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Showing 15 results for Curcumin
Fatemeh Attari , Gholamreza Hassanzadeh, Hadi Aligholi ,
Volume 2, Issue 4 (12-2014)
Abstract
Traumatic brain injury resulting road accidents create damage to the brain. The severe brain injury may cause extensive tissue loss of several parenchyma which results in cavities due to primary destruction and secondary injuries such as ischemia and inflammation. Recent findings suggest that neuronal precursors in the adult mammalian brain can be a therapeutic target in ischemic brain injuries. It has been reported that curcumin reduces oxidative stress and stimulates neurogenesis in the brain. The present study was undertaken to evaluate the neuroprotective and neurogenesis effects of curcumin in a rat model of transient global ischemia (TGI). Fourty-eight adult male Wistar rats were randomly chosen as control, sham (animals only underwent TGI), treatment (animals were treated with 100 or 300 mg/kg curcumin following TGI) and vehicle groups. 5-bromo-2-deoxyuridine was injected intra pritoneally twice daily for three consecutive days. Then, animals were decapitated for 3 and 4 weeks after treatment. Neurogenesis, cell injury and apoptosis in the hippocampus, somatosensory neocortex, subventricular as well as subgranular zone and posterior periventricular region were assessed. We found that the number of dark neurons and apoptotic cells increased after TGI. Treatment with curcumin reduced the number of dark neurons and apoptotic cells in a dose-dependent manner. In addition, application of curcumin increased neurogenesis at low concentration in comparison to control and ischemia groups while higher concentration of curcumin reduced the neurogenesis. The present investigation provides evidences supporting the neuroprotective potential of curcumin in vivo and opens a new horizon for future experiments.
Parastoo Barati Dowom, Marzieh Darvishi, Mohammad Jabbarian, Azam Babakhani, Kambiz Roshanaei,
Volume 5, Issue 1 (3-2017)
Abstract
Introduction: Any traumatic spinal cord injury (SCI) may cause symptoms ranging from pain to complete loss of motor and sensory functions below the level of the injury. Despite of many advances in surgical techniques, treatment of SCI remains as a complex issue. Reduction of the initial inflammatory processes by creation of framework is suggested as a possible novel treatment. The aim of this study was evaluation of the effect of curcumin on the improvement of behavioral movement in rat contusion model in acute phase. Materials and Methods: In this in vivo study, rats were randomly assigned to experimental, laminectomy, sham operated (normal saline injected) and treatment groups. In treatment groups, the rats received daily intraperitoneal injection of curcumin (70, 60, 50, or 40 mg/ml/kg) at 6 h after the SCI. Spinal cord injury was performed by a standard procedure. After shaving, laminectomy was performed at T12-L1 level and the exposed spinal cord was exposed a 10 gram metal rod with a 2 mm diameter dropped from a height of 25 mm. The locomotor function was assessed by Basso-Beattie-Bresnahan (BBB) test for 12 weeks. Three months after SCI, the spinal cords were evaluated by morphometric, glial fibrillary acid protein (GFAP) expression, and the axonal regeneration. Results: Immunohistochemical staining and BBB test scores of spinal cord injured rats treated with curcumin were significantly improved at day 7 compared to sham rats. The level of GFAP was significantly decreased in curcumin treated group compared to sham group. Optimal dose of curcumin was 60 mg/ml/kg 6 h after SCI. Conclusion: The data demonstrate that curcumin improves behavioral movement in acute phase of SCI, possibly via the enhancement of axonal regeneration and reduction of astrogloisis.
