rats.- انتشار مقاله: 27-02-1396
- نویسندگان: Hamid Reza Sadeghnia,Ali Reza Taji,Fatemeh Forouzanfar,Hossein Hosseinzadeh
- مشاهده