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Research Publications on "Sho-saiko-to" (1990-2001)
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Is your "Sho-saiko-to" manufactured under the same quality standard as the ones approved by the Japanese Ministry of Health, Welfare, and Labor? Find out more... |
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Breakthrough Research: Two studies performed by a Japanese research group, published in 1998 and March 2000, have demonstrated an anti-tumor effect of "Sho-saiko-to" (Liver Kampo) on melanoma developed in RET-transgenic mice. The second research was published on The Journal of Investigative Dermatology on the March issue of 2000.
The Journal of Investigative Dermatology © 2000 by the Society for Investigative Dermatology, Inc. Volume 114(3) March 2000 pp 599-601 Further Characterization of the Sho-saiko-to-Mediated Anti-Tumor Effect on Melanoma Developed in RET-Transgenic Mice [Letters To The Editor]
Kato, Masashi; Isobe, Ken-ichi; Dai, Yan; Liu, Wei; Takahashi, Masahide*; Nakashima, Izumi Departments of Immunology and *Pathology, Nagoya University School of Medicine, Nagoya, Japan. Volume 111(4) October 1998 pp 640-644
The Herbal Medicine Sho-saiko-to Inhibits Growth and Metastasis of Malignant Melanoma Primarily Developed in ret-Transgenic Mice [Regular Articles]]
Kato, Masashi; Liu, Wei; Yi, Hong; Asai, Naoya*; Hayakawa, Akemi†; Kozaki, Ken-ichi‡; Takahashi, Masahide*; Nakashima, Izumi Departments of Immunology and *Pathology, and †Equipment Center for Research and Education, Nagoya University School of Medicine, Showa-ku, Nagoya, Japan; ‡Pathophysiology Unit, Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya, Aichi, Japan Authors Shimizu
I. Second Department of Internal Medicine, Tokushima University School of Medicine, Japan. shimizui@clin.med.tokushima-u.ac.jp Title Sho-saiko-to: Japanese herbal medicine for protection against hepatic fibrosis and carcinoma. [Review] [85 refs] Source Journal of Gastroenterology & Hepatology. 15 Suppl:D84-90, 2000 Mar. Abstract Herbal medicines, which have been used in China for thousands of years, are now being manufactured in Japan, in standardized form in terms of quality and quantities of ingredients. The Chinese herbal medicine Sho-saiko-to is a mixture of seven herbal preparations, which is widely administered in Japan to patients with chronic hepatitis and cirrhosis. In a prospective study, this herbal medicine was found to play a chemopreventive role in the development of hepatocellular carcinoma in cirrhotic patients. However, little is known about the mechanism by which Sho-saiko-to protects against hepatic fibrosis and carcinoma. Several laboratories, including ours, have clearly demonstrated the preventive and therapeutic effects of Sho-saiko-to on experimental hepatic fibrosis, as well as its inhibitory effect on the activation of hepatic stellate cells, which are the major types of collagen-producing cells. We provided evidence that Sho-saiko-to functions as a potent anti-fibrosuppressant via the inhibition of oxidative stress in hepatocytes and hepatic stellate cells and that its active components are baicalin and baicalein. In addition, Sho-saiko-to has anti-carcinogenic properties in that it inhibits chemical hepatocarcinogenesis in animals, acts as a biological response modifier and suppresses the proliferation of hepatoma cells by inducing apoptosis and arrests the cell cycle. Among the active components of Sho-saiko-to, baicalin, baicalein and saikosaponin-a have the ability to inhibit cell proliferation. It should be noted that baicalin and baicalein are flavonoids with chemical structures very similar to silybinin, which shows anti-fibrogenic activities. This may provide valuable information on the search for novel anti-fibrogenic agents. [References: 85]
