Objective: The new adipokine, which is asprosin, affects glucose release from the liver to the blood, and thus, influences exercise metabolism. This is the first study assessing whether single anaerobic exercise affects asprosin secretion in women and men.Methods: 10 men and 10 women (aged 21.64 ± 1.22 and 22.64 ± 1.49, respectively) performed a single 20-s bicycle sprint. Blood samples were collected before exercise and in the 3′, 15′, 30′, and 60′ of recovery, and 24 h after competition.Results: Only in women did asprosin (P = 0.001) (15′, 30′, 60′, and 24 h after exercise) and irisin (P < 0.001) (15′, 30′, and 60′) concentrations increase. Leptin, however, decreased (P = 0.001) at 3′, 15′, and 30′ in women. There was an increase in interleukin-6 (P < 0.001) at 3′, 15′, 30′, and 60′ of recovery in men, at 15′, 30′, 60′, and 24 h of recovery in women, along with a simultaneous decrease in interleukin-1β (P < 0.001) at 15′, 30′, and 60′ of recovery in men, and at 15′ and 30′ of recovery in women (r = -0.35, P < 0.001). There was a positive correlation between asprosin and adiponectin and a negative one between asprosin and leptin. The increase in irisin concentration at 30′ of recovery was positively correlated with the increase in asprosin concentration and percentage fat content, while being negatively correlated with total and lean body mass (LBM).Conclusion: The single anaerobic effort induced an increase in asprosin and irisin secretion while reducing leptin secretion in women. Adipocytokine concentration changes are inter-related. Regardless of sex, anaerobic efforts induce anti-inflammatory effects.

Objective: Physical exercise changes redox balance in the blood. The study aim is to determine gender-related differences in enzymatic antioxidant defense [superoxide dismutase, catalase (CAT), and glutathione peroxidase (GPx)] during the initial period following anaerobic exercise and 24 h after its completion.Methods: Young, non-training participants (10 women and 10 men) performed a single anaerobic exercise, which was a 20-s maximal cycling sprint test. Blood was collected before and after completing the anaerobic exercise, i.e., after 3, 15, 30, and 60 min and after 24 h. Lactate concentration, and the superoxide dismutase, CAT, and GPx activity were determined. The results were adapted to the changes in plasma volume.Results: Anaerobic exercise induced a significant increase in lactate concentration, similar among both sexes. Anaerobic exercise evokes identical changes in the activity of antioxidant enzymes in the blood plasma of women and men, which is dependent on anaerobic capacity. In the early phase of restitution, the activity of antioxidant enzymes decreases; 24 h after anaerobic exercise, GPx activity in the blood plasma of women and men is higher than before the exercise.Conclusion: There are no gender-related differences concerning changes in plasma antioxidant activity after anaerobic exercise. Depending on the antioxidant enzyme, changes of activity differ in time after the end of the anaerobic exercise.

PurposeThe aim of this study was to compare changes in total oxidative status (TOS), total antioxidative capacity (TAC) and the concentration of VitA, VitE, VitC, uric acid (UA), reduced (GSH) and oxidized glutathione (GSSG) in blood within 24 hours following anaerobic exercise (AnEx) among men and women.Methods10 women and 10 men performed a 20-second bicycle sprint (AnEx). Concentrations of oxidative stress indicators were measured before AnEx and 3, 15 and 30 minutes and 1 hour afterwards. UA, GSH and GSSH were also measured 24 hours after AnEx. Lactate and H+ concentrations were measured before and 3 minutes after AnEx.ResultsThe increase in lactate and H+ concentrations following AnEx was similar in both sexes. Changes in the concentrations of all oxidative stress indicators were significant and did not differ between men and women. In both sexes, TOS, TAC, TOS/TAC and VitA and VitE concentrations were the highest 3 minutes, VitC concentration was the highest 30 minutes, and UA concentration was the highest 1 hour after AnEx. GSH concentration was significantly lower than the initial concentration from 15 minutes to 24 hour after AnEx. GSSG concentration was significantly higher, while the GSH/GSSG ratio was significantly lower than the initial values 1 hour and 24 hour after AnEx.ConclusionsWith similar changes in lactate and H+ concentrations, AnEx induces the same changes in TAC, TOS, TOS/TAC and non-enzymatic antioxidants of low molecular weight in men and women. Oxidative stress lasted at least 24 hours after AnEx.

