Pavlovskiy Yaroslav
@new.meduniv.lviv.ua
Danylo Halytsky Lviv National Medical University
RESEARCH, TEACHING, or OTHER INTERESTS
Surgery
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
V.O. Serhiyenko, A.Yu. Oliinyk, Ya.I. Pavlovskiy, O.S. Kruk, and O.O. Serhiyenko
Publishing House Zaslavsky
The basis for the pathogenesis of cardiovascular, cancer, metabolic diseases, low-grade chronic inflammation (LGCI) and many other disorders is an imbalance between prooxidants and the antioxidant defense system. It is believed that the link between post-traumatic stress disorder (PTSD) and metabolic syndrome (MetS) is based on oxidative stress (OS), increased autonomic nervous system activity, glucocorticoid synthesis activation, or immunological dysregulation. Moreover, pathophysiological changes in the systemic LGCI pathways that result from modifications in glucocorticoid receptor reactivity (secondary to emotional and physiological arousal) may be the basis for inappropriate social behavior consistent with PTSD and MetS manifestations. Recently, evidence has emerged suggesting that a combination of high levels of systemic OS and activation of LGCI plays an important role in the pathogenesis of PTSD. On the other hand, PTSD is a type of recurrent and long-term trauma that exacerbates OS and accelerates cellular aging. LGCI is accompanied by the release of reactive oxygen and nitrogen species, proinflammatory cytokines, and other biologically active substances that cause OS. The purpose of this review was to discuss the role of individual antioxidants, in particular polyphenols, flavonoids, carotenoids, N-acetylcysteine, melatonin, L-arginine, C and E vitamins, zinc, copper, and selenium, in the prevention/treatment of comorbid pathology of PTSD and MetS, as well as to analyze new trends and directions for future research. The search was conducted in Scopus, Science Direct (from Elsevier) and PubMed, including MEDLINE databases. The keywords used were “post-traumatic stress disorder,” “metabolic syndrome,” and “antioxidants.” To identify research results that could not be found during the online search, a manual search of the bibliography of publications was used.
A.A. Serhiyenko, T.V. Tsaryk, Y.I. Pavlovskiy, and V.A. Serhiyenko
Publishing House Zaslavsky
Cardiac autonomic neuropathy (CAN) is closely associated with an approximately five-fold increase in the risk of cardiovascular mortality in patients with diabetes mellitus (DM). Impaired autonomic function of the cardiovascular system in DM, which leads to the development of CAN, can be accompanied by coronary artery ischemia, heart rhythm disturbances, “silent” myocardial infarction, severe orthostatic hypotension, and sudden cardiac death syndrome. The article provides an analysis of literature data on the impact of glycemic variability (GV) on diabetic CAN development. This review analyzed the possible relationships between GV in people with diabetic CAN. In particular, the issues related to glycemic control and CAN, the link between GV and CAN in diabetes were analyzed. Unsatisfactory glycemic control and uncontrolled glycemic status are considered the main risk factors for chronic complications of DM, in particular CAN. An increase of GV is associated with a higher risk of chronic complications of DM, cardiovascular risk, all-cause mortality and morbidity. The clinical trial results demonstrated that time in range might be a promising metric for assessing glycemic control and prognosis of diabetic complications. This review is based on a search in PubMed and MEDLINE, Scopus, BIOSIS, EMBASE, Google Scholar and Springer Online Archives Collection. The following keywords were used: glycemic variability, cardiac autonomic neuropathy and diabetes mellitus. Research findings missed by the web search have been identified through a manual search of the bibliography of publications. CAN is one of the frequent long-term complications of DM, and reasonable control of GV may be necessary for its prevention. Determination of GV may have advantages for predicting future complications of DM in clinical trials and practice. The association of autonomic dysfunction and glucose levels, insulin resistance, and HbA1c variability suggest further research to reduce chronic complications development. Further investigation is needed to study the mechanisms of GV and evaluate them as therapeutic targets in the treatment of patients with T2DM.