M Beiraghi Toosi , K Hassanpour, J Akhondian, F Ashrafzadeh, F Ebrahimzadeh,
Volume 5, Issue 2 (4-2017)
Abstract
Epilepsy is a neurological disease of the central nervous system. It is estimated that about 50-70 million people worldwide suffer from this chronic disorder and 20 to 30% are resistant to conventional anti-epileptic drugs. In the epilepsy therapeutic arena, there is real need for developing novel antiepileptogenesis treatments that offer a way to prevent the onset or the progression of the disease. Such treatments are still lacking. Numerous experimental and clinical findings demonstrate that brain inflammation plays a key role in the generation of seizures and the pathogenesis of epilepsy. Some conventional corticosteroid therapies are used for seizures in infantile spasm, lafora disease and Rasmussen syndrome. There are some herbal drugs that have anti-inflammatory effects but small side effects, like curcumin. Curcumin is the active component of turmeric which is used in every day cooking. Molecular investigations reveal that curcumin has anti-inflammatory, antimicrobial, anti-hepatotoxic and anti-hyperlipidemic affects. Curcumin has recently been reported to have anticonvulsant effects in several animal models of epilepsy and in our investigation, has effect on refractory myoclonic seizures in children with no significant side effect.
Masoomeh Mohamadpour, Leila Kamali Dolatabadi,
Volume 5, Issue 2 (4-2017)
Abstract
Introduction: Multiple sclerosis (MS) is a progressive and autoimmune neurodegenerative disease of the central nervous system (CNS). This disease is renowned through symptoms like inflammation, demyelination and the damage of neurological actions. Melittin is one of components of bee venom and has anti-neuroinflammatory effects. Curcumin also, a dietary spice from turmeric, has outstanding anti-inflammation and neuroprotective effects. Materials and Methods: Experimental allergic encephalomyelitis (EAE) is a widely accepted animal model for MS. EAE is created in animals by injecting the tissue of myelin basic protein (MBP), CNS, or myelin oligodendrocyte glycoprotein (MOG) along with the adjuvant. EAE and MS are similar diseases. EAE was induced in 40 rats randomly placed in four groups of 10: Group 1: Named E-S received normal saline (0.2 mL) every day. Group 2: Named E-mel, received 10 mg/Kg melittin every day. Group 3: Named E-cur, received 100 mg/Kg curcumin every day and Group 4: Named E-cur+mel .The treatments started from the first day of post immunization through GPSH-CFA and lasted until the tenth day. The ELISA and the high performance liquid chromatography (HPLC) were used for the assessment of tumor necrosis factor alpha (TNF-α) and nitrate in rats serum. Results: In this study, we indicated that the treatment of EAE with melittin and curcumin decreased the symptoms of clinical disorder, level of serum TNF-α and the serum nitrates in rat EAE. Conclusion: This activity of melittin and curcumin may be caused by the anti-inflammatory effects and the immuno-modulatory and antioxidant effects of these.
Alireza Hoseini, Amirreza Memari, Houshang Rafatpanah, Hamid Reza Rahimi,
Volume 5, Issue 2 (4-2017)
Abstract
Human T-lymphotropic virus type I (HTLV-1) is an endemic virus in Iran and other regions that is associated with multiple diseases including adult T-cell leukemia/ lymphoma and a chronic debilitating neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HAM/TSP is seen in approximately 2% of HTLV-1-infected people with symptoms such as back pain, weakness or paralysis of the lower limbs, and urinary tract symptoms. Immunological and Inflammatory responses cause Tissue damage in HAM/TSP patients and influence proviral load of HTLV-1. Curcumin (Diferuloylmethane), a natural compound derived from rhizome of turmeric, has been shown to possess anti-oxidant, anti-inflammatory and anti-microbial characteristics. Turmeric is a GRAS (Generally Recognized as Safe) agent, which is used widely in Iranian traditional medicine. Several kinds of immune cells can be infected by HTLV-1, but CD4+ cells as main target for htlv1 drew attention to themself. Patients with HAM/TSP have an increased level of inflammatory cytokines. Recent researches focused on effect of curcumin on four subsets of cd4+ cells: t regulatory (Treg), Th1, Th2, and Th17. curcumin drive the Th17/Treg balance toward the Treg dominance, which in turn suppresses the inflammatory process. Another presumable mechanism of curcumin, as an anti-inflammatory substance, is its regulatory effect that shifts immune system from Th1 to Th2 responses and could inhibit NF-КB inflammatory pathway. Curcumin has also showed Anti-viral properties that may be attributed to direct inhibition of virus replication or due to blockage of viral replication pathways. Considering the important role of proviral load in HAM/TSP development, curcumin may be efficient in lowering this load, too. Few studies have evaluated the efficacy of curcumin in treatment of HAM/TSP, but lack of randomized clinical trials and retraction of papers on this issue due to duplication caused doubts about the efficacy of this substance and urges new researches in this field.
