Posttraumatic stress disorder and metabolic syndrome: the role of some biofactors in treatment V.A. Serhiyenko, A.Y. Oliinyk, Y.I. Pavlovskiy, O.S. Kruk, A.A. Serhiyenko International Neurological Journal Ukraine, 2024 Post-traumatic stress disorder (PTSD) and metabolic syndrome (MetS) are often comorbidities and share neurobiological and clinical features. In particular, the results of meta-analyses indicate a higher prevalence of MetS in patients with PTSD compared to the general population. At the same time, PTSD is also a known risk factor for MetS. The involvement of common pathogenetic mechanisms characteristic of both conditions partially explains this coincidence. Insufficient intake and deficiency of certain biofactors, especially micronutrients (vitamins and essential minerals), are associated with an increased risk of MetS, type 2 diabetes mellitus, and cardiovascular diseases, and maintaining their physiological content in the body reduces this risk. Taking nutritional supplements with certain biofactors may help as an adjunct to conventional therapy to prevent and treat PTSD and, more often than not, MetS at the same time. This is because both conditions are linked to deficiencies in a number of biofactors. This review aims to discuss the role of several biofactors, including α-lipoic acid, vitamin B1/benfotiamine, L-carnitine and acetyl-L-carnitine, ω-3 polyunsaturated fatty acids, quercetin, magnesium, vitamins D and E, polyphenols, in the prevention and treatment of PTSD and MetS comorbidity, as well as to analyze new trends and future research directions. We conducted the search in databases such as Scopus, Science Direct (from Elsevier), PubMed, and MEDLINE. The keywords used were “post-traumatic stress disorder”, “metabolic syndrome”, and “biofactors”. We manually searched the bibliography of publications to identify research results that were not found during the online search.
Glycemic variability and diabetic cardiac autonomic neuropathy A.A. Serhiyenko, T.V. Tsaryk, Y.I. Pavlovskiy, V.A. Serhiyenko Miznarodnij Endokrinologicnij Zurnal, 2024 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.
Post-traumatic stress disorder and metabolic syndrome: the role of some antioxidants in treatment V.O. Serhiyenko, A.Yu. Oliinyk, Ya.I. Pavlovskiy, O.S. Kruk, O.O. Serhiyenko Miznarodnij Endokrinologicnij Zurnal, 2024 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.
Hydrogen Sulfide Prevents Mesenteric Adipose Tissue Damage, Endothelial Dysfunction, and Redox Imbalance From High Fructose Diet-Induced Injury in Aged Rats Oleh Revenko, Yaroslav Pavlovskiy, Maryana Savytska, Antonina Yashchenko, Vasyl Kovalyshyn, et al. Frontiers in Pharmacology, 2021 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.
H2S Donors Reverse Age-Related Gastric Malfunction Impaired Due to Fructose-Induced Injury via CBS, CSE, and TST Expression Yaroslav Pavlovskiy, Antonina Yashchenko, Oksana Zayachkivska Frontiers in Pharmacology, 2020 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.
Effect of hydrogen sulfide-releasing aspirin on esophageal and gastric mucosa compromised by stress injury O. S. Zayachkivska, N. S. Bula, Ya. I. Pavlovskiy, I. O. Pshyk-Titko, E. M. Gavriluk, et al. Ukrainian Biochemical Journal, 2017 Recent data of study H2S in gastrointestinal tract has proven its potent cytoprotection on mucosal defense among acid-related diseases in the gut. The aim was to evaluate the effects of H2S-releasing aspirin derivative (ATB-340) on esophageal and gastric mucosa compromised by stress injury. Rats were treated with vehicle (control), aspirin (10 mg/kg), ATB-340 (17.5 mg/kg) single or 9 days duration, with or without induction of stress injury. Esophageal mucosa, gastric mucosa were estimated by histopathological damage scoring. Serological levels of VCAM-1, IL-6 by ELISA. ATB-340 treatment resulted in protective effect and lower grade of damage score in esophageal mucosa and gastric mucosa lesions vs effect of aspirin in single or 9 days applications. The serum levels of VCAM, IL-6 in rats who were aspirin-treated and subjected to stressinjury were higher than those in control animals. Treatment with ATB-340 produced an anti-inflammatory effect by decreasing VCAM and IL-6 vs aspirin. Cytoprotective effect of ATB-340 on esophageal mucosa and gastric mucosa was modulated by inhibi ting inflammation and improving endothelial functions.
