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  • 1.
    Bagheri, Maryam
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Neuroprotective Effect of Genistein: Studies in Rat Models of Parkinson’s and Alzheimer’s Disease2012Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Parkinson’s disease (PD) and Alzheimer’s disease (AD) are neurodegenerative disorders that mainly affect the elderly population. It is believed that oxidative stress is involved in development of both these diseases and that estrogen deficiency is a risk factor for development of AD. Genistein is a plant-derived compound that is similar in structure to estrogen and has anti-oxidative properties. The general objective of the present research was to evaluate the effects of genistein on neurodegeneration in rat models of PD and AD.

    Using a rat model of PD, we found that a single intraperitoneal dose of genistein 1 h before intrastriatal injection of 6-hydroxydopamine (6-OHDA) attenuated apomorphine-induced rotational behavior and protected the neurons of substantia nigra pars compacta against 6-OHDA toxicity.

    To produce an animal model of AD, we injected Aβ1–40 into the hippocampus of rats. Using groups of these Aβ1–40-lesioned animals, the involvement of estrogen receptors (ERs) was evaluated by intracerebroventricular injection of the estrogen receptor antagonist fulvestrant, and the role of oxidative stress was studied by measuring levels of malondialdehyde (MDA), nitrite, and superoxide dismutase (SOD) activity. The results showed that intrahippocampal injection of Aβ1–40 caused the following: lower spontaneous alternation score in Y-maze tasks, impaired retention and recall capability in the passive avoidance test, and fewer correct choices and more errors in a radial arm maze (RAM task), elevated levels of MDA and nitrite, and a signiHcant reduction in SOD activity in the brain tissue. Furthermore, hippocampus in theses rats exhibited Aβ1–40 immunoreactive aggregates close to the lateral blade of the dentate gyrus (DGlb), extensive neuronal degeneration in the DGlb, high intracellular iNOS+ and nNOS+ immunoreactivity, and extensive astrogliosis.

    Genistein pretreatment ameliorated the Aβ-induced impairment of short-term spatial memory, and this effect occurred via an estrogenic pathway and through attenuation of oxidative stress. Genistein also ameliorated the degeneration of neurons, inhibited the formation of Aβ1–40-positive aggregates, and alleviated Aβ1–40-induced astrogliosis in the hippocampus.

    Delarbeten
    1. Neuroprotective Effect of Genistein in 6-Hydroxydopamine Hemi-parkinsonian Rat Model
    Öppna denna publikation i ny flik eller fönster >>Neuroprotective Effect of Genistein in 6-Hydroxydopamine Hemi-parkinsonian Rat Model
    2008 (Engelska)Ingår i: Phytotherapy Research, ISSN 0951-418X, E-ISSN 1099-1573, Vol. 23, nr 1, s. 132-135Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    A large body of experimental evidence supports a role for oxidative stress as a mediator of nerve cell death in Parkinson-s disease (PD). Phytoestrogens such as genistein have been reported to prevent neuronal degeneration caused by increased oxidative burden, therefore, this study examined whether genistein administration at a high dose would attenuate behavioral and structural abnormalities in an experimental model of PD in rat. For this purpose, unilateral intrastriatal 6-hydroxydopamine (6-OHDA, 12.5 μg/5 μL of saline-ascorbate)- lesioned rats were intraperitoneally pretreated with a single and high dose of genistein (10 mg/kg) 1 h before surgery. Apomorphine-induced rotations and the number of Nissl-stained neurons in the substantia nigra pars compacta (SNC) were counted after 2 weeks. Genistein administration could attenuate the rotational behavior in lesioned rats and protect the neurons of SNC against 6-OHDA toxicity. Genistein administration has a protective effect against 6-OHDA toxicity. 