Oleh Revenko, Yaroslav Pavlovskiy, Iryna Kovalchuk, Maryana Savytska, and Oksana Zayachkivska
Elsevier
Oleh Revenko, Yaroslav Pavlovskiy, Maryana Savytska, Antonina Yashchenko, Vasyl Kovalyshyn, Ilona Chelpanova, Olena Varyvoda, and Oksana Zayachkivska
Frontiers Media SA
A high fructose diet (HFD) and advanced age are key factors for the gradual loss of physiological integrity of adipose tissue. Endogenous hydrogen sulfide (H2S) has beneficial effects on cytoprotection and redox balance. But its interactive effects on age-related damage of mesenteric vessels and connective and adipose tissues (MA) during HFD which could be the base of the development of effective physiological-based therapeutic strategy are unknown. The aim of study was to investigate age- and HFD-induced mesenteric cellular changes and activities of enzymes in H2S synthesis and to test the effects of sodium hydrosulfide (NaHS) which is considered an H2S donor on them. Adult and aged male rats on a standard diet (SD) or 4-week HFD were exposed to acute water-immersion restraint stress (WIRS) for evaluation of mesenteric subcellular and cellular adaptive responses by electron microscopy. The effects of exogenous NaHS (5.6 mg/kg/day for 9 days) versus vehicle on mesentery changes were investigated. Serum glucose level, thiobarbituric acid reactive substances (TBARS), and activities of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS), thiosulfate-dithiol sulfurtransferase (TST), and sulfite oxidase (SO) were examined by spectrophotometry. In both adult and aged SD groups, treatment with NaHS protected mesenteric cells after WIRS. In both groups, the treatment with NaHS also protected MA mitochondria, microvascular endothelial and sub-endothelial structures, and fibroblasts versus the vehicle-treated group that had signs of damage. HFD increased MA injury and mitochondrial changes in both aged and adult rats. HFD-associated malfunction is characterized by low activities of CSE, CBS, TST, SO, and increased TBARS. Finally, we demonstrated that pretreatment with NaHS inhibited MA and mitochondria alterations in aged rats exposed to HFD and WIRS, lowered TBARS, and enhanced H2S enzyme activities in contrast to the vehicle-treated group. Mitochondrial integrity alterations, endothelial damage, and redox imbalance are key factors for rat mesenteric adipose tissue damage during advanced age. These alterations and MA hypertrophic changes retain the central for HFD-induced damage. Moreover, H2S signaling contributes to MA and mitochondria redox balance that is crucial for advanced age and HFD injury. The future study of H2S donors’ effects on mesenteric cells is fundamental to define novel therapeutic strategies against metabolic changes.
Yaroslav Pavlovskiy, Antonina Yashchenko, and Oksana Zayachkivska
Frontiers Media SA
Objective Excess of fructose consumption is related to life-treating conditions that affected more than a third of the global population. Therefore, to identify a newer therapeutic strategy for the impact prevention of high fructose injury in age-related malfunctions of the gastric mucosa (GM) in the animal model is important. Methods Adult and aged male rats were divided into control groups (standard diet, SD) and high fructose diet (HFD) groups; acute water immersion restraint stress (WIRS) was induced for evaluation of GM adaptive response and effects of testing the therapeutic potential of H2S-releasing compounds (H2S donors). Histological examination of gastric damage was done on hematoxylin-eosin stained slides. Cystathionine beta-synthase (CBS), Cystathionine gamma-lyase (CSE), and Thiosulfate-dithiol sulfurtransferase (TST) activities and oxidative index were assessed during exogenous administration of H2S donors: sodium hydrosulfide (NaHS) and the novel hybrid H2S-releasing aspirin (ATB-340). The results showed that HFD increased gastric damage in adult and aged rats. HFD-associated malfunction characterized by low activities of H2S key enzymes, inducing increased oxidation. Pretreatment with NaHS, ATB-340 of aged rats in the models of HFD, and WIRS attenuated gastric damage in contrast to vehicle-treated group (p < 0.05). The effect of ATB-340 was characterized by reverse oxidative index and increased CBS, CSE, and TST activities. In conclusion, H2S donors prevent GM age-related malfunctions by enhancement of CBS, CSE, and TST expression against fructose excess injury though reduction of oxidative damage.