RECENT SCHOLAR PUBLICATIONS
New insight into the role of TST-derived hydrogen sulfide, a key regulator of mesenteric homeostasis in health and during chronic fructose intake O Revenko, Y Pavlovskiy, I Kovalchuk, M Savytska, O Zayachkivska Sulfurtransferases, 165-175 , 2023 2023 Citations: 1
Yashchenko A and Zayachkivska O (2020) H2S Donors Reverse Age-Related Gastric Malfunction Impaired Due to Fructose-Induced Injury via CBS, CSE, and TST Expression Y Pavlovskiy Oxidative Stress, Antioxidants, Transcription Factors, and Assimilation of … , 2021 2021
Hydrogen sulfide prevents mesenteric adipose tissue damage, endothelial dysfunction, and redox imbalance from high fructose diet-induced injury in aged rats O Revenko, Y Pavlovskiy, M Savytska, A Yashchenko, V Kovalyshyn, ... Frontiers in pharmacology 12, 693100 , 2021 2021 Citations: 15
H 2 S Donors Reverse Age-Related Gastric Malfunction Impaired Due to Fructose-Induced Injury via CBS, CSE, and TST Expression Y Pavlovskiy, A Yashchenko, O Zayachkivska Frontiers in Pharmacology 11, 1134 , 2020 2020 Citations: 20
Physiological basis for novel drug hydrogen sulfide‐related therapy used to treat oxidative stress in the model of fructose‐induced injury O Zayachkivska, Y Pavlovskiy, O Revenko, A Yashchenko The FASEB Journal 33 (S1), lb67-lb67 , 2019 2019 Citations: 1
ATB 340, a modulator of Sulfite Oxidase activity, reduces oxidative stress in hyperglycemia and stress exposed gastric mucosa in old rats Y Pavlovskiy, M Lutsyk, A Yashchenko, N Zaichko, J Wallace, ... Proceeding of the Shevchenko Scientific Society. Medical Sciences 54 (2), 33-41 , 2018 2018 Citations: 10
Translational aspects of place of hydrogen sulfide-releasing non-steroidal anti-inflammatory drugs on the tomorrow’s landscape for stressassociated disorders N Bula, Y Pavlovsky, V Student, O Revenko, JL Wallace, O Zayachkivska Proceeding of the Shevchenko Scientific Society. Medical Sciences 49 (1), 21-21 , 2017 2017 Citations: 3
Effect of hydrogen sulfide-releasing aspirin on esophageal and gastric mucosa compromised by stress injury OS Zayachkivska, NS Bula, YI Pavlovskiy, IO Pshyk-Titko, EM Gavriluk, ... The Ukrainian Biochemical Journal 89 (Special issue), 93-101 , 2017 2017 Citations: 9
AGE PROPERTIES COMPARATIVE CHARACTERISTICS OF STOMACH MUCOSA ENDOTHELIAL FUNCTIONS WITH THE HELP OF VCAM AND IL-1Β EXPRESSION Y Pavlovskyj, O Gavryliuk, O Grushka, O Zayachkivska Proceeding of the Shevchenko Scientific Society. Medical Sciences 47 (2 … , 2016 2016
H 2 S‐RELEASING ASPIRIN EXERTS PROTECTIVE EFFECT IN ESOPHAGEAL AND GASTRIC MUCOSAL STRESS‐ASSOCIATED INJURY O Zayachkivska, N Bula, Y Pavlovsky, E Gavriluk, J Wallace The FASEB Journal 30, 1271.1-1271.1 , 2016 2016 Citations: 3
Infl uence of Hydrogen Sulfi de-releasing aspirin on mucosal integrity of esophageal and gastric mucosa J Wallace, I Pshyk-Titko, MN Muscara, N Bula, Y Pavlovsky, E Gavriluk, ... Праці наукового товариства ім. Шевченка. Медичні науки. Лікарський збірник … , 2015 2015 Citations: 10
