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1.
Article in English | MEDLINE | ID: mdl-19332457

ABSTRACT

In post-stroke patients, the recurrence of stroke and progression of impairments lead to a bedridden state and dementia. As for their treatments, only anti-hypertension and anti-coagulation therapies to prevent the recurrence of stroke are available. In Asia, post-stroke patients with impairments are often treated with herbal medicine. The present study evaluated the effectiveness of tokishakuyakusan (TS) in improving the impairment and independence in post-stroke patients. Thirty-one post-stroke patients (mean age = 81.4 years) were recruited and enrolled. Participants were randomly assigned to the TS group (n = 16) or non-treatment (control) group (n = 15) and treated for 12 months. Impairments were assessed using the Stroke Impairment Assessment Set (SIAS). Independence was evaluated using the functional independence measure (FIM). For each outcome measure, mean change was calculated every 3 months. The results were that impairments according to SIAS did not significantly change in the TS group. In contrast, SIAS significantly worsened in the control group. There was a significant difference between the two groups. In each term of SIAS, affected lower extremity scores, abdominal muscle strength, function of visuospatial perception, and so forth. in the TS group were better than those in the control group. Independence according to FIM did not change significantly in the TS group. In contrast, FIM significantly worsened in the control group. There was also a significant difference between the two groups. In conclusion, TS was considered to suppress the impairments of lower limbs and to exert a favorable effect on cerebral function for post-stroke patients.

2.
Biol Pharm Bull ; 32(1): 79-85, 2009 Jan.
Article in English | MEDLINE | ID: mdl-19122285

ABSTRACT

In this study we elucidated the effects of berberine, a major alkaloid component contained in medicinal herbs, such as Phellodendri Cortex and Coptidis Rhizoma, on ischemic neuronal damage in mouse organotypic hippocampal slice cultures (OHSCs) caused by oxygen and glucose deprivation (OGD) and N-methyl-D-aspartate (NMDA) -type glutamate receptor stimulation. Hippocampal slices obtained from 7-d-old ICR mice were cultured for 10 d before the experiments. Ischemia-related damage was induced by OGD (5, 15, 45 min) or NMDA (10 microM) treatment, and was evaluated by measuring propidium iodide (PI) uptake. Levels of apoptotic marker proteins, B-cell lymphoma 2 (Bcl-2) and phosphorylated-Bcl-2 (p-Bcl-2), in the OHSCs were measured as indices of biochemical neuronal cell damage by Western blotting. Berberine (5, 25 microM) or the NMDA antagonist MK-801 (25 microM) was added to the medium 30 min before OGD or NMDA treatment. OGD time-dependently increased PI uptake of the OHSCs. Both berberine (5, 25 microM) and MK-801 (25 microM) significantly inhibited PI uptake at 24 h after 45-min OGD treatment and PI uptake in OHSCs exposed to NMDA for 24 h. OGD treatment also significantly increased the level of p-Bcl-2 but not that of Bcl-2 or glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in OHSCs. Berberine (5-25 microM) significantly suppressed the OGD-induced increase of p-Bcl-2 level in OHSCs when tissue was exposed to the alkaloid prior to OGD or simultaneously with OGD. These findings suggest that berberine has protective effects against ischemic damage in mouse OHSCs and that the effects are at least partly mediated by suppression of Bcl-2 phosphorylation.


Subject(s)
Berberine/chemistry , Berberine/pharmacology , Docosahexaenoic Acids/pharmacology , Hippocampus/pathology , Neurons/drug effects , Animals , Berberine/therapeutic use , Cell Death/drug effects , Docosahexaenoic Acids/therapeutic use , Excitatory Amino Acid Agonists/pharmacology , Glucose/deficiency , Hippocampus/drug effects , Hippocampus/physiopathology , Hypoxia/complications , Hypoxia/drug therapy , Ischemia/complications , Ischemia/pathology , Isoxazoles/pharmacology , Isoxazoles/therapeutic use , Mice , Mice, Inbred ICR , N-Methylaspartate/pharmacology , Organ Culture Techniques , Phosphorylation , Propidium , Proto-Oncogene Proteins c-bcl-2/metabolism , Sulfonamides/pharmacology , Sulfonamides/therapeutic use , Time Factors
3.
Am J Chin Med ; 36(6): 1171-83, 2008.
Article in English | MEDLINE | ID: mdl-19051344