Authors Ono M. Miyamura M. Kyotani S. Saibara T. Ohnishi S. Nishioka Y Institution Department of Pharmacy, Kochi Medical School Hospital, Nankoku, Japan. Title Effect of Sho-saiko-to extract on HGF and TGF-beta levels of intraorgans in liver-injured rats after partial hepatectomy. Source Journal of Pharmacy & Pharmacology. 52(1):111-8, 2000 Jan. Abstract To examine the effects of Sho-saiko-to extract on liver regeneration, Sho-saiko-to extract (0.75%, 1.5% or 3%) was administered to 70% partial hepatectomized rats with dimethylnitrosamine-induced liver-injury. S phase cell number, liver retinoid levels, hepatocyte growth factor (HGF) and transforming growth factor-beta (TGF-beta) levels in each intraorgan were measured as indicators of liver regeneration. Three to seven days after hepatectomy, HGF and TGF-beta levels of the liver and spleen of the Sho-saiko-to extract groups were significantly different from the levels of the ordinary food group (P < 0.05-0.1). HGF levels in the Sho-saiko-to extract groups were approximately 1.3-1.8 times higher in the liver and approximately 1.8-2.1 times higher in the spleen compared with the levels found in the ordinary food group. TGF-beta levels in the Sho-saiko-to extract groups were approximately 0.38-0.47 times the level in the liver and 0.58-0.77 times the level in the spleen of the ordinary food group. There was no difference in HGF and TGF-beta levels of the kidney and lung between the Sho-saiko-to extract group and the ordinary food group. There was a significant and positive correlation between HGF level and S phase cell number in the liver (r = 0.826, P < 0.01). There was a significant and negative correlation between TGF-beta level and the retinoid level in the liver (r = -0.696, P < 0.01). In addition, the levels of the active constituents of Sho-saiko-to extract (glycyrrhetic acid, baicalin and baicalein) showed high values in the liver and spleen of partial hepatectomized rats, and increased from the third day after partial hepatectomy. These results show that Sho-saiko-to extract induces liver regeneration by increasing the production of HGF and suppressing the production of TGF-beta in the liver and spleen of partial hepatectomized rats. It was considered that the increase in the Sho-saiko-to extract active constituent levels in the liver and spleen greatly influences this action.
Authors Thatte U. Bagadey S. Dahanukar S. Institution Department of Pharmacology and Therapeutics, Seth GS Medical College, Parel, Mumbai, India. kemarc@vsnl.com Title Modulation of programmed cell death by medicinal plants. [Review] [85 refs] Source Cellular & Molecular Biology. 46(1):199-214, 2000 Feb. Abstract Programmed cell death (apoptosis), a form of cell death, described by Kerr and Wyllie some 20 years ago, has generated considerable interest in recent years. The mechanisms by which this mode of cell death (seen both in animal and plant cells), takes place have been examined in detail. Extracellular signals and intracellular events have been elaborated. Of interest to the clinician, is the concentrated effort to study pharmacological modulation of programmed cell death. The attempt to influence the natural phenomenon of programmed cell death stems from the fact that it is reduced (like in cancer) or increased (like in neurodegenerative diseases) in several clinical situations. Thus, chemicals that can modify programmed cell death are likely to be potentially useful drugs. From foxglove, which gave digitalis to the Pacific Yew from which came taxol, plants have been a source of research material for useful drugs. Recently, a variety of plant extracts have been investigated for their ability to influence the apoptotic process. This article discusses some of the interesting data. The ability of plants to influence programmed cell death in cancerous cells in an attempt to arrest their proliferation has been the topic of much research. Various cell-lines like HL60, human hepatocellular carcinoma cell line (KIM-1), a cholangiocarcinoma cell-line (KMC-1), B-cell hybridomas, U937 a monocytic cell-line, HeLa cells, human lymphoid leukemia (MOLT-4B) cells and K562 cells have been studied. The agents found to induce programmed cell death (measured either morphologically or flow cytometrically) included extracts of plants like mistletoe and Semicarpus anacardium. Isolated compounds like bryonolic acid (from Trichosanthes kirilowii var. Japonica, crocin (from saffron) and allicin (from Allium sativum) have also been found to induce programmed cell death and therefore arrest proliferation. Even Chinese herbal medicine "Sho-saiko-to" induces programmed cell death in selected cancerous cell lines. Of considerable interest is the finding that Panax ginseng prevents irradiation-induced programmed cell death in hair follicles, suggesting important therapeutic implications. Nutraceuticals (dietary plants) like soya bean, garlic, ginger, green tea, etc. which have been suggested, in epidemiological studies, to reduce the incidence of cancer may do so by inducing programmed cell death. Soy bean extracts have been shown to prevent development of diseases like polycystic