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      A Review on Medicinal Properties of Orientin

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          Abstract

          Medicinal plants continue to play an important role in modern medications and healthcare as consumers generally believe that most of them cause fewer or milder adverse effects than the conventional modern medicines. In order to use the plants as a source of medicinal agents, the bioactive compounds are usually extracted from plants. Therefore, the extraction of bioactive compounds from medicinal plants is a crucial step in producing plant-derived drugs. One of the bioactive compounds isolable from medicinal plants, orientin, is often used in various bioactivity studies due to its extensive beneficial properties. The extraction of orientin in different medicinal plants and its medicinal properties, which include antioxidant, antiaging, antiviral, antibacterial, anti-inflammation, vasodilatation and cardioprotective, radiation protective, neuroprotective, antidepressant-like, antiadipogenesis, and antinociceptive effects, are discussed in detail in this review.

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          Most cited references75

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          Plants as source of drugs.

          This work presents a study of the importance of natural products, especially those derived from higher plants, in terms of drug development. It describes the main strategies for obtaining drugs from natural sources, fields of knowledge involved, difficulties and perspectives. It also includes a brief discussion of the specific situation in Brazil regarding the use of, trade in, and research into therapeutic resources of natural origin and the general lack of awareness of the use of potentially toxic plants, mainly in folk medicine.
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            Cytokines in acute and chronic inflammation.

            Inflammation is mediated by a variety of soluble factors, including a group of secreted polypeptides known as cytokines. Inflammatory cytokines can be divided into two groups: those involved in acute inflammation and those responsible for chronic inflammation. This review describes the role played in acute inflammation by IL-1, TNF-alpha, IL-6, IL-11, IL-8 and other chemokines, G-CSF, and GM-CSF. It also describes the involvement of cytokines in chronic inflammation. This latter group can be subdivided into cytokines mediating humoral responses such as IL-4, IL-5, IL-6, IL-7, and IL-13, and those mediating cellular responses such as IL-1, IL-2, IL-3, IL-4, IL-7, IL-9, IL-10, IL-12, interferons, transforming growth factor-beta, and tumor necrosis factor alpha and beta. Some cytokines, such as IL-1, significantly contribute to both acute and chronic inflammation. This review also summarizes features of the cell-surface receptors that mediate the inflammatory effects of the described cytokines.
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              Vascular inflammation and the renin-angiotensin system.

              It is now well established that vascular inflammation is an independent risk factor for the development of atherosclerosis. In otherwise healthy patients, chronic elevations of circulating interleukin-6 or its biomarkers are predictors for increased risk in the development and progression of ischemic heart disease. Although multifactorial in etiology, vascular inflammation produces atherosclerosis by the continuous recruitment of circulating monocytes into the vessel wall and by contributing to an oxidant-rich inflammatory milieu that induces phenotypic changes in resident (noninflammatory) cells. In addition, the renin-angiotensin system (RAS) has important modulatory activities in the atherogenic process. Recent work has shown that angiotensin II (Ang II) has significant proinflammatory actions in the vascular wall, inducing the production of reactive oxygen species, inflammatory cytokines, and adhesion molecules. These latter effects on gene expression are mediated, at least in part, through the cytoplasmic nuclear factor-kappaB transcription factor. Through these actions, Ang II augments vascular inflammation, induces endothelial dysfunction, and, in so doing, enhances the atherogenic process. Our recent studies have defined a molecular mechanism for a biological positive-feedback loop that explains how vascular inflammation can be self-sustaining through upregulation of the vessel wall Ang II tone. Ang II produced locally by the inflamed vessel induces the synthesis and secretion of interleukin-6, a cytokine that induces synthesis of angiotensinogen in the liver through a janus kinase (JAK)/signal transducer and activator of transcription (STAT)-3 pathway. Enhanced angiotensinogen production, in turn, supplies more substrate to the activated vascular RAS, where locally produced Ang II synergizes with oxidized lipid to perpetuate atherosclerotic vascular inflammation. These observations suggest that one mechanism by which RAS antagonists prevent atherosclerosis is by reducing vascular inflammation. Moreover, antagonizing the vascular nuclear factor-kappaB and/or hepatic JAK/STAT pathways may modulate the atherosclerotic process.
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                Author and article information

                Journal
                Adv Pharmacol Sci
                Adv Pharmacol Sci
                APS
                Advances in Pharmacological Sciences
                Hindawi Publishing Corporation
                1687-6334
                1687-6342
                2016
                19 May 2016
                : 2016
                : 4104595
                Affiliations
                1School of Postgraduate Studies and Research, International Medical University, 57000 Kuala Lumpur, Malaysia
                2Division of Biomedical Science and Biotechnology, School of Health Sciences, International Medical University, 57000 Kuala Lumpur, Malaysia
                3Department of Biomedical Science, Faculty of Science, Universiti Tunku Abdul Rahman, Perak Campus, 31900 Kampar, Perak, Malaysia
                Author notes
                *Anna Pick Kiong Ling: anna_ling@ 123456imu.edu.my

                Academic Editor: Hansen Wang

                Article
                10.1155/2016/4104595
                4889806
                27298620
                652eddc9-a982-42c4-9719-f8320eddf284
                Copyright © 2016 Kit Ying Lam et al.

                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
                : 17 November 2015
                : 4 March 2016
                : 14 April 2016
                Categories
                Review Article

                Pharmacology & Pharmaceutical medicine
                Pharmacology & Pharmaceutical medicine

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