We studied pathways of apoptosis regulation during experimental hepatopathy caused by treatment with antitubercular drugs and involvement of some hepatoprotectors and immunomodulators in the regulation of hepatocyte apoptosis induced by antitubercular drugs. The intensity of apoptosis and expression of apoptosis-associated molecules were evaluated. It was shown that antitubercular drugs induce apoptosis in hepatocytes by triggering external signaling pathway and p53-dependent signaling pathway and simultaneously reducing the level of anti-apoptotic Bcl-2 protein. Runihol, remaxol, and cycloferon reduced degenerative effects in the liver, though the level of apoptosis remained high. Ademetionine in tablets and reamberin improved the microstructure of the liver by inhibiting both apoptotic pathways induced by the antitubercular drugs; in other words, they have distinct hepatoprotective and apoptosis-protective effects, which is especially important at the late stages of ontogeny.
Cough is one of the most frequent symptoms of the new coronavirus infection (COVID-19). It reduces the quality of life and contributes to the development of life-threatening conditions.Aim. This article analyzes modern approaches to the pharmacotherapy of cough in patients with the new coronavirus infection from the standpoint of pathogenetic justification of the use of drugs. The main mechanisms of cough development in COVID-19 presented in the literature are considered. The cough is associated with virus-induced damage to the epithelium and subsequent release of biologically active substances that irritate the afferent endings of the vagus nerve. Approaches to cough management in COVID-19 with the possible use of antitussive (central and peripheral action) and mucoactive drugs (expectorants, mucokinetics, mucolytics, mucoregulators) are addressed.Conclusion. Based on the literature data and pathogenesis, antitussive drugs play a crucial role in the treatment of cough in COVID-19.
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