Sara Abbassi,
Volume 5, Issue 2 (4-2017)
Abstract
Multiple sclerosis (MS) is the most common autoimmune disease, especially among young’s. Neuroinflammation results from inflammation in CNS and it may cause different disorders and diseases .It is also known as a detriment in multiple sclerosis. In fact, it causes problems and symptoms in MS. In MS the self-immune cells attack the myelin of neurons, it maybe the nerve in brain or spinal cord. Demyelination causes inflammation in the area and activation of the microglial cells. Microglial cells (macrophages in nervous system) protect nervous system and they are also important in neuroinflammation especially in autoimmune condition. Microglial cells can cause inflammation in MS in these ways: Presenting of neural autoantigens to autoreactive T cells, Secreting of proinflammatory cytokines.) TNF-alpha, IL-1 beta, IL-6), increasing permeability of blood vessels, releasing nitric oxide (NO). Anti-inflammatory drugs can decrease symptoms of MS. As we know Curcumin or diferuloylmethane is a yellow pigment and principal curcuminoid of turmeric. Anti-inflammatory properties of curcumin are obtained by the control of secretion nitric acid through decreasing the level of MRNA and protein producing nitric oxide and restraining LPS that result in releasing cytokines. Regulating inflammatory cytokines such as IL-1beta, IL-6, IL-12, TNF-alpha and IFN-gamma and associated JAK-STAT, AP-1, and NF-kappaB signaling pathways in immune cells are decreased by curcumin. The purpose of this study is to suggest that turmeric can be as a natural herbal drug for inflammatory diseases like MS. According to the evidences , we can say turmeric, which contains curcumin can use as a prevention in MS or any diseases with inflammation like autoimmune diseases and Curcumin as an herbal matter has anti-inflammatory effects especially on microglial cells so it can be considered as a benefit dietary factor in patients with MS.
Mokhtar Ahmadi, Pouya Ghaderi, Fatemeh Shahbeigi, Seyed Reza Hosseini,
Volume 5, Issue 2 (4-2017)
Abstract
Curcumin is a hydrophobic polyphenol and major bioactive component of turmeric with known anti-inflammatory, neurogenesis, antioxidant, and anti-carcinogenic effect. Curcumin antagonizes many steps in the inflammatory cascade, including Inhibition of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), activator protein-1 transcription and iNOS (induced Nitric oxide synthases). Inhibition of NFkB is believed to be the central pathway of curcumin’s mechanism. Curcumin induced the antioxidative protein HO-1 which reduced the microglial pro-inflammatory cytokines such as TNF α, IL 1β and IL 6. All these mechanisms indicate the anti-inflammatory effect and neuroprotective action of this chemical against neuroinflammation also Neuroinflammation is implicated in the pathogenesis of many neurodegenerative diseases. Curcumin administration has been reported to attenuate neuroinflammation.in contrast to nonsteroidal anti-inflammatory drugs whose adverse side effects includes gastrointestinal ulceration and liver or kidney toxicity, curcumin seems to be relatively safe but Despite its multi anti-inflammatory properties, curcumin’s clinical use is limited because its poor oral absorption, rapid systemic elimination, rapid metabolism and limited blood brain barrier permeability but the most challenging factor is curcumin’s low aqueous solubility. Clinical studies on humans and rodents have reported low bioavailability of curcumin shown by the lower level of serum and tissue curcumin.in this study we aim to overview the prospective and challenges on curcumin use as an anti-inflammatory drug. Curcumin’s anti-inflammatory effect is well-established but clinical administration of this chemical is limited due to its poor bioavailability, so approaches to enhance the bioavailability of curcumin is needed and maybe using the structural analogues of curcumin, adjuvants like piperine, phospholipids and biodegradable nanoparticle mediated delivery of curcumin are the best ways to increase curcumin’s bioavailability.
