Clinical-morphological study of lung diseases in basic treatment with the use of antioxidants of different origin and without

Т М Korol ,K M Ahafonov

doi:10.31393/reports-vnmedical-2019-23(4)-28

Abstract

Annotation. The purpose of the work is to analyze contemporary views on the morphological changes of lung tissue in inflammatory disease in the clinical and experimental conditions and results of correction by using the antioxidants. The analysis is based in a review if foreign articles for 2014-2019, using the scientometric databases PubMed, Web of Science and Google Scholar. According to the latest data from WHO and WORLD HEALTH RANKINGS 5-year mortality rate of such disease as COPD typically ranges from 40% to 70%, depending on disease severity, while the 2-year mortality rate for people with severe COPD is about 50%. We know that almost 90% of COPD deaths occur in low- and middle-income countries such as Ukraine. Thereby mortality rate from lung tissue diseases in Ukraine is 11.11%. These diseases often accompanied by inflammation and oxidative stress. The last can cause mitochondrial dysfunction, dynamic changes and mitophagy impairment, which leads to increase the number of superoxide anions, hydrogen peroxide etc., inflammatory responses and cellular senescence. They all play important roles in the pathogenesis of chronic lung diseases, such as chronic obstructive pulmonary disease, pulmonary fibrosis and bronchopulmonary dysplasia. Many studies in vitro approved the role of antioxidants in the decreasing of the degree of morphological changes: inflammatory cells infiltration and alveolar edema, permeability and inflammation. In vivo disease development is mainly related to the many conditions, but closely to its severity and possible of combination with other diseases. Thereby treatment of such diseases by using e.g. leaves extract of different herbs can be prescribe to ameliorate the level of reactive oxygen species and decrease the possible cell injure made by anti-inflammatory medicines.

Highlights

Ahmad T. and co-authors discovered the defects of mitochondria by the methods by which the quality of it is controlled - mitophagy, which has been shown to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD)
Authors have shown that cigarette smoke impairs mitophagy, leading to incomplete degradation of damaged mitochondria [1]. These damaged mitochondria may accumulate in the perinuclear region where generating excessive mitochondrial reactive oxygen species (ROS) (mtROS) leads to nuclear DNA damage and subsequent cellular senescence. This is corroborated by the finding that restoration of mitophagy by the overexpression of Parkin reduces cigarette smoke-induced DNA damage and cellular senescence when used in combination with an mtROS scavenger [1, 34]
The use of direct antioxidants, like N-acetyl cysteine (NAC), has some degree of beneficial effects but Shasha Tao and co-authors suggested that activating the body's own defensive responses through upregulation of the nuclear factor-erythroid-related factor 2 (NRF2) pathway in combination with low tidal ventilator strategies will result in greater benefits for the patients [30, 23]

Summary

Introduction

There are many questions concerning developing lung tissue diseases, it is progressing and relation of impact of oxidative stress on mortality rate and morphological changes These we can highlight the main causes of formation of reactive oxygen, peroxide radicals and others products of cell metabolism. The use of direct antioxidants, like N-acetyl cysteine (NAC), has some degree of beneficial effects but Shasha Tao and co-authors suggested that activating the body's own defensive responses through upregulation of the NRF2 pathway in combination with low tidal ventilator strategies will result in greater benefits for the patients [30, 23] Another histological study revealed that inflammatory cells infiltration and alveolar edema, permeability and inflammation induced by ventilation were significantly severe in VILI as compared to other groups treated by curcumin. Mairead Hayes and co-authors observed that human mesenchymal stem cells (hMSCs) improved lung compliance, reducing alveolar edema, and restoring lung architecture. hMSCs attenuated lung inflammation, decreasing alveolar cellular infiltration, and decreasing cytokine-induced neutrophil chemoattractant-1 and interleukin-6 while increasing keratinocyte growth factor concentrations, as result level of ROS and mtROS [10]

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Conclusion