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Single-dose Intravenous Toxicology Testing of Daebohwalryeok Pharmcopuncture in Sprague-Dawley Rats

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      Abstract

      Objectives:The aims of the study were to test the single-dose intravenous toxicity of Daebohwalryeok pharmacopuncture (DHRP) in Sprague-Dawley (SD) rats and to estimate the crude lethal dose.Methods:The experiments were conducted at Biotoxtech Co., a Good Laboratory Practice (GLP) laboratory, according to the GLP regulation and were approved by the Institutional Animal Care and Use Committee of Biotoxtech Co. (Approval no: 110156). The rats were divided into three groups: DHRP was injected into the rats in the two test groups at doses of 10 mL/kg and 20 mL/kg, respectively, and normal saline solution was injected into the rats in the control group. Single doses of DHRP were injected intravenously into 6 week old SD rats (5 male and 5 female rats per group). General symptoms were observed and weights were measured during the 14 day observation period after the injection. After the observation period, necropsies were done. Then, histopathological tests were performed. Weight data were analyzed with a one-way analysis of variance (ANOVA) by using statistical analysis system (SAS, version 9.2).Results:No deaths and no statistical significant weight changes were observed for either male or female SD rats in either the control or the test groups during the observation period. In addition, no treatment related general symptoms or necropsy abnormalities were observed. Histopathological results showed no DHRP related effects in the 20 mL/kg DHRP group for either male or female rats.Conclusion:Under the conditions of this study, the results from single-dose intravenous injections of DHRP showed that estimated lethal doses for both male and female rats were above 20 mL/kg.

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      Anti-fatigue activity of the water-soluble polysaccharides isolated from Panax ginseng C. A. Meyer.

      Panax ginseng C. A. Meyer (ginseng) is a well-known Chinese herb often used in Asian countries for physical strength development. Ginseng polysaccharides are its active component and have a lot of pharmaceutical activities. However, anti-fatigue activity of ginseng polysaccharides has not yet been tested. The current study was designed to evaluate the anti-fatigue activity of ginseng polysaccharides (WGP) in an animal test for fatigue and compare the activities between the neutral (WGPN) and acidic (WGPA) portion in an attempt to determine whether the medicinal uses are supported by pharmacological effects. WGP, WGPN and WGPA were orally administrated to mice once daily for 15 days. Anti-fatigue activity was assessed using the forced swim test (FST) and serum biochemical parameters were determined by autoanalyzer and commercially available kits. While all compounds were found to reduce immobility in the FST, the effect of WGPA was demonstrated in lower doses compared with WGP and WGPN. Moreover, the FST-induced reduction in glucose (GLU) and glutathione peroxidase (GPx) and increase in creatine phosphokinase (CK), lactic dehydrogenase (LDH) and malondialdehyde (MDA) levels, all indicators of fatigue, were inhibited by the corresponding doses of WGP, WGPN and WGPA. Ginseng polysaccharides have anti-fatigue activity, also reflected in the effects on the physiological markers for fatigue. The acidic polysaccharide is more potent than the neutral polysaccharide. Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
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        Neuroprotective effects of ginsenoside Rd against oxygen-glucose deprivation in cultured hippocampal neurons.

        We previously found that ginsenoside Rd (GSRd), one of the main active ingredients in Panax Ginseng, attenuates H(2)O(2)-induced oxidative injury in PC12 cells. Mounting evidence suggests that the oxidative stress is crucially involved in the pathophysiologic process of ischemia. In the present study, we examined the protective role of GSRd to attenuate ischemic neuronal injury in vitro. Cultured hippocampal neurons were exposed to oxygen-glucose deprivation (OGD) for 2h followed by a 24-h reoxygenation. GSRd exhibited remarkable neuroprotection when presented during OGD and reoxygenation, which may be ascribed to its antioxidative properties by reducing the intracellular reactive oxygen species and malondialdehyde production; increasing glutathione content; and enhancing the antioxidant enzymatic activities of catalase, superoxide dismutase and glutathione peroxidase. Additionally, GSRd could stabilize the mitochondrial membrane potential and attenuate apoptotic death of hippocampal neurons after OGD exposure. These findings suggested that GSRd may be a potential neuroprotective agent for cerebral ischemic injury and should encourage further in vivo studies on stroke to explore the potential neuroprotective efficacy of GSRd.
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          The lignan-rich fractions of Fructus Schisandrae improve insulin sensitivity via the PPAR-γ pathways in in vitro and in vivo studies.

