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Post-COVID-19-Syndrom : Ein heterogenes Krankheitsbild aus der Sicht der Neurologie <span class="so-article-trans-title" dir="auto"> Translated title: Post COVID-19 Condition : A Heterogeneous Clinical Picture from a Neurological Point of View </span>
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      Poly-Ingredient Formulation Bresol ® Ameliorates Experimental Chronic Obstructive Pulmonary Disease (COPD) in Rats

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          Abstract

          In the present study, the protective effect of Bresol ® – a polyherbal formulation – was evaluated in an experimental model of cigarette smoke (CS)-induced COPD in rats. Ten minutes daily exposure to CS for 7 weeks caused significant elevation of TNF-α (p<0.01) and total protein (p<0.01) in the bronchoalveolar lavage fluid (BALF) of positive untreated control animals, indicating ongoing inflammatory process in the lungs. Further, histopathological findings have confirmed the presence of pathological lesions in the trachea and lungs. Five weeks of post-treatment with Bresol ® (250 and 500 mg/kg, p.o.) showed significant and dose-dependent anti-inflammatory effects against CS-induced lung abnormalities by maintaining the TNF-α and total protein levels within the normal range. Additionally, Bresol ®-treated animals showed normal cyto-architecture of the trachea and lungs. In conclusion, Bresol ® showed dose-dependent protection against CS-induced lung and tracheal injury in rats, which further indicates, Bresol ® is a useful healing agent, may help to decelerate the progression of COPD, and reduce the exacerbations in patients.

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          Oxidative stress and redox regulation of lung inflammation in COPD.

          I Rahman, I M Adcock (2006)
          Reactive oxygen species, either directly or via the formation of lipid peroxidation products, may play a role in enhancing inflammation through the activation of stress kinases (c-Jun activated kinase, extracellular signal-regulated kinase, p38) and redox-sensitive transcription factors, such as nuclear factor (NF)-kappaB and activator protein-1. This results in increased expression of a battery of distinct pro-inflammatory mediators. Oxidative stress activates NF-kappaB-mediated transcription of pro-inflammatory mediators either through activation of its activating inhibitor of kappaB-alpha kinase or the enhanced recruitment and activation of transcriptional co-activators. Enhanced NF-kappaB-co-activator complex formation results in targeted increases in histone modifications, such as acetylation leading to inflammatory gene expression. Emerging evidence suggests the glutathione redox couple may entail dynamic regulation of protein function by reversible disulphide bond formation on kinases, phosphatases and transcription factors. Oxidative stress also inhibits histone deacetylase activity and in doing so further enhances inflammatory gene expression and may attenuate glucocorticoid sensitivity. The antioxidant/anti-inflammatory effects of thiol molecules (glutathione, N-acetyl-L-cysteine and N-acystelyn, erdosteine), dietary polyphenols (curcumin-diferuloylmethane, cathechins/quercetin and reserveratol), specific spin traps, such as alpha-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (extracellular superoxide dismutase (SOD) mimetic, SOD mimetic M40419 and SOD, and catalase manganic salen compound, eukarion-8), porphyrins (AEOL 10150 and AEOL 10113) and theophylline have all been shown to play a role in either controlling NF-kappaB activation or affecting histone modifications with subsequent effects on inflammatory gene expression in lung epithelial cells. Thus, oxidative stress regulates both key signal transduction pathways and histone modifications involved in lung inflammation. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in chronic obstructive pulmonary disease are also discussed.
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            Differences in interleukin-8 and tumor necrosis factor-alpha in induced sputum from patients with chronic obstructive pulmonary disease or asthma.

