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Article ; Online: Involvement of the Restoration of Cerebral Blood Flow and Maintenance of eNOS Expression in the Prophylactic Protective Effect of the Novel Ferulic Acid Derivative FAD012 against Ischemia/Reperfusion Injuries in Rats.

Asano, Takashi / Xuan, Meiyan / Iwata, Naohiro / Takayama, Jun / Hayashi, Kousuke / Kato, Yosuke / Aoyama, Toshiya / Sugo, Hiroshi / Matsuzaki, Hirokazu / Yuan, Bo / Kamiuchi, Shinya / Hibino, Yasuhide / Sakamoto, Takeshi / Okazaki, Mari

International journal of molecular sciences

2023 Volume 24, Issue 11

Abstract: Tissue plasminogen activator, aiming to restore cerebral blood flow (CBF), has been used for acute ischemic strokes in clinics; however, its narrow therapeutic time window remains a serious concern. To develop novel prophylactic drugs to alleviate ... ...

Abstract	Tissue plasminogen activator, aiming to restore cerebral blood flow (CBF), has been used for acute ischemic strokes in clinics; however, its narrow therapeutic time window remains a serious concern. To develop novel prophylactic drugs to alleviate cerebral ischemia/reperfusion injuries, ferulic acid derivative 012 (FAD012) was synthesized and showed comparable antioxidant properties to ferulic acid (FA) and probably possesses the potent ability to cross the blood-brain barrier. A more potent cytoprotective effect of FAD012 against H
MeSH term(s)	Animals ; Rats ; Brain Ischemia/drug therapy ; Cerebrovascular Circulation ; Endothelial Cells/metabolism ; Hydrogen Peroxide/therapeutic use ; Infarction, Middle Cerebral Artery/metabolism ; Neuroprotective Agents/pharmacology ; Nitric Oxide Synthase ; Rats, Sprague-Dawley ; Reperfusion Injury/drug therapy ; Reperfusion Injury/prevention & control ; Reperfusion Injury/metabolism ; Tissue Plasminogen Activator/therapeutic use
Chemical Substances	ferulic acid (AVM951ZWST) ; Hydrogen Peroxide (BBX060AN9V) ; Neuroprotective Agents ; Nitric Oxide Synthase (EC 1.14.13.39) ; Tissue Plasminogen Activator (EC 3.4.21.68) ; FAD012
Language	English
Publishing date	2023-06-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24119663
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Enhanced Cytotoxic Effects of Arenite in Combination with Active Bufadienolide Compounds against Human Glioblastoma Cell Line U-87.

Yuan, Bo / Li, Jingmei / Miyashita, Shin-Ich / Kikuchi, Hidetomo / Xuan, Meiyan / Matsuzaki, Hirokazu / Iwata, Naohiro / Kamiuchi, Shinya / Sunaga, Katsuyoshi / Sakamoto, Takeshi / Hibino, Yasuhide / Okazaki, Mari

Molecules (Basel, Switzerland)

2022 Volume 27, Issue 19

Abstract: The cytotoxicity of a trivalent arsenic derivative (arsenite, ... ...

Abstract	The cytotoxicity of a trivalent arsenic derivative (arsenite, As
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis ; Arsenic/metabolism ; Arsenites/pharmacology ; Bufanolides/pharmacology ; Caspase 8/metabolism ; Caspase 9/metabolism ; Cell Line ; Cell Line, Tumor ; Glioblastoma/drug therapy ; Glioblastoma/metabolism ; Humans
Chemical Substances	Antineoplastic Agents ; Arsenites ; Bufanolides ; Caspase 8 (EC 3.4.22.-) ; Caspase 9 (EC 3.4.22.-) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2022-10-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules27196577
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Article: Orally Administrated Ascorbic Acid Suppresses Neuronal Damage and Modifies Expression of SVCT2 and GLUT1 in the Brain of Diabetic Rats with Cerebral Ischemia-Reperfusion

Iwata, Naohiro / Okazaki, Mari / Xuan, Meiyan / Kamiuchi, Shinya / Matsuzaki, Hirokazu / Hibino, Yasuhide

Nutrients. 2014 Apr. 15, v. 6, no. 4

2014

Abstract: Diabetes mellitus is known to exacerbate cerebral ischemic injury. In the present study, we investigated antiapoptotic and anti-inflammatory effects of oral supplementation of ascorbic acid (AA) on cerebral injury caused by middle cerebral artery ... ...

