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      Medicinal Profile, Phytochemistry, and Pharmacological Activities of Murraya koenigii and Its Primary Bioactive Compounds

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          Abstract

          The discovery of several revitalizing molecules that can stop or reduce the pathology of a wide range of diseases will be considered a major breakthrough of the present time. Available synthetic compounds may provoke side effects and health issues, which heightens the need for molecules from plants and other natural resources under discovery as potential methods of replacing synthetic compounds. In traditional medicinal therapies, several plant extracts and phytochemicals have been reported to impart remedial effects as better alternatives. Murraya koenigii ( M. koenigii) belongs to the Rutaceae family, which is commonly used as a medicinally important herb of Indian origin in the Ayurvedic system of medicine. Previous reports have demonstrated that the leaves, roots, and bark of this plant are rich sources of carbazole alkaloids, which produce potent biological activities and pharmacological effects. These include antioxidant, antidiabetic, anti-inflammatory, antitumor, and neuroprotective activities. The present review provides insight into the major components of M. koenigii and their pharmacological activities against different pathological conditions. The review also emphasizes the need for more research on the molecular basis of such activity in various cellular and animal models to validate the efficacy of M. koenigii and its derivatives as potent therapeutic agents.

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          Antioxidant activity and phenolic compounds in 32 selected herbs

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            Increased nigral iron content and alterations in other metal ions occurring in brain in Parkinson's disease.

            Levels of iron, copper, zinc, manganese, and lead were measured by inductively coupled plasma spectroscopy in parkinsonian and age-matched control brain tissue. There was 31-35% increase in the total iron content of the parkinsonian substantia nigra when compared to control tissue. In contrast, in the globus pallidus total iron levels were decreased by 29% in Parkinson's disease. There was no change in the total iron levels in any other region of the parkinsonian brain. Total copper levels were reduced by 34-45% in the substantia nigra in Parkinson's disease; no difference was found in the other brain areas examined. Zinc levels were increased in substantia nigra in Parkinson's disease by 50-54%, and the zinc content of the caudate nucleus and lateral putamen was also raised by 18-35%. Levels of manganese and lead were unchanged in all areas of the parkinsonian brain studied when compared to control brains, except for a small decrease (20%) in manganese content of the medial putamen. Increased levels of total iron in the substantia nigra may cause the excessive formation of toxic oxygen radicals, leading to dopamine cell death.
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              Mitochondrial metabolism, redox signaling, and fusion: a mitochondria-ROS-HIF-1alpha-Kv1.5 O2-sensing pathway at the intersection of pulmonary hypertension and cancer.

              Pulmonary arterial hypertension (PAH) is a lethal syndrome characterized by vascular obstruction and right ventricular failure. Although the fundamental cause remains elusive, many predisposing and disease-modifying abnormalities occur, including endothelial injury/dysfunction, bone morphogenetic protein receptor-2 gene mutations, decreased expression of the O(2)-sensitive K(+) channel (Kv1.5), transcription factor activation [hypoxia-inducible factor-1alpha (HIF-1alpha) and nuclear factor-activating T cells], de novo expression of survivin, and increased expression/activity of both serotonin transporters and platelet-derived growth factor receptors. Together, these abnormalities create a cancerlike, proliferative, apoptosis-resistant phenotype in pulmonary artery smooth muscle cells (PASMCs). A possible unifying mechanism for PAH comes from studies of fawn-hooded rats, which manifest spontaneous PAH and impaired O(2) sensing. PASMC mitochondria normally produce reactive O(2) species (ROS) in proportion to P(O2). Superoxide dismutase 2 (SOD2) converts intramitochondrial superoxide to diffusible H(2)O(2), which serves as a redox-signaling molecule, regulating pulmonary vascular tone and structure through effects on Kv1.5 and transcription factors. O(2) sensing is mediated by this mitochondria-ROS-HIF-1alpha-Kv1.5 pathway. In PAH and cancer, mitochondrial metabolism and redox signaling are reversibly disordered, creating a pseudohypoxic redox state characterized by normoxic decreases in ROS, a shift from oxidative to glycolytic metabolism and HIF-1alpha activation. Three newly recognized mitochondrial abnormalities disrupt the mitochondria-ROS-HIF-1alpha-Kv1.5 pathway: 1) mitochondrial pyruvate dehydrogenase kinase activation, 2) SOD2 deficiency, and 3) fragmentation and/or hyperpolarization of the mitochondrial reticulum. The pyruvate dehydrogenase kinase inhibitor, dichloroacetate, corrects the mitochondrial abnormalities in experimental models of PAH and human cancer, causing a regression of both diseases. Mitochondrial abnormalities that disturb the ROS-HIF-1alpha-Kv1.5 O(2)-sensing pathway contribute to the pathogenesis of PAH and cancer and constitute promising therapeutic targets.
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                Author and article information

                Journal
                Antioxidants (Basel)
                Antioxidants (Basel)
                antioxidants
                Antioxidants
                MDPI
                2076-3921
                24 January 2020
                February 2020
                : 9
                : 2
                : 101
                Affiliations
                [1 ]Department of Applied Life Sciences and Integrated Bioscience, Graduate School, Konkuk University, Chungju 27478, Korea; rmbalabio@ 123456gmail.com (R.B.); wowsong333@ 123456naver.com (S.-H.J.)
                [2 ]Department of Biochemistry, Rev. Jacob Memorial Christian College, Ambilikkai 624612, Tamilnadu, India; dvijayraja@ 123456gmail.com
                [3 ]Department of Integrated Bio Science and Biotechnology, College of Biomedical and Health Science, Nanotechnology Research Center, Konkuk University, Chungju 27478, Korea; palanivel@ 123456kku.ac.kr
                Author notes
                [* ]Correspondence: kis5497@ 123456kku.ac.kr (I.S.-K.); choidk@ 123456kku.ac.kr (D.-K.C.)
                Author information
                https://orcid.org/0000-0001-5755-8433
                https://orcid.org/0000-0001-7041-1524
                Article
                antioxidants-09-00101
                10.3390/antiox9020101
                7070712
                31991665
                705046ac-1afe-4766-8efd-7539635ffaab
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 13 December 2019
                : 13 January 2020
                Categories
                Review

                murraya koenigii,antioxidant,bioactive compounds,pharmacological activity,traditional medicine

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