kidneys, while Artemisia asiatica attenuates cerulein-induced pancreatitis in rats. Interestingly enough, a number of food items as well as herbal medicines have been reported to produce toxic effects by inducing programmed cell death. For example, programmed cell death in isolated rat hepatocytes has been implicated in the hepatitis induced by a herbal medicine containing diterpinoids from germander. Other studies suggest that rapid progression of the betel- and tobacco-related oral squamous cell carcinomas may be associated with a simultaneous involvement of p53 and c-myc leading to inhibition of programmed cell death. Several mechanisms have been identified to underlie the modulation of programmed cell death by plants including endonuclease activation, induction of p53, activation of caspase 3 protease via a Bcl-2-insensitive pathway, potentiate free-radical formation and accumulation of sphinganine. Programmed cell death is a highly conserved mechanism of self-defense, also found to occur in plants. Hence, it is natural to assume that chemicals must exist in them to regulate programmed cell death in them. Thus, plants are likely to prove to be important sources of agents that will modulate programmed cell death. [References: 85]
Authors Yagura M. Murai S. Kojima H. Tokita H. Kamitsukasa H. Harada H. Institution Department of Gastroenterology, Tokyo National Chest Hospital, Kiyose, Japan. Title Changes of liver fibrosis in chronic hepatitis C patients with no response to interferon-alpha therapy: including quantitative assessment by a morphometric method. Source Journal of Gastroenterology. 35(2):105-11, 2000. Abstract The aim of this study was to evaluate the antifibrotic effect of interferon (IFN)-alpha in chronic hepatitis C (CH-C) patients with no response to IFN-alpha therapy. We studied 76 patients (46 men, 30 women; mean age, 55.6 years) who received IFN-alpha intramuscularly, at a total close of 480 to 880MU for 6 months (group A). As a control group, we studied 50 patients (32 men and 18 women; mean age, 58.5 years) with CH-C who received medication other than IFN (ie, Strong-Neo-Minophagen C, ursodeoxycholic acid, and a herbal medicine, Sho-saiko-to [TJ-9]) and who had persistent alanine aminotransferase (ALT) elevation (group B). All patients were subdivided into three subgroups according to different patterns of ALT changes during the observation period, ie, (a) persistent ALT level < 60IU/ 1 (below about twice the upper limit of the normal range), (b) persistent ALT level > or = 60IU/1, (c) ALT levels other than (a) and (b). Liver biopsy was performed within 6 months prior to IFN therapy and more than 6 months after IFN therapy, while two liver biopsies were performed during therapy in group B. Liver fibrosis was compared between two specimens by staging. When the fibrosis stage was the same in the two specimens, we determined whether the fibrosis had improved or worsened by comparing the fibrotic ratio, ie, the ratio of the area of fibrosis to the area of the entire liver tissue specimen, calculated using computed graphic software. Serum aminoterminal peptide of type III procollagen (PIIIP) levels were measured on the day of the liver biopsy and their mean yearly changes were compared between the two groups. Improvement of liver fibrosis was found in 12% to 30% of patients in each ALT subgroup and in 24% of all patients in group A and there were no significant differences in liver fibrosis in comparison with findings in of group B when assessed by staging alone. However, these percentages rose to 59% to 75% and 66%, respectively, when liver fibrosis was assessed by the fibrotic ratio together with staging, resulting in a significant difference in fibrosis between groups A and B in total (P < 0.01). The mean yearly changes in serum PIIIP levels in each subgroup and in all patients in group A were below zero, indicating a tendency to improvement of fibrosis after IFN therapy, while these changes in group B were all above zero, except for subgroup (c). Improvement of fibrosis after IFN therapy was found in 15 of 24 patients (64%) whose ALT changes had the same pattern before and after IFN therapy, although no significant difference was noted between improved and worsened patients. These results suggest that IFN-alpha may have an antifibrotic effect even in CH-C patients with no overt response to IFN-alpha therapy, compared with the effect of medications other than IFN.
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