Abstract	Diabetes mellitus is known to exacerbate cerebral ischemic injury. In the present study, we investigated antiapoptotic and anti-inflammatory effects of oral supplementation of ascorbic acid (AA) on cerebral injury caused by middle cerebral artery occlusion and reperfusion (MCAO/Re) in rats with streptozotocin-induced diabetes. We also evaluated the effects of AA on expression of sodium-dependent vitamin C transporter 2 (SVCT2) and glucose transporter 1 (GLUT1) after MCAO/Re in the brain. The diabetic state markedly aggravated MCAO/Re-induced cerebral damage, as assessed by infarct volume and edema. Pretreatment with AA (100 mg/kg, p.o.) for two weeks significantly suppressed the exacerbation of damage in the brain of diabetic rats. AA also suppressed the production of superoxide radical, activation of caspase-3, and expression of proinflammatory cytokines (tumor necrosis factor-α and interleukin-1β) in the ischemic penumbra. Immunohistochemical staining revealed that expression of SVCT2 was upregulated primarily in neurons and capillary endothelial cells after MCAO/Re in the nondiabetic cortex, accompanied by an increase in total AA (AA + dehydroascorbic acid) in the tissue, and that these responses were suppressed in the diabetic rats. AA supplementation to the diabetic rats restored these responses to the levels of the nondiabetic rats. Furthermore, AA markedly upregulated the basal expression of GLUT1 in endothelial cells of nondiabetic and diabetic cortex, which did not affect total AA levels in the cortex. These results suggest that daily intake of AA attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-apoptotic and anti-inflammatory effects via the improvement of augmented oxidative stress in the brain. AA supplementation may protect endothelial function against the exacerbated ischemic oxidative injury in the diabetic state and improve AA transport through SVCT2 in the cortex.
Keywords	animal disease models ; anti-inflammatory activity ; ascorbic acid ; brain ; caspase-3 ; cortex ; dehydroascorbic acid ; diabetes mellitus ; edema ; endothelial cells ; glucose transporters ; immunohistochemistry ; infarction ; interleukin-1beta ; neoplasms ; neurons ; oxidative stress ; oxidative toxicity ; rats ; staining ; superoxide anion ; tumor necrosis factor-alpha
Language	English
Dates of publication	2014-0415
Size	p. 1554-1577.
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu6041554
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Effects of Etanercept against Transient Cerebral Ischemia in Diabetic Rats.

Iwata, Naohiro / Takayama, Hiroko / Xuan, Meiyan / Kamiuchi, Shinya / Matsuzaki, Hirokazu / Okazaki, Mari / Hibino, Yasuhide

BioMed research international

2015 Volume 2015, Page(s) 189292

Abstract: Diabetes mellitus is known to exacerbate acute cerebral ischemic injury. Previous studies have demonstrated that infarction volumes caused by transient cerebral ischemia were greater in diabetic rats than in nondiabetic rats. Tumor necrosis factor-α (TNF- ...

Abstract	Diabetes mellitus is known to exacerbate acute cerebral ischemic injury. Previous studies have demonstrated that infarction volumes caused by transient cerebral ischemia were greater in diabetic rats than in nondiabetic rats. Tumor necrosis factor-α (TNF-α) is a proinflammatory protein produced in the brain in response to cerebral ischemia that promotes apoptosis. Etanercept (ETN), a recombinant TNF receptor (p75)-Fc fusion protein, competitively inhibits TNF-α. Therefore, we evaluated the neuroprotective effects of chronic or acute treatment with ETN on cerebral injury caused by middle cerebral artery occlusion/reperfusion (MCAO/Re) in rats with streptozotocin-induced diabetes. Furthermore, we evaluated the effects of ETN against the apoptosis and myeloperoxidase activity. Single administration of ETN before MCAO significantly suppressed exacerbation of cerebral damage in nondiabetic rats, as assessed by infarct volume. In contrast, the diabetic state markedly aggravated MCAO/Re-induced cerebral damage despite ETN treatment within 24 h before MCAO. However, the damage was improved by repeated administration of ETN at 900 μg/kg/daily in rats in an induced diabetic state. These results suggested that repeated administration of ETN can prevent exacerbation of cerebral ischemic injury in the diabetic state and is mainly attributed to anti-inflammatory effects.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Experimental/physiopathology ; Etanercept/administration & dosage ; Humans ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/genetics ; Infarction, Middle Cerebral Artery/physiopathology ; Inflammation/drug therapy ; Inflammation/genetics ; Inflammation/pathology ; Ischemic Attack, Transient/complications ; Ischemic Attack, Transient/drug therapy ; Ischemic Attack, Transient/genetics ; Ischemic Attack, Transient/physiopathology ; Neuroprotective Agents ; Rats ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Neuroprotective Agents ; Tumor Necrosis Factor-alpha ; Etanercept (OP401G7OJC)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2015/189292
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Protective Effects of Ferulic Acid against Chronic Cerebral Hypoperfusion-Induced Swallowing Dysfunction in Rats.

