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      Drug Design, Development and Therapy (submit here)

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      Antioxidant compounds and activities of the stem, flower, and leaf extracts of the anti-smoking Thai medicinal plant: Vernonia cinerea Less

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          Abstract

          Vernonia cinerea (VC) Less has been proposed as a medicinal plant with interesting activities, such as an aid for smoking cessation worldwide. Despite its previous clinical success in smoking cessation by exhibiting reduced oxidative stress, it has not been approved. The aim of this study was to investigate various antioxidant activity and active compounds that have not been approved, including the protective activity in human red blood cells (RBCs), from the stem, flower, and leaf extracts of VC Less in vitro. These extracts were tested for their antioxidant activity in scavenging 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals and analyzed by high-performance liquid chromatography (HPLC) for their active compounds: total tannin, five catechin (C) compounds (epicatechin gallate [ECG], C, epicatechin [EC], epigallocatechin gallate [EGCG], and (−)-epigallocatechin [EGC]), flavonoid, nitrite, nitrate, caffeine, and nicotine. Moreover, antioxidant activities of the extracts were evaluated in 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH)-treated RBCs. The results showed that the flower and leaf of VC Less had higher activity than the stem in scavenging DPPH radicals. The tannin content in the flower and leaf was higher than that in the stem. The leaf had the highest content of the five catechins (C, EC, EGCG, ECG, and EGC), the same as in the flavonoid, when compared to the stem and flower. Furthermore, the leaf extract had higher nitrate and nitrite than the stem. Nicotine content was found to be higher in the leaf when compared to the flower. In addition, the leaf showed protective activity in glutathione (GSH), malondialdehyde (MDA), and protein carbonyl, with a dose response in AAPH-oxidized RBCs, the same as in standard EGCG. Thus, this study concluded that radical scavenging and antioxidant compounds such as catechins, flavonoid, nitrate and nitrite, and nicotine are present in different VC Less parts and are included in the AAPH-oxidized RBC model.

          Most cited references35

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          Estimates of global mortality attributable to smoking in 2000.

          Majid Ezzati, Alan Lopez (2003)
          Smoking is a risk factor for several diseases and has been increasing in many developing countries. Our aim was to estimate global and regional mortality in 2000 caused by smoking, including an analysis of uncertainty. Following the methods of Peto and colleagues, we used lung-cancer mortality as an indirect marker for accumulated smoking risk. Never-smoker lung-cancer mortality was estimated based on the household use of coal with poor ventilation. Relative risks were taken from the American Cancer Society Cancer Prevention Study, phase II, and the retrospective proportional mortality analysis of Liu and colleagues in China. Relative risks were corrected for confounding and extrapolation to other regions. We estimated that in 2000, 4.83 (uncertainty range 3.94-5.93) million premature deaths in the world were attributable to smoking; 2.41 (1.80-3.15) million in developing countries and 2.43 (2.13-2.78) million in industrialised countries. 3.84 million of these deaths were in men. The leading causes of death from smoking were cardiovascular diseases (1.69 million deaths), chronic obstructive pulmonary disease (0.97 million deaths), and lung cancer (0.85 million deaths). Smoking was an important cause of global mortality in 2000. In view of the expected demographic and epidemiological transitions and current smoking patterns in the developing world, the health loss due to smoking will grow even larger unless effective interventions and policies that reduce smoking among men and prevent increases among women in developing countries are implemented.
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            Free-radical chemistry of cigarette smoke and its toxicological implications.

            D Church, W A Pryor (1985)
            Cigarette smoke contains two very different populations of free radicals, one in the tar and one in the gas phase. The tar phase contains several relatively stable free radicals; we have identified the principal radical as a quinone/hydroquinone (Q/QH2) complex held in the tarry matrix. We suggest that this Q/QH2 polymer is an active redox system that is capable of reducing molecular oxygen to produce superoxide, eventually leading to hydrogen peroxide and hydroxyl radicals. In addition, we have shown that the principal radical in tar reacts with DNA in vitro, possibly by covalent binding. The gas phase of cigarette smoke contains small oxygen- and carbon-centered radicals that are much more reactive than are the tar-phase radicals. These gas-phase radicals do not arise in the flame, but rather are produced in a steady state by the oxidation of NO to NO2, which then reacts with reactive species in smoke such as isoprene. We suggest that these radicals and the metastable products derived from these radical reactions may be responsible for the inactivation of alpha 1-proteinase inhibitor by fresh smoke. Cigarette smoke oxidizes thiols to disulfides; we suggest the active oxidants are NO and NO2. The effects of smoke on lipid peroxidation are complex, and this is discussed. We also discuss the toxicological implications for the radicals in smoke in terms of a number of radical-mediated disease processes, including emphysema and cancer.
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              The antioxidant effects of the flavonoids rutin and quercetin inhibit oxaliplatin-induced chronic painful peripheral neuropathy

