At the end of 2019, a new coronavirus infection occurred in the People’s Republic of China with an epicentre in the city of Wuhan. On February 11th, 2020, the World Health Organization assigned the official name of the infection caused by the new coronavirus – COVID-19. COVID-19 has affected people from all over the world given that the infection was noted in 200 countries resulting in annunciation of the pandemic situation. Human corona viruses cause mild to moderate respiratory infections. At the end of 2002, a new coronavirus appeared (SARS-CoV), the causal agent of atypical pneumonia, which caused acute respiratory distress syndrome (ARDS). The initial stage of COVID-19 infection is the penetration of SARS-CoV-2 into target cells that have angiotensin converting enzyme type II receptors. The virus enters the body through the respiratory tract and interacts primarily with toll-like receptors (TLRs). The events in SARS-Cov-2 induced infection follow the next scenario: epithelial cells via TLRs recognize and identify SARS-Cov-2, and after that the information is transmitted to the transcriptional NF-κB, which causes expression of the corresponding genes. Activated in this way, the epithelial cells begin to synthesize various biologically active molecules. The results obtained on preclinical material indicate that ROS generation increases and the antioxidant protection decreases, which plays a major role in the pathogenesis of SARS-CoV, as well as in the progression and severity of this respiratory disease.

Type 2 diabetes (T2DM) is characterized by well-preserved insulin secretion; however, the surrounding tissue is insensitive to insulin, resulting in increased blood glucose level due to the inability of tissues to convert glucose into energy. As a result of chronic non-regulation of glucose levels and high daily fluctuations in the blood, the micro- and macrovascular complications occur in these patients. Complications develop through two main mechanisms: induction of oxidative stress and innate immunity. In this regard, the aim of this study was to examine the effect of four week administration of DPP4 inhibitors (saxagliptin, sitagliptin and vildagliptin) to the parameters of oxidative stress and antioxidant defense in the group of rats with diabetes type 2 (T2DM). Sixty Wistar albino rats were divided randomly into 5 groups: group I: control healthy group; group II: rats with diabetes type 2; group III: rats with diabetes type 2 treated with 0.6 mg/kg of sitagliptin; group IV: rats with diabetes type 2 treated with 0.45 mg/kg of saxagliptin, group V: rats with diabetes type 2 treated with 9 mg/kg vildagliptin. The rats from experimental groups were fed with a high-fat diet for 4 weeks and after 6–8 h of starvation received one dose of streptozotocin (STZ) intraperitoneally (25 mg/kg body weight) to induce T2DM. Animals with fasting glucose above 7 mmol / L and insulin over 6 mmol / L were included in the study as rats with T2DM. Upon completion of the experiments, the blood was collected from the anesthetized animals and used for sphectrophotometrical determination of parameters of oxidative stress, and antioxidative defense. T2DM induced significant increase in production of reacitve oxygen species (ROS) (superoxide anion radical and hydrogen peroxide), but additional four-week administration of gliptins induced decrease in ROS values. On the other hand, T2DM induced decrease of nitric oxide, superoxide dismutase, catalaze, and reduced gluthation and concomitant therapy with gliptins induced increase of these parametars, suggesting significant antioxidant potential of this group of drugs.