Seyed Damoon Sadoughi, Jina Khayatzadeh,
Volume 6, Issue 1 (1-2018)
Abstract
Introduction: Alzheimer's disease (AD) is a progressive neurodegenerative disease of the central nervous system. Neuronal injury and oxidative stress in AD increases the level of inflammatory cytokines. Curcumin has antioxidant and neuroprotective properties. The aim of this study was to determine the effect of curcumin on hippocampal levels of brain-derived neurotrophic factor (BDNF) and serum levels of inflammatory cytokines in an experimental model of AD. Materials and Methods: 28 male rats divided into 4 groups: Control group (30 days, intraperitoneal injection of DMSO), AD control group (30 days, intraperitoneal injection of DMSO, after induction of AD) and two AD treatment groups with application of 50 and 100 mg/kg of curcumin (30 days, intraperitoneal injection of curcumin, after induction of AD). AD was induced by intraperitoneal injection of 8 mg/kg trimethyltin chloride. At the end of the treatment period, the hippocampal levels of BDNF and serum levels of different cytokines (TNF-α, IL-1β and IL-6) were measured by ELISA method. Results: Compared to AD control group, administration of curcumin with dose of 100 mg/kg significantly increased the hippocampal levels of BDNF (P=0.002) and decreased the serum levels of TNF-α, IL-1β and IL-6 (P=0.001). Conclusion: Administration of curcumin may decrease the serum levels of inflammatory cytokines in AD, possibly via enhancement of the hippocampal levels of BDNF. This study suggests the protective effect of curcumin against neuronal damages and oxidative stress in AD.
Homa Talebi, Akbar Hajizadeh Moghaddam, Mahbobe Zare, Sedigheh Khanjani Jelodar,
Volume 6, Issue 2 (4-2018)
Abstract
Ischemic stroke causes the depletion of energy and induces excitotoxicity and neuroinflammation in the brain that results from thrombotic blockage. Cerebral ischemia leads to many types of memory loss, including impairment of working, spatial and object recognition memoreis. Curcumin shows strong anti-oxidoinflammatory activities but it terapathics limited by its low solubility in water and corresponding poor intestinal absorption. So, in this study curcumin used in conjugate with dextran as polymeric carriers in novel drug delivery system. The purpose of this study was to determine the effect of dextran-curcumin on memory impairment induced by global ischemia. In this study 35 rats individed 5 groups. Pre-treatment and positive control groups, were treated with curcumin and dextran- curcumin (15mg/kg - orally) for 30 days and the vehicle and disease groups received distillated water. For induction of ischemic stroke model, rat were anaesthetized and both right and left carotid arteries were selected and clamped for 5 min by vascular clamps (time of ischemia), There after the vascular clamps were removed for the next 10 min (time of reperfusion), and both carotid arteries were clamped again for 5 min. Finally, the vascular clamps were removed and blood circulation was return in both carotid arteries, 48 hours after induction of model, Novel Object Recognition test was used to determine memory impairment in all rats. Our study indicated that memory impairment increace in ischemic groupe and dextran curcumin has memory-improving effects after global ischemic stroke (p˂ 0.01): Dextran-curcumin has memory-improving capacity better than curcumin in lower does.
Meysam Gachpazan, Sadra Habbibirad, Hoda Kashani, Hamid Reza Rahimi,
Volume 6, Issue 2 (4-2018)
Abstract
Curcumin is active component of turmeric and isolated from the rhizome of turmeric, a phenolic natural product. One of inflammatory disease is multiple sclerosis, a multifocal chronic autoimmune inflammatory disease of the CNS, which is also known as a perivascular demyelinating disease. Studies have been shown that neuro-inflammation can have both harmful and beneficial effects on the neuronal and glial cells function, transcription factor nuclear factor-kappa B(NF-κB) has a determinant role in controlling this process. The involvement of NF-κB signaling pathway in multiple sclerosis has been suggested by genome-wide association studies. Selective anti-NF-κB therapeutic strategies could be beneficial for minimizing damages during acute and chronic inflammation. Genes that can be induced by NF-κB signaling include those that encode important molecules such as TNF-α, IL-1, IL-6, SOD, Bcl-2, and inhibitors of apoptosis proteins. Curcumin, have been shown exhibit anti-inflammatory and anti-mutagenic in addition to anti-carcinogenic activity. Downregulation expression of the NF-κB-regulated gene products such as COX-2, TNF, 5-LOX, IL-1, IL-6 and others, inhibition multiple pro-inflammatory pathways.