MOST CITED SCHOLAR PUBLICATIONS
H 2 S Donors Reverse Age-Related Gastric Malfunction Impaired Due to Fructose-Induced Injury via CBS, CSE, and TST Expression Y Pavlovskiy, A Yashchenko, O Zayachkivska Frontiers in Pharmacology 11, 1134 , 2020 2020 Citations: 20
Hydrogen sulfide prevents mesenteric adipose tissue damage, endothelial dysfunction, and redox imbalance from high fructose diet-induced injury in aged rats O Revenko, Y Pavlovskiy, M Savytska, A Yashchenko, V Kovalyshyn, ... Frontiers in pharmacology 12, 693100 , 2021 2021 Citations: 15
ATB 340, a modulator of Sulfite Oxidase activity, reduces oxidative stress in hyperglycemia and stress exposed gastric mucosa in old rats Y Pavlovskiy, M Lutsyk, A Yashchenko, N Zaichko, J Wallace, ... Proceeding of the Shevchenko Scientific Society. Medical Sciences 54 (2), 33-41 , 2018 2018 Citations: 10
Infl uence of Hydrogen Sulfi de-releasing aspirin on mucosal integrity of esophageal and gastric mucosa J Wallace, I Pshyk-Titko, MN Muscara, N Bula, Y Pavlovsky, E Gavriluk, ... Праці наукового товариства ім. Шевченка. Медичні науки. Лікарський збірник … , 2015 2015 Citations: 10
Effect of hydrogen sulfide-releasing aspirin on esophageal and gastric mucosa compromised by stress injury OS Zayachkivska, NS Bula, YI Pavlovskiy, IO Pshyk-Titko, EM Gavriluk, ... The Ukrainian Biochemical Journal 89 (Special issue), 93-101 , 2017 2017 Citations: 9
Translational aspects of place of hydrogen sulfide-releasing non-steroidal anti-inflammatory drugs on the tomorrow’s landscape for stressassociated disorders N Bula, Y Pavlovsky, V Student, O Revenko, JL Wallace, O Zayachkivska Proceeding of the Shevchenko Scientific Society. Medical Sciences 49 (1), 21-21 , 2017 2017 Citations: 3
H 2 S‐RELEASING ASPIRIN EXERTS PROTECTIVE EFFECT IN ESOPHAGEAL AND GASTRIC MUCOSAL STRESS‐ASSOCIATED INJURY O Zayachkivska, N Bula, Y Pavlovsky, E Gavriluk, J Wallace The FASEB Journal 30, 1271.1-1271.1 , 2016 2016 Citations: 3
New insight into the role of TST-derived hydrogen sulfide, a key regulator of mesenteric homeostasis in health and during chronic fructose intake O Revenko, Y Pavlovskiy, I Kovalchuk, M Savytska, O Zayachkivska Sulfurtransferases, 165-175 , 2023 2023 Citations: 1
Physiological basis for novel drug hydrogen sulfide‐related therapy used to treat oxidative stress in the model of fructose‐induced injury O Zayachkivska, Y Pavlovskiy, O Revenko, A Yashchenko The FASEB Journal 33 (S1), lb67-lb67 , 2019 2019 Citations: 1
Yashchenko A and Zayachkivska O (2020) H2S Donors Reverse Age-Related Gastric Malfunction Impaired Due to Fructose-Induced Injury via CBS, CSE, and TST Expression Y Pavlovskiy Oxidative Stress, Antioxidants, Transcription Factors, and Assimilation of … , 2021 2021
AGE PROPERTIES COMPARATIVE CHARACTERISTICS OF STOMACH MUCOSA ENDOTHELIAL FUNCTIONS WITH THE HELP OF VCAM AND IL-1Β EXPRESSION Y Pavlovskyj, O Gavryliuk, O Grushka, O Zayachkivska Proceeding of the Shevchenko Scientific Society. Medical Sciences 47 (2 … , 2016 2016