Asano, Takashi / Matsuzaki, Hirokazu / Iwata, Naohiro / Xuan, Meiyan / Kamiuchi, Shinya / Hibino, Yasuhide / Sakamoto, Takeshi / Okazaki, Mari

International journal of molecular sciences

2017 Volume 18, Issue 3

Abstract: Ferulic acid (FA), a phenolic phytochemical, has been reported to exert antioxidative and neuroprotective effects. In this study, we investigated the protective effects of FA against the dysfunction of the swallowing reflex induced by ligation of ... ...

Abstract	Ferulic acid (FA), a phenolic phytochemical, has been reported to exert antioxidative and neuroprotective effects. In this study, we investigated the protective effects of FA against the dysfunction of the swallowing reflex induced by ligation of bilateral common carotid arteries (2VO) in rats. In 2VO rats, topical administration of water or citric acid to the pharyngolaryngeal region evoked a diminished number of swallowing events with prolonged latency compared to sham-operated control rats. 2VO rats had an increased level of superoxide anion radical, and decreased dopamine and tyrosine hydroxylase enzyme levels in the striatum, suggesting that 2VO augmented cerebral oxidative stress and impaired the striatal dopaminergic system. Furthermore, substance P (SP) expression in the laryngopharyngeal mucosa, which is believed to be positively regulated by dopaminergic signaling in the basal ganglia, was decreased in 2VO rats. Oral treatment with FA (30 mg/kg) for 3 weeks (from one week before 2VO to two weeks after) improved the swallowing reflex and maintained levels of striatal dopamine and laryngopharyngeal SP expression in 2VO rats. These results suggest that FA maintains the swallowing reflex by protecting the dopamine-SP system against ischemia-induced oxidative damage in 2VO rats.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Brain Ischemia/drug therapy ; Brain Ischemia/etiology ; Brain Ischemia/pathology ; Brain Ischemia/physiopathology ; Cerebral Cortex/blood supply ; Cerebral Cortex/drug effects ; Cerebral Cortex/pathology ; Cerebral Cortex/physiopathology ; Cerebrovascular Circulation/drug effects ; Corpus Striatum/blood supply ; Corpus Striatum/drug effects ; Corpus Striatum/metabolism ; Coumaric Acids/pharmacology ; Disease Models, Animal ; Dopamine/biosynthesis ; Dopaminergic Neurons/metabolism ; Gene Expression ; Male ; Neuroprotective Agents/pharmacology ; Oxidative Stress/drug effects ; Rats ; Tyrosine 3-Monooxygenase/genetics ; Tyrosine 3-Monooxygenase/metabolism
Chemical Substances	Coumaric Acids ; Neuroprotective Agents ; ferulic acid (AVM951ZWST) ; Tyrosine 3-Monooxygenase (EC 1.14.16.2) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2017-03-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms18030550
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Article ; Online: Orally administrated ascorbic acid suppresses neuronal damage and modifies expression of SVCT2 and GLUT1 in the brain of diabetic rats with cerebral ischemia-reperfusion.

Iwata, Naohiro / Okazaki, Mari / Xuan, Meiyan / Kamiuchi, Shinya / Matsuzaki, Hirokazu / Hibino, Yasuhide