Mahmoud Gorji Valokola, Bibi Marjan Razavi, Gholamreza Karimi, Mohsen Imenshahidi,
Volume 6, Issue 2 (4-2018)
Abstract
Bisphenol A (BPA) is used in the manufacture of polycarbonate plastics and epoxy resins; therefore, exposure to BPA is increasing every day. BPA has toxic effects on various human tissues. Curcumin, a yellow polyphenol, is the active turmeric ingredient. It is an efficacious and safe compound with multiple pharmacological activities including antioxidant, ant carcinogenic, ant proliferative, and anti-inflammatory properties. This study was designed to determine the potential protective effect of nanomicelle curcumin on BPA-induced subacute brain toxicity in rats. The wistar rats were divided into six groups (8 rats/group). The first group served as the control (dextrose 5% + sesame oil); the second group received 50 mg/kg nanomicelle curcumin; the third group was fed 50 mg/kg BPA; the fourth, fifth, and sixth groups received 10, 25, and 50 mg/kg nanomicelle curcumin, respectively, supplemented with 50 mg/kg BPA, after one hour. At the end of the study period (4 weeks), MDA level and GSH content were measured in the cerebellum, cortex and hippocampus. This study revealed that the dose of 50 mg/kg of BPA significantly increased malondialdehyde in the cerebellum (P< 0.001), cortex (P< 0.001) and hippocampus (P< 0.01). In addition, BPA decreased glutathione content in the cerebellum (P< 0.001), cortex (P< 0.001) and hippocampus (P< 0.01) as well. However, nanomicelle curcumin (50 mg/kg) significantly improved these toxic effects of BPA in rat brain tissue. The results provide evidence that nanomicelle curcumin has preventive effects in subacute exposure to BPA (50 mg/kg) induced toxicity in rat brain tissue.
Leila Kamali Dolatabadi, Masoumeh Emamghoreishi, Mohammad Reza Namavar,
Volume 6, Issue 2 (4-2018)
Abstract
Global cerebral ischemia (GCI) leads to inflammation and neuronal death in CA1. Curcumin with neuroprotective and anti-inflammatory properties is a potential candidate for suppressing cell death. The aim of this study was to determine the effects of curcumin on neuronal number in the CA1 area following GCI. 28 Sprague-Dawley male rats were randomly assigned into four groups including sham, control, and curcumin 50 and 100 mg/kg (n= 7/group). Two treatment groups were orally received curcumin for 28 days. Control group was received PBS, Sham group did not receive anything. Cresyl violet staining following GCI was performed in 40μm paraformaldehyde perfused sections. Then the volume “v (CA1)” was estimated using the Cavalieri method and the total number of neurons in the CA1 area was determined using the optical dissector method. There were no significant differences in the volume of CA1 between studied groups. Total number of neurons significantly reduced in control group compare with sham group (p<0.01). Also there was no significant difference between curcumin 50 mg/kg and control group in total number of neurons. But, curcumin 100 mg/kg significantly increased number of neurons in comparison with curcumin 50 mg/kg (p<0.05) and control group (p<0.01). We found two effects̛ curcumin dose dependently: the first, curcumin cause to prevent neuronal death, the second, curcumin increased neuronal number of CA1.