    Nyckelord
    genistein • Parkinson's disease • 6-hydroxydopamine • rotation • rat
    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:liu:diva-44303 (URN)10.1002/ptr.2564 (DOI)18693302 (PubMedID)76209 (Lokalt ID)76209 (Arkivnummer)76209 (OAI)
    Tillgänglig från: 2009-10-10 Skapad: 2009-10-10 Senast uppdaterad: 2017-12-13
    2. Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease
    Öppna denna publikation i ny flik eller fönster >>Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease
    2011 (Engelska)Ingår i: Neurobiology of Learning and Memory, ISSN 1074-7427, E-ISSN 1095-9564, Vol. 95, nr 3, s. 270-276Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Alzheimers disease (AD) is a debilitating neurodegenerative disorder characterized by increased beta-amyloid (A beta) deposition and neuronal dysfunction leading to impaired learning and recall. Ageing, heredity, and induced oxidative stress are among proposed risk factors. The increased frequency of the disease in women also suggests a role for estrogen in development of AD. In the present study, effects of the phytoestrogen genistein (10 mg/kg) on learning and memory impairments was assessed in intrahippocampal A beta((1-40))-injected rats. The estrogen receptor antagonist fulvestrant was injected intracerebroventricularly in a group of A beta-lesioned rats. The A beta-injected animals exhibited the following: lower spontaneous alternation score in Y-maze tasks, impaired retention and recall capability in the passive avoidance test, and fewer correct choices and more errors in the RAM task. Genistein, but not genistein and fulvestrant, significantly improved most of these parameters. Measurements of oxidative stress markers in hippocampal tissue of A beta-injected rats showed an elevation of malondialdehyde (MDA) and nitrite content, and a reduction of superoxide dismutase (SOD) activity. Genistein significantly attenuated the increased MDA content but did not affect the nitrite content or SOD activity. These results indicate that genistein pretreatment ameliorates A beta-induced impairment of short-term spatial memory in rats through an estrogenic pathway and by inducing attenuation of oxidative stress.

    Ort, förlag, år, upplaga, sidor
    Elsevier Science B.V., Amsterdam, 2011
    Nyckelord
    Alzheimers disease, Beta-amyloid, Genistein, Learning and memory
    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:liu:diva-67550 (URN)10.1016/j.nlm.2010.12.001 (DOI)000288774300006 ()
    Anmärkning
    Original Publication: Maryam Bagheri, Mohammad-Taghi Joghataei, Simin Mohseni and Mehrdad Roghani, Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease, 2011, NEUROBIOLOGY OF LEARNING AND MEMORY, (95), 3, 270-276. http://dx.doi.org/10.1016/j.nlm.2010.12.001 Copyright: Elsevier Science B.V., Amsterdam http://www.elsevier.com/Tillgänglig från: 2011-04-18 Skapad: 2011-04-18 Senast uppdaterad: 2017-12-11Bibliografiskt granskad
    3. Genistein inhibits aggregation of exogenous amyloid-beta(1-40) and alleviates astrogliosis in the hippocampus of rats
    Öppna denna publikation i ny flik eller fönster >>Genistein inhibits aggregation of exogenous amyloid-beta(1-40) and alleviates astrogliosis in the hippocampus of rats
    2012 (Engelska)Ingår i: Brain Research, ISSN 0006-8993, E-ISSN 1872-6240, Vol. 1429, s. 145-154Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    We addressed the question of whether injection of Amyloid beta (Aβ)(1-40) in the rat brain is associated with pathology in the hippocampus, and if genistein has any protective effect against the neuronal damage caused by Aβ(1-40). Genistein is a plant-derived compound with a structure similar to that of the female sex hormone estrogen and it was recently shown that pretreatment with a single dose of genistein ameliorated learning and memory deficits in an (Aβ)(1-40) rat model of Alzheimer's disease. Here, we report that injection of the amyloid peptide into the hippocampus of rats led to formation of Aβ(1-40) positive aggregates close to the lateral blade of the dentate gyrus (DGlb). We also observed the following in the hippocampus: extensive cell death in the DGlb (P<0.0001), CA1 (P=0.03), and CA3 (P=0.002); an increased number of iNOS-expressing cells (P=0.01) and gliosis. Genistein given to rats by gavage 1h before injection of Aβ(1-40) inhibited the formation of Aβ(1-40) positive aggregates in the brain tissue and led to increased number of nNOS(+) (P=0.0001) cells in the hippocampus compared to sham-operated genistein-treated controls. Treatment with genistein also alleviated the extensive astrogliosis that occurred in Aβ(1-40)-injected hippocampus to a level similar to that observed in sham-operated rats. We conclude that the neurons in the DGlb are most sensitive to Aβ(1-40), and a single dose of genistein can ameliorate Aβ(1-40) induced pathology.