Nutrients

2014 Volume 6, Issue 4, Page(s) 1554–1577

Abstract	Diabetes mellitus is known to exacerbate cerebral ischemic injury. In the present study, we investigated antiapoptotic and anti-inflammatory effects of oral supplementation of ascorbic acid (AA) on cerebral injury caused by middle cerebral artery occlusion and reperfusion (MCAO/Re) in rats with streptozotocin-induced diabetes. We also evaluated the effects of AA on expression of sodium-dependent vitamin C transporter 2 (SVCT2) and glucose transporter 1 (GLUT1) after MCAO/Re in the brain. The diabetic state markedly aggravated MCAO/Re-induced cerebral damage, as assessed by infarct volume and edema. Pretreatment with AA (100 mg/kg, p.o.) for two weeks significantly suppressed the exacerbation of damage in the brain of diabetic rats. AA also suppressed the production of superoxide radical, activation of caspase-3, and expression of proinflammatory cytokines (tumor necrosis factor-α and interleukin-1β) in the ischemic penumbra. Immunohistochemical staining revealed that expression of SVCT2 was upregulated primarily in neurons and capillary endothelial cells after MCAO/Re in the nondiabetic cortex, accompanied by an increase in total AA (AA + dehydroascorbic acid) in the tissue, and that these responses were suppressed in the diabetic rats. AA supplementation to the diabetic rats restored these responses to the levels of the nondiabetic rats. Furthermore, AA markedly upregulated the basal expression of GLUT1 in endothelial cells of nondiabetic and diabetic cortex, which did not affect total AA levels in the cortex. These results suggest that daily intake of AA attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-apoptotic and anti-inflammatory effects via the improvement of augmented oxidative stress in the brain. AA supplementation may protect endothelial function against the exacerbated ischemic oxidative injury in the diabetic state and improve AA transport through SVCT2 in the cortex.
MeSH term(s)	Administration, Oral ; Animals ; Apoptosis/drug effects ; Ascorbic Acid/administration & dosage ; Brain/drug effects ; Caspase 3 ; Diabetes Mellitus, Experimental/drug therapy ; Dietary Supplements ; Endothelial Cells/drug effects ; Glucose Transporter Type 1/genetics ; Glucose Transporter Type 1/metabolism ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/pathology ; Interleukin-1beta/metabolism ; Male ; Neurons/drug effects ; Oxidative Stress/drug effects ; Rats ; Rats, Sprague-Dawley ; Sodium-Coupled Vitamin C Transporters/genetics ; Sodium-Coupled Vitamin C Transporters/metabolism ; Streptozocin ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation
Chemical Substances	Glucose Transporter Type 1 ; Interleukin-1beta ; Slc23a2 protein, rat ; Slc2a1 protein, rat ; Sodium-Coupled Vitamin C Transporters ; Tumor Necrosis Factor-alpha ; Streptozocin (5W494URQ81) ; Casp3 protein, rat (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2014-04-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu6041554
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Antidepressant-like effects of a water-soluble extract from the culture medium of Ganoderma lucidum mycelia in rats

Matsuzaki, Hirokazu / Shimizu, Yuta / Iwata, Naohiro / Kamiuchi, Shinya / Suzuki, Fumiko / Iizuka, Hiroshi / Hibino, Yasuhide / Okazaki, Mari

BMC Complement Altern Med. 2013 Dec., v. 13, no. 1 p.370-370

2013

Abstract: BACKGROUND: Ganoderma lucidum is a popular medicinal mushroom used for promoting health and longevity in Asian countries. Previously, we reported that a water-soluble extract from a culture medium of Ganoderma lucidum mycelia (MAK) exerts antioxidative ... ...

Abstract	BACKGROUND: Ganoderma lucidum is a popular medicinal mushroom used for promoting health and longevity in Asian countries. Previously, we reported that a water-soluble extract from a culture medium of Ganoderma lucidum mycelia (MAK) exerts antioxidative and cerebroprotective effects against ischemia–reperfusion injury in vivo. Here, we evaluated the antidepressant and anxiolytic activities of MAK in rats. METHODS: MAK (0.3 or 1 g/kg, p.o.) was administered in the experimental animals 60 min before the forced swimming, open-field, elevated plus-maze, contextual fear-conditioning, and head twitch tests. Additionally, the mechanisms involved in the antidepressant-like action of MAK were investigated by the serotonin precursor 5-hydroxy-L-tryptophan (5-HTP)- or 5-HT₂A agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI)-induced head twitch responses. RESULTS: Treatment with MAK (1 g/kg) exhibited antidepressant-like effects in the forced swimming test, attenuated freezing behavior in the contextual fear-conditioning test, and decreased the number of head twitches induced by DOI, but not with 5-HTP. No significant response was observed in locomotion or anxiety-like behavior, when the animals were evaluated in the open-field or elevated plus-maze test, respectively. CONCLUSIONS: These data suggest that MAK has antidepressant-like potential, which is most likely due to the antagonism of 5-HT₂A receptors, and possesses anxiolytic-like effects toward memory-dependent and/or stress-induced anxiety in rats.
Keywords	5-hydroxytryptophan ; Ganoderma lucidum ; agonists ; antagonism ; antidepressants ; anxiety ; complement ; culture media ; head ; locomotion ; longevity ; medicinal fungi ; mycelium ; serotonin ; tranquilizers ; water solubility
Language	English
Dates of publication	2013-12
Size	p. 370.
Publishing place	BioMed Central
Document type	Article ; Online
ZDB-ID	2050429-9
ISSN	1472-6882
ISSN	1472-6882
DOI	10.1186/1472-6882-13-370
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Article: Chronic Treatment with a Water-Soluble Extract from the Culture Medium of Ganoderma lucidum Mycelia Prevents Apoptosis and Necroptosis in Hypoxia/Ischemia-Induced Injury of Type 2 Diabetic Mouse Brain.