            V Keatings, P Collins, D. M. Scott … (1996)
            Asthma and chronic obstructive pulmonary disease are characterized by chronic airway inflammation. Studies using bronchoalveolar lavage (BAL) have shown an increased proportion of eosinophils in the BAL fluid from asthmatics compared with that from normal subjects, whereas studies of chronic obstructive pulmonary disease (COPD) have shown increased numbers of neutrophils. Induced sputum allows sampling of respiratory tract secretions from patients and control subjects, providing a noninvasive method of studying airway secretions and allowing characterization of cells and measurement of soluble markers. We investigated whether induced sputum was a useful method of studying airway fluid from patients with moderate to severe COPD and whether it could be used to compare inflammation in this condition with that in asthma. An initial reproducibility study was undertaken. Sputum was induced twice in 13 patients with severe COPD at a 14-d interval. Total and differential cell counts were carried out and were found to be reproducible over this period. Sputum was then induced in 14 patients with COPD, 23 patients with asthma, 12 healthy cigarette smokers, and 16 normal nonsmoking control subjects. We found a significant increase in neutrophils and increased concentrations of tumor necrosis factor-alpha (TNF alpha) and interleukin-8 (IL-8) in the patients with COPD compared with the smoking and nonsmoking control subjects. Interleukin-8, but not TNF alpha, was significantly higher in the COPD group than in the asthmatic group. We conclude that the cytokines TNF alpha and IL-8 may be involved in the inflammation in COPD.
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              Pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease.

              Toshinori YOSHIDA, Rubin M Tuder (2007)
              Chronic obstructive pulmonary diseases (COPD), comprised of pulmonary emphysema, chronic bronchitis, and structural and inflammatory changes of small airways, is a leading cause of morbidity and mortality in the world. A better understanding of the pathobiology of COPD is critical for the developing of novel therapies, as the majority of patients with the disease have little therapeutic options at the present time. The pathobiology of COPD encompasses multiple injurious processes including inflammation (excessive or inappropriate innate and adaptive immunity), cellular apoptosis, altered cellular and molecular alveolar maintenance program, abnormal cell repair, extracellular matrix destruction (protease and anti-protease imbalance), and oxidative stress (oxidant and antioxidant imbalance). These processes are triggered by urban and rural air pollutants and active and/or passive cigarette smoke and modified by cellular senescence and infection. A series of receptor-mediated signal transduction pathways are activated by reactive oxygen species and tobacco components, resulting in impairment of a variety of cell signaling and cytokine networks, subsequently leading to chronic airway responses with mucus production, airway remodeling, and alveolar destruction. The authors provide an updated insight into the molecular and cellular pathobiology of COPD based on human and/or animal data.
              Article 0 comments Cited 131 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Sci Pharm
                Journal ID (iso-abbrev): Sci Pharm
                Journal ID (publisher-id): Scientia Pharmaceutica
                Title: Scientia Pharmaceutica
                Publisher: Österreichische Apotheker-Verlagsgesellschaft
                ISSN (Print): 0036-8709
                ISSN (Electronic): 2218-0532
                Publication date Collection: September 2013
                Publication date (Electronic): 09 May 2013
                Volume: 81
                Issue: 3
                Pages: 833-842
                Affiliations
                Department of Pharmacology, R&D Center, The Himalaya Drug Company, Makali, Bangalore, Karnataka, India.
                Author notes
                [* ]Corresponding author. E-mail: dr.rafiq@ 123456himalayahealthcare.com (M. Rafiq)
                Article
                Publisher ID: scipharm_2013_81_833
                DOI: 10.3797/scipharm.1212-06
                PMC ID: 3791943
                SO-VID: f994dec5-19b7-4ce4-963b-e09d4c590c4c
                Copyright © © Rafiq et al.; licensee Österreichische Apotheker-Verlagsgesellschaft m. b. H., Vienna, Austria.
                License:

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

                History
                Date received : 06 December 2012
                Date accepted : 09 May 2013
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: bresol®,cigarette smoke-induced lung injury,bronchitis,broncheoalveolar lavage fluid,tnf-α
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: bresol®, cigarette smoke-induced lung injury, bronchitis, broncheoalveolar lavage fluid, tnf-α

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