    Ort, förlag, år, upplaga, sidor
    Elsevier, 2012
    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:liu:diva-72775 (URN)10.1016/j.brainres.2011.10.020 (DOI)000300268200016 ()22079317 (PubMedID)
    Anmärkning
    funding agencies|Cellular and Molecular Research Center at Tehran University of Medical Sciences (Tehran)||Linkoping University (Linkoping, Sweden)||County Council of Ostergotland||Tillgänglig från: 2011-12-07 Skapad: 2011-12-07 Senast uppdaterad: 2017-12-08Bibliografiskt granskad
    4. Genistein inhibits Aβ1-40-induced astrogliosis: A three-dimensional confocal morphometric analysis
    Öppna denna publikation i ny flik eller fönster >>Genistein inhibits Aβ1-40-induced astrogliosis: A three-dimensional confocal morphometric analysis
    Visa övriga...
    (Engelska)Manuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Astrocytes are highly involved in regulation and homeostasis of the extracellular environment in the healthy brain. In pathological conditions, these cells play a major role in the inflammatory response seen in CNS tissues, which is called reactive astrogliosis and includes hypertrophy, proliferation, and remodeling. Here, we performed 3D confocal microscopy to evaluate the morphology of reactive glial fibrillary acidic protein (GFAP-positive) astrocytes in an animal model of Alzheimer’s disease, and we also assessed the effect of the antiinflammatory agent genistein on amyloid-beta-induced astrogliosis. In 50 astrocytes/animal, we measured the area and volume of the nucleus, cell body, astrocyte (soma and branches) and territory (tissue covered by each astrocyte), and total length of the branches. Moreover, we quantified the intensity of GFAP immunoreactivity in the hippocampus. Injecting amyloid beta (Aβ)1–40 into the brain caused astrogliosis, observed as significantly higher GFAP intensity in the hippocampus, and also led to significant enlargement of astrocytes in this area, indicated by increased values for all the above-mentioned parameters. In Aβ1–40-injected rats pretreated with genistein, GFAP intensity was decreased to the level seen in the shamoperated group, and Aβ1–40-induced enlargement of astrocytes was significantly inhibited. Interestingly, genistein also ameliorated the astrogliosis that was initiated by mechanical injury caused by insertion of the injection needle into the brain tissue. This  was indicated by the observation that the mean cell body volume and area of astrocytes were significantly smaller in the genistein-treated rats, even in comparison with the sham-operated animals.

    Nyckelord
    Alzheimer’s disease; astrocytes; amyloid beta; genistein; gliosis
    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:liu:diva-77172 (URN)
    Tillgänglig från: 2012-05-07 Skapad: 2012-05-07 Senast uppdaterad: 2016-02-29Bibliografiskt granskad
  • 2.
    Bagheri, Maryam
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi.
    Joghataei, Mohammad-Taghi
    University of Tehran Medical Science.
    Mohseni, Simin
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Roghani, Mehrdad
    Shahed University.
    Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease2011Ingår i: Neurobiology of Learning and Memory, ISSN 1074-7427, E-ISSN 1095-9564, Vol. 95, nr 3, s. 270-276Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Alzheimers disease (AD) is a debilitating neurodegenerative disorder characterized by increased beta-amyloid (A beta) deposition and neuronal dysfunction leading to impaired learning and recall. Ageing, heredity, and induced oxidative stress are among proposed risk factors. The increased frequency of the disease in women also suggests a role for estrogen in development of AD. In the present study, effects of the phytoestrogen genistein (10 mg/kg) on learning and memory impairments was assessed in intrahippocampal A beta((1-40))-injected rats. The estrogen receptor antagonist fulvestrant was injected intracerebroventricularly in a group of A beta-lesioned rats. The A beta-injected animals exhibited the following: lower spontaneous alternation score in Y-maze tasks, impaired retention and recall capability in the passive avoidance test, and fewer correct choices and more errors in the RAM task. Genistein, but not genistein and fulvestrant, significantly improved most of these parameters. Measurements of oxidative stress markers in hippocampal tissue of A beta-injected rats showed an elevation of malondialdehyde (MDA) and nitrite content, and a reduction of superoxide dismutase (SOD) activity. Genistein significantly attenuated the increased MDA content but did not affect the nitrite content or SOD activity. These results indicate that genistein pretreatment ameliorates A beta-induced impairment of short-term spatial memory in rats through an estrogenic pathway and by inducing attenuation of oxidative stress.