BET bromodomain proteins are important epigenetic regulators of gene expression that bind acetylated histone tails and regulate the formation of acetylation-dependent chromatin complexes. BET inhibitors suppress inflammatory responses in multiple cell types and animal models, and protect against bone loss in experimental periodontitis in mice. Here, we analyzed the role of BET proteins in inflammatory activation of gingival fibroblasts (GFs) and gingival epithelial cells (GECs). We show that the BET inhibitors I-BET151 and JQ1 significantly reduced expression and/or production of distinct, but overlapping, profiles of cytokine-inducible mediators of inflammation and bone resorption in GFs from healthy donors ( IL6, IL8, IL1B, CCL2, CCL5, COX2 , and MMP3 ) and the GEC line TIGK ( IL6, IL8, IL1B, CXCL10, MMP9 ) without affecting cell viability. Activation of mitogen-activated protein kinase and nuclear factor-κB pathways was unaffected by I-BET151, as was the histone acetylation status, and new protein synthesis was not required for the anti-inflammatory effects of BET inhibition. I-BET151 and JQ1 also suppressed expression of inflammatory cytokines, chemokines, and osteoclastogenic mediators in GFs and TIGKs infected with the key periodontal pathogen Porphyromonas gingivalis . Notably, P. gingivalis internalization and intracellular survival in GFs and TIGKs remained unaffected by BET inhibitors. Finally, inhibition of BET proteins significantly reduced P. gingivalis -induced inflammatory mediator expression in GECs and GFs from patients with periodontitis. Our results demonstrate that BET inhibitors may block the excessive inflammatory mediator production by resident cells of the gingival tissue and identify the BET family of epigenetic reader proteins as a potential therapeutic target in the treatment of periodontal disease.

Histone deacetylases (HDACs) are important regulators of gene expression that are aberrantly regulated in several inflammatory and infectious diseases. HDAC inhibitors (HDACi) suppress inflammatory activation of various cell types through epigenetic and non-epigenetic mechanisms, and ameliorate pathology in a mouse model of periodontitis. Activation of gingival fibroblasts (GFs) significantly contributes to the development of periodontitis and the anaerobic bacterium Porphyromonas gingivalis plays a key role in driving chronic inflammation. Here, we analyzed the role of HDACs in inflammatory responses of GFs. Pan-HDACi suberoylanilide hydroxamic acid (SAHA) and/or ITF2357 (givinostat) significantly reduced TNFα- and P. gingivalis–inducible expression and/or production of a cluster of inflammatory mediators in healthy donor GFs ( IL1B, CCL2, CCL5, CXCL10, COX2, and MMP3) without affecting cell viability. Selective inhibition of HDAC3/6, but not specific HDAC1, HDAC6, or HDAC8 inhibition, reproduced the suppressive effects of pan-HDACi on the inflammatory gene expression profile induced by TNFα and P. gingivalis, suggesting a critical role for HDAC3 in GF inflammatory activation. Consistently, silencing of HDAC3 expression with siRNA largely recapitulated the effects of HDAC3/6i on mRNA levels of inflammatory mediators in P. gingivalis–infected GFs. In contrast, P. gingivalis internalization and intracellular survival in GFs remained unaffected by HDACi. Activation of mitogen-activated protein kinases and NFκB signaling was unaffected by global or HDAC3/6-selective HDACi, and new protein synthesis was not required for gene suppression by HDACi. Finally, pan-HDACi and HDAC3/6i suppressed P. gingivalis–induced expression of IL1B, CCL2, CCL5, CXCL10, MMP1, and MMP3 in GFs from patients with periodontitis. Our results identify HDAC3 as an important regulator of inflammatory gene expression in GFs and suggest that therapeutic targeting of HDAC activity, in particular HDAC3, may be clinically beneficial in suppressing inflammation in periodontal disease.