ABSTRACT

We investigated the inhibitory effect of the conditioned medium (CM) from P338D1 (D1) cells, a murine macrophage cell line, stimulated for 10 hours with a fixed dose (100 mug/ml) of the extracts from the fruit bodies of Grifola frondosa (ME) or its ultra filtration-based fractions (MFs), on the growth of influenza A/Aichi/2/68 virus in Madin-Darby canine kidney cells. Direct addition of ME and 3 kinds of MFs (MF1, MF2 and MF3) to the infected cells had no obvious inhibitory effect. However, virus yields were reduced in the presence of CMs. Notably, the inhibitory effect of the CM prepared by using MF2 (molecular weight of 30 Kd to 100 Kd) was the strongest (28% reduction compared to the control). RT-PCR and ELISA assays showed that the CMs could induce the expression of TNF-alpha mRNA in D1 cells leading to production of TNF-alpha, known as an antiviral cytokine. These findings suggest that ME and MFs (especially MF-2) might induce the production of certain factors, including TNF-alpha, which are responsible for the inhibition of viral growth in vitro.


Subject(s)
Drugs, Chinese Herbal/pharmacology , Grifola/chemistry , Influenza A virus/growth & development , Macrophages/immunology , Tumor Necrosis Factor-alpha/pharmacology , Animals , Cell Line , Chick Embryo , Culture Media, Conditioned/chemistry , Culture Media, Conditioned/pharmacology , Dogs , Drugs, Chinese Herbal/chemistry , Influenza A virus/drug effects , Macrophages/chemistry , Macrophages/drug effects , Mice , Tumor Necrosis Factor-alpha/immunology
4.
Biol Pharm Bull ; 30(12): 2250-6, 2007 Dec.
Article in English | MEDLINE | ID: mdl-18057707

ABSTRACT

Macrophage colony stimulating factor (M-CSF) is a cytokine which has been recently reported to have a neuroprotective effect on ischemic rat brain. In this study, we investigated the effect of chotosan, an oriental medicine, which has been clinically demonstrated to be effective for the treatment of vascular dementia, on M-CSF gene expression in rats with permanent occlusion of bilateral common carotid arteries (P2VO) in vivo and in a C6Bu-1 glioma cell line in vitro. The expression level of M-CSF mRNA in the cerebral cortices of P2VO rats was significantly higher than that in the cerebral cortices of sham-operated animals. Repeated treatment of P2VO rats with chotosan (75 mg/kg per day) for 4 d after P2VO significantly increased the expression level of M-CSF mRNA in the cortex but it had no effect on the expression of beta-actin, granulocyte colony stimulating factor (G-CSF), granulocyte/macrophage colony stimulating factor (GM-CSF) mRNAs. Moreover, the present in vitro studies revealed that chotosan treatment (10-100 mug/ml) of C6Bu-1 glioma cells dose-dependently enhanced M-CSF mRNA expression without affecting the expression of G-CSF, GM-CSF, and inducible nitric oxide synthase mRNAs. The effect of chotosan was reversed by Ro 31-8220 (1 muM), a selective protein kinase C (PKC) inhibitor, but not by H-89 (10 muM), a selective protein kinase A (PKA) inhibitor. These findings suggest that the upregulatory effect of chotosan on M-CSF mRNA expression involves PKC and may play an important role in the anti-vascular dementia action of this formula.


Subject(s)
Brain Chemistry/drug effects , Brain Ischemia/metabolism , Brain Neoplasms/metabolism , Drugs, Chinese Herbal/pharmacology , Glioma/metabolism , Macrophage Colony-Stimulating Factor/antagonists & inhibitors , Macrophage Colony-Stimulating Factor/biosynthesis , RNA, Messenger/biosynthesis , Animals , Carotid Artery, Common/physiology , Carotid Stenosis/physiopathology , Cell Line, Tumor , Cell Survival/drug effects , Male , Protein Kinase C/physiology , Rats , Rats, Wistar , Receptors, Colony-Stimulating Factor/biosynthesis , Reverse Transcriptase Polymerase Chain Reaction , Signal Transduction/physiology , Tetrazolium Salts , Thiazoles
5.
J Pharmacol Sci ; 103(4): 360-73, 2007 Apr.
Article in English | MEDLINE | ID: mdl-17409635