  • 3.
    Bagheri, Maryam
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Rezakhani, Arjang
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Roghani, Mehrdad
    Neurophysiology Research Center, Shahed University, Iran.
    Joghataei, Mohammad T.
    Iran University of Medical Science, Iran.
    Mohseni, Simin
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Protocol for Three-dimensional Confocal Morphometric Analysis of Astrocytes2015Ingår i: Journal of Visualized Experiments, ISSN 1940-087X, E-ISSN 1940-087X, nr 106, s. e53113-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    As glial cells in the brain, astrocytes have diverse functional roles in the central nervous system. In the presence of harmful stimuli, astrocytes modify their functional and structural properties, a condition called reactive astrogliosis. Here, a protocol for assessment of the morphological properties of astrocytes is presented. This protocol includes quantification of 12 different parameters i.e. the surface area and volume of the tissue covered by an astrocyte (astrocyte territory), the entire astrocyte including branches, cell body, and nucleus, as well as total length and number of branches, the intensity of fluorescence immunoreactivity of antibodies used for astrocyte detection, and astrocyte density (number/1,000 mu m(2)). For this purpose three-dimensional (3D) confocal microscopic images were created, and 3D image analysis software such as Volocity 6.3 was used for measurements. Rat brain tissue exposed to amyloid beta(1-40) (A beta(1-40)) with or without a therapeutic intervention was used to present the method. This protocol can also be used for 3D morphometric analysis of other cells from either in vivo or in vitro conditions.

  • 4.
    Bagheri, Maryam
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Rezakhani, Arjang
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Roghani, Mehrdad
    Department of Physiology, Neurophysiology Research Group, Shahed University, Tehran, Iran.
    Joghataei, Mohammad-Taghi
    Cellular and Molecular Research Center & Department of Anatomy and Neuroscience, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
    Mohseni, Simin
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Genistein inhibits Aβ1-40-induced astrogliosis: A three-dimensional confocal morphometric analysisManuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Astrocytes are highly involved in regulation and homeostasis of the extracellular environment in the healthy brain. In pathological conditions, these cells play a major role in the inflammatory response seen in CNS tissues, which is called reactive astrogliosis and includes hypertrophy, proliferation, and remodeling. Here, we performed 3D confocal microscopy to evaluate the morphology of reactive glial fibrillary acidic protein (GFAP-positive) astrocytes in an animal model of Alzheimer’s disease, and we also assessed the effect of the antiinflammatory agent genistein on amyloid-beta-induced astrogliosis. In 50 astrocytes/animal, we measured the area and volume of the nucleus, cell body, astrocyte (soma and branches) and territory (tissue covered by each astrocyte), and total length of the branches. Moreover, we quantified the intensity of GFAP immunoreactivity in the hippocampus. Injecting amyloid beta (Aβ)1–40 into the brain caused astrogliosis, observed as significantly higher GFAP intensity in the hippocampus, and also led to significant enlargement of astrocytes in this area, indicated by increased values for all the above-mentioned parameters. In Aβ1–40-injected rats pretreated with genistein, GFAP intensity was decreased to the level seen in the shamoperated group, and Aβ1–40-induced enlargement of astrocytes was significantly inhibited. Interestingly, genistein also ameliorated the astrogliosis that was initiated by mechanical injury caused by insertion of the injection needle into the brain tissue. This  was indicated by the observation that the mean cell body volume and area of astrocytes were significantly smaller in the genistein-treated rats, even in comparison with the sham-operated animals.