Xuan, Meiyan / Okazaki, Mari / Iwata, Naohiro / Asano, Satoshi / Kamiuchi, Shinya / Matsuzaki, Hirokazu / Sakamoto, Takeshi / Miyano, Yoshiyuki / Iizuka, Hiroshi / Hibino, Yasuhide

Evidence-based complementary and alternative medicine : eCAM

2015 Volume 2015, Page(s) 865986

Abstract: Type 2 diabetes mellitus has been known to increase systemic oxidative stress by chronic hyperglycemia and visceral obesity and aggravate cerebral ischemic injury. On the basis of our previous study regarding a water-soluble extract from the culture ... ...

Abstract	Type 2 diabetes mellitus has been known to increase systemic oxidative stress by chronic hyperglycemia and visceral obesity and aggravate cerebral ischemic injury. On the basis of our previous study regarding a water-soluble extract from the culture medium of Ganoderma lucidum mycelia (designed as MAK), which exerts antioxidative and neuroprotective effects, the present study was conducted to evaluate the preventive effects of MAK on apoptosis and necroptosis (a programmed necrosis) induced by hypoxia/ischemia (H/I) in type 2 diabetic KKAy mice. H/I was induced by a combination of unilateral common carotid artery ligation with hypoxia (8% O2 for 20 min) and subsequent reoxygenation. Pretreatment with MAK (1 g/kg, p.o.) for a week significantly reduced H/I-induced neurological deficits and brain infarction volume assessed at 24 h of reoxygenation. Histochemical analysis showed that MAK significantly suppressed superoxide production, neuronal cell death, and vacuolation in the ischemic penumbra, which was accompanied by a decrease in the numbers of TUNEL- or cleaved caspase-3-positive cells. Furthermore, MAK decreased the expression of receptor-interacting protein kinase 3 mRNA and protein, a key molecule for necroptosis. These results suggest that MAK confers resistance to apoptotic and necroptotic cell death and relieves H/I-induced cerebral ischemic injury in type 2 diabetic mice.
Language	English
Publishing date	2015-04-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2171158-6
ISSN	1741-4288 ; 1741-427X
ISSN (online)	1741-4288
ISSN	1741-427X
DOI	10.1155/2015/865986
Database	MEDical Literature Analysis and Retrieval System OnLINE

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Antidepressant-like effects of a water-soluble extract from the culture medium of Ganoderma lucidum mycelia in rats.

Matsuzaki, Hirokazu / Shimizu, Yuta / Iwata, Naohiro / Kamiuchi, Shinya / Suzuki, Fumiko / Iizuka, Hiroshi / Hibino, Yasuhide / Okazaki, Mari

BMC complementary and alternative medicine

2013 Volume 13, Page(s) 370

Abstract: Background: Ganoderma lucidum is a popular medicinal mushroom used for promoting health and longevity in Asian countries. Previously, we reported that a water-soluble extract from a culture medium of Ganoderma lucidum mycelia (MAK) exerts antioxidative ... ...