ABSTRACT

We previously demonstrated that the Kampo formula chotosan (CTS) ameliorated spatial cognitive impairment via central cholinergic systems in a chronic cerebral hypoperfusion (P2VO) mouse model. In this study, the object discrimination tasks were used to determine if the ameliorative effects of CTS on P2VO-induced cognitive deficits are a characteristic pharmacological profile of this formula, with the aim of clarifying the mechanisms by which CTS enhances central cholinergic function in P2VO mice. The cholinesterase inhibitor tacrine (THA) and Kampo formula saikokeishito (SKT) were used as controls. P2VO impaired object discrimination performance in the object recognition, location, and context tests. Daily administration of CTS (750 mg/kg, p.o.) and THA (2.5 mg/kg, i.p.) improved the object discrimination deficits, whereas SKT (750 mg/kg, p.o.) did not. In ex vivo assays, tacrine but not CTS or SKT inhibited cortical cholinesterase activity. P2VO reduced the mRNA expression of m(3) and m(5) muscarinic receptors and choline acetyltransferase but not that of other muscarinic receptor subtypes in the cerebral cortex. Daily administration of CTS and THA but not SKT reversed these expression changes. These results suggest that CTS and THA improve P2VO-induced cognitive impairment by normalizing the deficit of central cholinergic systems and that the beneficial effect on P2VO-induced cognitive deficits is a distinctive pharmacological characteristic of CTS.


Subject(s)
Cholinergic Fibers/drug effects , Cognition Disorders/prevention & control , Drugs, Chinese Herbal/pharmacology , Recognition, Psychology/drug effects , Acetylcholinesterase/genetics , Actins/genetics , Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Brain Ischemia/complications , Cerebral Cortex/drug effects , Cerebral Cortex/metabolism , Cerebrovascular Circulation/drug effects , Choline O-Acetyltransferase/genetics , Cholinergic Fibers/pathology , Cholinesterase Inhibitors/pharmacology , Chronic Disease , Cognition Disorders/etiology , Discrimination, Psychological/drug effects , Exploratory Behavior/drug effects , Male , Medicine, Kampo , Mice , Mice, Inbred ICR , RNA, Messenger/genetics , RNA, Messenger/metabolism , Receptors, Muscarinic/genetics , Reverse Transcriptase Polymerase Chain Reaction , Tacrine/pharmacology
6.
Int J Cancer ; 119(12): 2760-7, 2006 Dec 15.
Article in English | MEDLINE | ID: mdl-16998795

ABSTRACT

Although obesity is known as a risk factor for several human cancers, the association of obesity with cancer recurrence and metastasis remains to be characterized. Here, B16-BL6 melanoma and Lewis lung carcinoma cells were intravenously injected into diabetic (db/db) and obese (ob/ob) mice. The number of experimental lung colonies was markedly promoted in these mice when compared with C57BL/6 mice. In contrast, tumor growth at the implanted site was comparable when cells were inoculated orthotopically. The use of B16-BL6 cells stably transfected with the luciferase gene revealed that the increased metastasis reflected a difference mainly within 6 hr after the intravenous inoculation of tumor cells. Administration of recombinant leptin in ob/ob mice abolished the increase in metastasis early on as well as the decrease in the splenic NK cell number. In addition, depletion of NK cells by an anti-asialo-GM1 antibody abrogated the enhanced metastasis in db/db mice. These results demonstrate that metastasis is markedly promoted in diabetic and obese mice mainly because of decreased NK cell function during the early phase of metastasis.


Subject(s)
Carcinoma, Lewis Lung/pathology , Lung Neoplasms/secondary , Melanoma, Experimental/pathology , Animals , Carcinoma, Lewis Lung/genetics , Carcinoma, Lewis Lung/metabolism , Cell Line, Tumor , Hypoglycemic Agents/pharmacology , Killer Cells, Natural/drug effects , Killer Cells, Natural/pathology , Leptin/genetics , Leptin/pharmacology , Luciferases/genetics , Luciferases/metabolism , Lung/drug effects , Lung/metabolism , Lung/pathology , Lung Neoplasms/prevention & control , Lymphocyte Count , Melanoma, Experimental/genetics , Melanoma, Experimental/metabolism , Mice , Mice, Obese , Pioglitazone , Recombinant Proteins/pharmacology , Thiazolidinediones/pharmacology , Time Factors , Transfection
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