              Maria Isabel Azevedo, Anamaria Falcão Pereira, Ricardo Braz Nogueira … (2013)
              Background Oxaliplatin, the third-generation platinum compound, has evolved as one of the most important therapeutic agents in colorectal cancer chemotherapy. The main limiting factor in oxaliplatin treatment is painful neuropathy that is difficult to treat. This side effect has been studied for several years, but its full mechanism is still inconclusive, and effective treatment does not exist. Data suggest that oxaliplatin’s initial neurotoxic effect is peripheral and oxidative stress-dependent. A spinal target is also suggested in its mechanism of action. The flavonoids rutin and quercetin have been described as cell-protecting agents because of their antioxidant, antinociceptive, and anti-inflammatory actions. We proposed a preventive effect of these agents on oxaliplatin-induced painful peripheral neuropathy based on their antioxidant properties. Methods Oxaliplatin (1 mg/kg, i.v.) was injected in male Swiss mice, twice a week (total of nine injections). The development of sensory alterations, such as thermal and mechanical allodynia, was evaluated using the tail immersion test in cold water (10°C) and the von Frey test. Rutin and quercetin (25-100 mg/kg, i.p.) were injected 30 min before each oxaliplatin injection. The animals’ spinal cords were removed for histopathological and immunohistochemical evaluation and malondialdehyde assay. Results Oxaliplatin significantly increased thermal and mechanical nociceptive response, effects prevented by quercetin and rutin at all doses. Fos immunostaining in the dorsal horn of the spinal cord confirmed these results. The oxidative stress assays mainly showed that oxaliplatin induced peroxidation in the spinal cord and that rutin and quercetin decreased this effect. The flavonoids also decreased inducible nitric oxide synthase and nitrotyrosine immunostaining in the dorsal horn of the spinal cord. These results suggest that nitric oxide and peroxynitrite are also involved in the neurotoxic effect of oxaliplatin and that rutin and quercetin can inhibit their effect in the spinal cord. We also observed the preservation of dorsal horn structure using histopathological analyses. Conclusions Oxaliplatin induced painful peripheral neuropathy in mice, an effect that was prevented by rutin and quercetin. The mechanism of action of oxaliplatin appears to be, at least, partially oxidative stress-induced damage in dorsal horn neurons, with the involvement of lipid peroxidation and protein nitrosylation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Drug Des Devel Ther
                Journal ID (iso-abbrev): Drug Des Devel Ther
                Journal ID (publisher-id): Drug Design, Development and Therapy
                Title: Drug Design, Development and Therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 1177-8881
                Publication date Collection: 2017
                Publication date (Electronic): 13 February 2017
                Volume: 11
                Pages: 383-391
                Affiliations
                [1 ]Department of Physical Therapy
                [2 ]Department of Radiologic Technology
                [3 ]Department of Medical Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand
                Author notes
                Correspondence: Jirakrit Leelarungrayub, Department of Physical Therapy, Faculty of Associated Medical Sciences, Chiang Mai University, Intawaroroj Road, Sripoom, Chiang Mai 50200, Thailand, Tel +66 53 94 9272, Fax +66 53 94 6042, Email donrawee.leela@ 123456cmu.ac.th
                Article
                Publisher ID: dddt-11-383
                DOI: 10.2147/DDDT.S126882
                PMC ID: 5317266
                SO-VID: 001b0ad7-46e2-42e0-9f98-77a0a6ac8086
                Copyright © © 2017 Ketsuwan et al. This work is published and licensed by Dove Medical Press Limited
                License:

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Subject: Original Research

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: antioxidant activity,anti-smoking aid,bioactive compounds,vernonia cinerea
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: antioxidant activity, anti-smoking aid, bioactive compounds, vernonia cinerea

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