          Fructus Schisandrae, the fruit of Schisandra chinensis (Turcz.) Baillon, has been traditionally used as a hypoglycemic agent in Asia and its extracts have been shown to improve insulin-stimulated glucose uptake in cell-based assays in previous studies. We set out to determine which fractions of Fructus Schisandrae improved peroxisome proliferator-activated receptor (PPAR)-γ activity and glucose-stimulated insulin secretion in cell-based experiments. The fractions that enhance glucose homeostasis were then tested for their hypoglycemic effects and mechanism was examined. The fractions (FS-0, FS-20, FS-40, FS-60, FS-80, FS-100) were made by extracting Fructus Schisandrae with 70% ethanol followed by its fractionation with a XDA column with a different ratio of methanol and water. The insulin-stimulated glucose uptake and PPAR-γ agonistic actions of each fraction were investigated in 3T3-L1 adipocytes and glucose-stimulated insulin secretion was determined in Min6 cells. The fraction(s) that were efficacious (200mg/kg bw) were orally given to 90% pancreatectomized (Px) diabetic rats for 8 weeks to evaluate insulin sensitivity in euglycemic hyperinsulinemic clamp and insulin secretion at hyperglycemic clamp. FS-60 contains schizandrin, gomisin A and angeloylgomisin H while FS-80 contains deoxyschizandrin, γ-schizandrin, and gomisin N. A PPAR-γ agonistic action was greater in the ascending order of the control, FS-80 and FS-60 in 3T3-L1 adipocytes. FS-60 increased the glucose disposal rates of Px rats as much as rosiglitazone during euglycemic hyperinsulinemic clamp while hepatic glucose output at hyperinsulinemic clamped states decreased in the descending order of the control, FS-80, FS-60 with potentiating insulin signaling. At hyperglycemic clamp only FS-60 potentiated first phase insulin secretion in diabetic animals; the second phase was not increased. FS-60, a lignan-rich fraction, improves glucose homeostasis by increasing glucose disposal rates and enhancing hepatic insulin sensitivity by working as a PPAR-γ agonist in type-2 diabetic rats. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
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            Author and article information

            Affiliations
            [1 ]Department of Internal Medicine, College of Korean Medicine, Sangji University, Wonju, Korea
            [2 ]Department of Preventive Medicine, College of Korean Medicine, Daejeon University, Daejeon, Korea
            [3 ]Department of Acupuncture & Moxibustion Medicine, College of Korean Medicine, Sangji University, Wonju, Korea
            [4 ]Department of Sasang Constitutional Medicine, College of Korean Medicine, Sangji University, Wonju, Korea
            [5 ]Department of Ophthalmology, Otolaryngology, and Dermatology, Korean Medicine Hospital, Pusan National University, Yangsan, Korea
            [6 ]Research Center of the Korean Pharmacopuncture Institute, Seoul, Korea
            Author notes
            * Corresponding Author Kirok Kwon. Korean Pharmacopuncture Institute, 4F, Association of Korean Oriental Medicine B/D 26-27, Gayang-dong, Gangseo-gu, Seoul 157-200, Korea. Tel: +82-33-744-9304 Fax: +82-33-744-9305 E-mail: drkwon5031@daum.net
            Contributors
            drkwon5031@daum.net
            Journal
            J Pharmacopuncture
            J Pharmacopuncture
            J Pharmacopunct
            10.3831
            Journal of Pharmacopuncture
            KOREAN PHARMACOPUNCTURE INSTITUTE
            2093-6966
            2234-6856
            June 2015
            : 18
            : 2
            : 42-50
            26120487
            4481398
            10.3831/KPI.2015.18.014
            Copyright ©2015, KOREAN PHARMACOPUNCTURE INSTITUTE

            This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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