Abstract	Background: Ganoderma lucidum is a popular medicinal mushroom used for promoting health and longevity in Asian countries. Previously, we reported that a water-soluble extract from a culture medium of Ganoderma lucidum mycelia (MAK) exerts antioxidative and cerebroprotective effects against ischemia-reperfusion injury in vivo. Here, we evaluated the antidepressant and anxiolytic activities of MAK in rats. Methods: MAK (0.3 or 1 g/kg, p.o.) was administered in the experimental animals 60 min before the forced swimming, open-field, elevated plus-maze, contextual fear-conditioning, and head twitch tests. Additionally, the mechanisms involved in the antidepressant-like action of MAK were investigated by the serotonin precursor 5-hydroxy-L-tryptophan (5-HTP)- or 5-HT2A agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI)-induced head twitch responses. Results: Treatment with MAK (1 g/kg) exhibited antidepressant-like effects in the forced swimming test, attenuated freezing behavior in the contextual fear-conditioning test, and decreased the number of head twitches induced by DOI, but not with 5-HTP. No significant response was observed in locomotion or anxiety-like behavior, when the animals were evaluated in the open-field or elevated plus-maze test, respectively. Conclusions: These data suggest that MAK has antidepressant-like potential, which is most likely due to the antagonism of 5-HT2A receptors, and possesses anxiolytic-like effects toward memory-dependent and/or stress-induced anxiety in rats.
MeSH term(s)	5-Hydroxytryptophan/toxicity ; Analysis of Variance ; Animals ; Antidepressive Agents/chemistry ; Antidepressive Agents/pharmacology ; Antidepressive Agents/therapeutic use ; Behavior, Animal/drug effects ; Culture Media, Conditioned ; Fear/drug effects ; Male ; Mycelium/metabolism ; Plant Extracts/chemistry ; Plant Extracts/pharmacology ; Rats ; Rats, Sprague-Dawley ; Reishi/chemistry ; Reishi/metabolism ; Stress, Physiological ; Stress, Psychological ; Tics/chemically induced ; Tics/drug therapy ; Tics/physiopathology
Chemical Substances	Antidepressive Agents ; Culture Media, Conditioned ; Plant Extracts ; 5-Hydroxytryptophan (C1LJO185Q9)
Language	English
Publishing date	2013-12-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2050429-9
ISSN	1472-6882 ; 1472-6882
ISSN (online)	1472-6882
ISSN	1472-6882
DOI	10.1186/1472-6882-13-370
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Functional TFIIH is required for UV-induced translocation of CSA to the nuclear matrix.

Saijo, Masafumi / Hirai, Tamami / Ogawa, Akiko / Kobayashi, Aki / Kamiuchi, Shinya / Tanaka, Kiyoji

Molecular and cellular biology

2007 Volume 27, Issue 7, Page(s) 2538–2547

Abstract: Transcription-coupled repair (TCR) efficiently removes a variety of lesions from the transcribed strand of active genes. Mutations in Cockayne syndrome group A and B genes (CSA and CSB) result in defective TCR, but the molecular mechanism of TCR in ... ...

Abstract	Transcription-coupled repair (TCR) efficiently removes a variety of lesions from the transcribed strand of active genes. Mutations in Cockayne syndrome group A and B genes (CSA and CSB) result in defective TCR, but the molecular mechanism of TCR in mammalian cells is not clear. We have found that CSA protein is translocated to the nuclear matrix after UV irradiation and colocalized with the hyperphosphorylated form of RNA polymerase II and that the translocation is dependent on CSB. We developed a cell-free system for the UV-induced translocation of CSA. A cytoskeleton (CSK) buffer-soluble fraction containing CSA and a CSK buffer-insoluble fraction prepared from UV-irradiated CS-A cells were mixed. After incubation, the insoluble fraction was treated with DNase I. CSA protein was detected in the DNase I-insoluble fraction, indicating that it was translocated to the nuclear matrix. In this cell-free system, the translocation was dependent on UV irradiation, CSB function, and TCR-competent CSA. Moreover, the translocation was dependent on functional TFIIH, as well as chromatin structure and transcription elongation. These results suggest that alterations of chromatin at the RNA polymerase II stall site, which depend on CSB and TFIIH at least, are necessary for the UV-induced translocation of CSA to the nuclear matrix.
MeSH term(s)	Cell Line, Transformed ; Cell Nucleus/metabolism ; Cell-Free System ; Chromatin/physiology ; Chromatin/ultrastructure ; DNA Repair Enzymes/genetics ; DNA Repair Enzymes/metabolism ; Fibroblasts/cytology ; Humans ; Nuclear Matrix/metabolism ; Protein Transport/radiation effects ; RNA Polymerase II/metabolism ; Transcription Factor TFIIH/genetics ; Transcription Factor TFIIH/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic ; Ultraviolet Rays
Chemical Substances	Chromatin ; ERCC8 protein, human ; Transcription Factors ; Transcription Factor TFIIH (148710-81-0) ; RNA Polymerase II (EC 2.7.7.-) ; DNA Repair Enzymes (EC 6.5.1.-)
Language	English
Publishing date	2007-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.01288-06
Database	MEDical Literature Analysis and Retrieval System OnLINE

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