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      Effectiveness of Keishibukuryogan on Chronic-Stage Lichenification Associated with Atopic Dermatitis

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          Abstract

          Atopic dermatitis (AD) is a common inflammatory skin disease with recurring episodes of itching and a chronic relapsing course. Keishibukuryogan (KBG) is a traditional herbal medicine, composed of five kinds of medical plants and has been administered to patients with blood stagnation in Japan. This study investigated the effect of KBG on the disease activity in AD ( n = 45) patients. AD patients were administered KBG for 4 to 6 weeks in addition to their prescribed medications. The results showed that the SCORAD index and VAS score were significantly decreased after the administration of KBG ( P < 0.01). KBG also decreased the serum LDH level significantly ( P < 0.01). The global assessment of the clinical response in SCORAD index showed that 88.5% of the patients with moderate improvement to excellent response ( n = 26) had a high lichenification score (lichenification score ≥2 in SCORAD). On the other hand, only 42.1% of the patients with no improvement to mild improvement ( n = 19) had a high lichenification score. Furthermore, long-term administration of KBG for 9–67 weeks showed a marked improvement in patients with a high lichenification score. Therefore, KBG was found to be effective against AD, particularly in cases presenting with lichenified lesions.

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          New insights into atopic dermatitis.

          Donald Y M Leung, Mark Boguniewicz, Michael Howell … (2004)
          Atopic dermatitis is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental triggers and is often the first step in the atopic march that results in asthma and allergic rhinitis. The clinical phenotype that characterizes atopic dermatitis is the product of interactions between susceptibility genes, the environment, defective skin barrier function, and immunologic responses. This review summarizes recent progress in our understanding of the pathophysiology of atopic dermatitis and the implications for new management strategies.
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            Thymus and activation regulated chemokine (TARC)/CCL17 and skin diseases.

            Kunihiko Tamaki, Hidehisa Saeki (2006)
            Thymus and activation-regulated chemokine (TARC)/CCL17 is constitutively expressed in the thymus and is produced by dendritic cells (DC), endothelial cells, keratinocytes (KC) and fibroblasts. TARC is designated a Th2 type chemokine since it binds to CCR4. We review the pathogenic role of TARC in skin diseases such as atopic dermatitis (AD), bullous pemphigoid (BP) and mycosis fungoides (MF) focusing on epidermal KC and Langerhans cells (LC), which are epidermal DC. We have determined that serum TARC levels sharply reflect the disease activity of AD, which is thought to be a Th2-dominant inflammatory skin disease especially in the acute phase. Serum TARC levels are also related to the disease activity of BP, which is a blistering autoimmune skin disease, and MF, which is a cutaneous T-cell lymphoma, but very high serum TARC levels are only seen in a limited number of various other skin diseases. TARC may be a useful laboratory marker for the diagnosis of AD, especially cases which are moderate to severe, and for the evaluation of disease activity of AD. IL-4 and TGF-beta1 downregulate TNF-alpha and IFN-gamma induced TARC production in the human KC cell line, HaCaT cells, while IL-4 upregulates, and IFN-gamma downregulates TARC production by mouse LC. Because TARC and its receptor CCR4 are believed to play important roles in the pathogenesis of AD, BP and MF, TARC and CCR4 may be possible future targets for therapy of these diseases.
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              Neuroprotective effect of paeoniflorin on cerebral ischemic rat by activating adenosine A1 receptor in a manner different from its classical agonists.

              Zhi Liu, Liang Jiang, Xing Zhu … (2005)
              The effects of paeoniflorin (PF), a compound isolated from Paeony radix, on neurological impairment and histologically measured infarction volume following transient and permanent focal ischemia were examined in Sprague-Dawley rats. In transient ischemia model, rats were subjected to a 1.5-h occlusion of the middle cerebral artery (MCA). The administration of PF (2.5 and 5 mg kg(-1), s.c.) produced a dose-dependent decrease in both neurological impairment and the histologically measured infarction volume. Similar results were also obtained when PF (2.5, 5, and 10 mg kg(-1), s.c.) was given in permanent ischemia model. The neuroprotective effect of PF (10 mg kg(-1), s.c.) was abolished by pretreatment of DPCPX (0.25 mg kg(-1), s.c.), a selective adenosine A1 receptor (A1R) antagonist. PF (10, 40, and 160 mg kg(-1), i.v.) had no effect on mean arterial pressure (MAP) and heart rates (HR) in the conscious rat. Additionally, PF (10(-3) mol l(-1)) had no effect on noradrenaline- (NA-) or high K+ concentration-induced contractions of isolated rabbit primary artery. In competitive binding experiments, PF did not compete with the binding of [3H]DPCPX, but displaced the binding of [3H]NECA to the membrane preparation of rat cerebral cortex. This binding manner was distinguished from the classical A1R agonists. The results demonstrated that activation of A1R might be involved in PF-induced neuroprotection in cerebral ischemia in rat. However, PF had no 'well-known' cardiovascular side effects of classical A1R agonists. The results suggest that PF might have the potential therapeutic value as an anti-stroke drug.
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                Author and article information

                Journal
                Journal ID (nlm-ta): ISRN Dermatol
                Journal ID (iso-abbrev): ISRN Dermatol
                Journal ID (publisher-id): ISRN.DERMATOLOGY
                Title: ISRN Dermatology
                Publisher: International Scholarly Research Network
                ISSN (Print): 2090-4592
                ISSN (Electronic): 2090-4606
                Publication date Collection: 2012
                Publication date (Electronic): 14 November 2012
                Volume: 2012
                Electronic Location Identifier: 158598
                Affiliations
                1Department of Dermatology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Sugitani, Toyama 2630, Japan
                2Department of Japanese Oriental Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Sugitani, Toyama 2630, Japan
                Author notes

                Academic Editors: S.-C. Chao, M. Feinmesser, E. Pasmatzi, and J. F. Val Bernal

                Article
                DOI: 10.5402/2012/158598
                PMC ID: 3504367
                PubMed ID: 23213558
                SO-VID: 35f5d21b-be74-49a9-9c6f-75f1f18ba07a
                Copyright © Copyright © 2012 Megumi Mizawa et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 September 2012
                Date accepted : 10 October 2012
                Categories
                Subject: Clinical Study

                ScienceOpen disciplines: Dermatology
                Data availability:
                ScienceOpen disciplines: Dermatology

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