Parnia Tarahomi, Hossein Ali Safakhah, Farzaneh Mohammadzadeh, Seyed Ali Seyedinia, Ali Rashidy-Pour, Abbas Ali Vafaei,
Volume 6, Issue 2 (4-2018)
Abstract
Treatment of neuropathic pain is still a major challenge because of its noresponsiveness to most available pharmacotherapy. Curcumin has been reported to play an active role in the treatment of various neurological disorders, such as neuropathic pain. In this study, the role of curcumin has been evaluated in pain behavioral responses of chronic Constriction injury (CCI) in rat. In this experimental study male Wistar rats (200–250 g) were used. Animals have been categorized as random based on groups of CCI, CCI with vehicle injection and CCI with 30 and 60 mg/kg Curcumin injection. For induction of CCI, Bennett & Xie (1988) method has been used applying CCI by 4 loose ligatures. Fourteen days after creation of neural injury, IP Injection of Vehicle and Curcumin have been started and continued to 26th day as daily. Animal behavioral responses have been measured using mechanical allodynia (Von Frey) and thermal hyperalgesia in 14 to 40th days After CCI. Data analyzed by one-way ANOVA and tukey test. Results indicated that CCI increases pain behavioral responses as significantly (P<0.05). Curcumin injection (30mg/Kg) leads to decrease of mechanical allodynia from 20th day and thermal hyperalgesia from 23th day. These effects have been continued to 40th day. Curcumin injection (60 mg/kg) leads to decrease of mechanical allodynia and thermal hyperalgesia only in 26th day. Based on findings, probably, curcumin can be effective on resulted neuropathy pains of CCI.
Saeideh Baradaran, Akbar Hajizadeh Moghaddam, Sedigheh Khanjani Jelodar,
Volume 6, Issue 2 (4-2018)
Abstract
Inflammatory disorders alone or as a consequence of neurological disease affecting patients in life. Experimental models of inflammation are use to evaluate the production of inflammatory mediators at site of inflammation. Curcumin is one of the flavonoids possesses potent anti-inflammatory activity. However, because of low water solubility curcumin, its clinical application has been limited. The present study attempts to assessment the effects of curcumin and nano-phytosome of curcumin on improve of behavioral impairment and reduce inflammation cytokines in carrageenan-induced inflammation model. Animals have received oral administration of curcumin or nano-phytosom of curcumin at dose of 15 mg/kg for 7 days before injection of carrageenan. Acute inflammation was induced by injection of carrageenan (1%,) into the subplantar region of left paw in mice. Tail pinch test and hotplate test (for evaluated the threshold of neuroinflammation pain) were performed on ½ h before injection and ½ h, 2 h, 24 h after injection of carrageenan. The results of behavioral testes showed enhance of antinociceptive effects in the animals recieved curcumin(p≤0.01) and nano-phytosome of curcumin (p≤0.001) compaired to other groups. These results suggested that curcumin and its nano-phytosome improvement behavioral impairment and reduce inflammation cytokines following local injection of carrageenan.
Golamhossein Tondro, Ghadir Rajabzade, Ali Mohammadi, Hamidreza Moradi, Sajad Sahab Negah,
Volume 10, Issue 3 (7-2022)
Abstract
Introduction: Glioblastoma multiforme is known as an aggressive brain tumor that is characterized by a high rate of recurrence. Current treatment strategies are not effective for GBM; therefore, novel targeted therapeutic options are urgently required. Nanocarrier-based drug delivery has recently gained attention due to the characteristics of blood-brain barrier permeability, continued drug release, improved solubility, and enhanced drug bioactivity. To this point, we investigated the superior effect of a nano-form of curcumin vs. free-form on the secretion of pro-inflammatory cytokines profile (i.e., IL6 and TNF-α) in the U87 cell line. Materials and Methods: The U87 cell line was purchased from the Iranian Biological Resource Center and expanded in the DMEM/F12 media with 10% FBS and 1% Pen/Strep. To synthesize nanoniosome containing curcumin, the thin-film hybridization method was used. To evaluate the production of IL6 and TNF-α by ELISA method, U87 cells were treated with 84.87 µg/ml of Nano-curcumin and 47 µg/ml of free curcumin. Results: Our results indicated that the production of IL6 and TNF-α was significantly decreased when treated with nano-form and free curcumin. Interestingly, we observed that nano-curcumin could significantly inhibit the secretion of IL6 and TNF-α compared to the curcumin group. Conclusion: The most obvious finding to emerge from this study is that nano-curcumin exerts antiimflammatory effects on glioblastoma.
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