  • 5.
    Bagheri, Maryam
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Roghani, Mehrdad
    Shahed University.
    Joghataei, Mohammad-Taghi
    Tehran University of Medical Sciences.
    Mohseni, Simin
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Genistein inhibits aggregation of exogenous amyloid-beta(1-40) and alleviates astrogliosis in the hippocampus of rats2012Ingår i: Brain Research, ISSN 0006-8993, E-ISSN 1872-6240, Vol. 1429, s. 145-154Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We addressed the question of whether injection of Amyloid beta (Aβ)(1-40) in the rat brain is associated with pathology in the hippocampus, and if genistein has any protective effect against the neuronal damage caused by Aβ(1-40). Genistein is a plant-derived compound with a structure similar to that of the female sex hormone estrogen and it was recently shown that pretreatment with a single dose of genistein ameliorated learning and memory deficits in an (Aβ)(1-40) rat model of Alzheimer's disease. Here, we report that injection of the amyloid peptide into the hippocampus of rats led to formation of Aβ(1-40) positive aggregates close to the lateral blade of the dentate gyrus (DGlb). We also observed the following in the hippocampus: extensive cell death in the DGlb (P<0.0001), CA1 (P=0.03), and CA3 (P=0.002); an increased number of iNOS-expressing cells (P=0.01) and gliosis. Genistein given to rats by gavage 1h before injection of Aβ(1-40) inhibited the formation of Aβ(1-40) positive aggregates in the brain tissue and led to increased number of nNOS(+) (P=0.0001) cells in the hippocampus compared to sham-operated genistein-treated controls. Treatment with genistein also alleviated the extensive astrogliosis that occurred in Aβ(1-40)-injected hippocampus to a level similar to that observed in sham-operated rats. We conclude that the neurons in the DGlb are most sensitive to Aβ(1-40), and a single dose of genistein can ameliorate Aβ(1-40) induced pathology.

  • 6.
    Baluchnejadmojarad, Tourandokht
    et al.
    Iran University of Medical Sciences, Tehran.
    Roghani, Mehrdad
    Shahed University, Tehran.
    Nadoushan, Mohammad Reza Jalali
    Shahed University, Tehran.
    Bagheri, Maryam
    Iran University of Medical Sciences.
    Neuroprotective Effect of Genistein in 6-Hydroxydopamine Hemi-parkinsonian Rat Model2008Ingår i: International Journal of Psychophysiology, ISSN 0167-8760, E-ISSN 1872-7697, Vol. 69, nr 3, s. 315-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A large body of experimental evidence supports a role for oxidative stress as a mediator of nerve cell death in Parkinson-s disease (PD). Phytoestrogens such as genistein have been reported to prevent neuronal degeneration caused by increased oxidative burden, therefore, this study examined whether genistein administration at a high dose would attenuate behavioral and structural abnormalities in an experimental model of PD in rat. For this purpose, unilateral intrastriatal 6-hydroxydopamine (6-OHDA, 12.5 μg/5 μL of saline-ascorbate)- lesioned rats were intraperitoneally pretreated with a single and high dose of genistein (10 mg/kg) 1 h before surgery. Apomorphine-induced rotations and the number of Nissl-stained neurons in the substantia nigra pars compacta (SNC) were counted after 2 weeks. Genistein administration could attenuate the rotational behavior in lesioned rats and protect the neurons of SNC against 6-OHDA toxicity. Genistein administration has a protective effect against 6-OHDA toxicity. 

  • 7.
    Baluchnejadmojarad, Tourandokht
    et al.
    Iran University of Medical Sciences, Tehran.
    Roghani, Mehrdad
    Shahed University, Tehran.
    Nadoushan, Mohammad Reza Jalali
    Shahed University, Tehran.
    Bagheri, Maryam
    Iran University of Medical Sciences.
    Neuroprotective Effect of Genistein in 6-Hydroxydopamine Hemi-parkinsonian Rat Model2008Ingår i: Phytotherapy Research, ISSN 0951-418X, E-ISSN 1099-1573, Vol. 23, nr 1, s. 132-135Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A large body of experimental evidence supports a role for oxidative stress as a mediator of nerve cell death in Parkinson-s disease (PD). Phytoestrogens such as genistein have been reported to prevent neuronal degeneration caused by increased oxidative burden, therefore, this study examined whether genistein administration at a high dose would attenuate behavioral and structural abnormalities in an experimental model of PD in rat. For this purpose, unilateral intrastriatal 6-hydroxydopamine (6-OHDA, 12.5 μg/5 μL of saline-ascorbate)- lesioned rats were intraperitoneally pretreated with a single and high dose of genistein (10 mg/kg) 1 h before surgery. Apomorphine-induced rotations and the number of Nissl-stained neurons in the substantia nigra pars compacta (SNC) were counted after 2 weeks. Genistein administration could attenuate the rotational behavior in lesioned rats and protect the neurons of SNC against 6-OHDA toxicity. Genistein administration has a protective effect against 6-OHDA toxicity. 

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