Background: Hypertension remains highly prevalent in postmenopausal women, along with vascular dysfunction and increased oxidative stress. In such context, regular exercises, yoga practice, and slow breathing have been recommended to treat hypertension. However, the effects of the multiple components of yoga, including the respiratory techniques involved in the practice, on hypertension and on vascular and endothelial function have never been evaluated. Objective: This study aimed to investigate the additional effects of respiratory technique on vascular function and oxidative stress profile in hypertensive postmenopausal women (HPMWs) following yoga or stretching video classes. Study Design: Hypertensive postmenopausal women were recruited and randomized for 12 weeks, twice a week, of supervised yoga or stretching video classes of 75 min for 12 weeks associated or not with respiratory technique. Baseline and post-intervention measurements included pulse wave velocity (PWV), flow-mediated dilation (FMD), and oxidative stress parameters. Hypertensive postmenopausal women (59 ± 0.7 years) who ended the protocol were distributed into three groups: (1) control group (yoga or stretching, C, n = 14); (2) yoga + respiratory technique (Y+, n = 10); (3) stretching + respiratory technique (S+, n = 9). Results: Diastolic blood pressure and FMD [baseline: C: 6.94 ± 1.97%, Y+: 7.05 ± 1.65%, and S+: 3.54 ± 2.01% vs. post: C: 16.59 ± 3.46% ( p = 0.006), Y+: 13.72 ± 2.81% ( p = 0.005), and S+: 11.79 ± 0.99% ( p = 0.0001)] have significantly increased in all groups when baseline and post-practice values were compared. However, resting heart rate and PWV [baseline: Y+: 10.44 ± 3.69 and S+: 9.50 ± 0.53 m/s vs. post: Y+: 9.45 ± 0.39 ( p = 0.003) and S+: 8.02 ± 0.47 m/s ( p = 0.003)] decreased significantly only in the Y+ and S+ groups (baseline vs. post). Systemic antioxidant enzyme activities (superoxide dismutase and catalase) increased in all groups, and hydrogen peroxide and lipoperoxidation reduced in Y+ and S+ (baseline vs. post). Conclusions: Twelve weeks of yoga or stretching video classes promoted positive changes in several outcomes generally regarded as cardiovascular risk factors in HPMWs, and these changes were even more pronounced by the association with respiratory technique.
Background: Cardiac rehabilitation with aerobic exercises is the first strategy for nonpharmacological treatment in the postoperative period of individuals undergoing coronary artery bypass grafting (CABG) to improve functional capacity and vascular health. However, other exercise modalities remain uncertain regarding the same benefits. Objectives: Evaluation of the effect of different modalities of exercise, such as early cardiac rehabilitation on subjects submitted to CABG in the six-minute walk test (6-MWT) and on the percentage of flow-mediated dilatation (FMD) of the brachial artery. Methods: A randomized clinical trial in which 15 patients (62.7 ± 6.7 years) who underwent CABG were randomly assigned to the following groups: isometric (IG, Handgrip Jamar®), ventilatory muscle training (VG, PowerBreathe®) and control (CG, conventional respiratory and motor physiotherapy). All patients were attended to physically twice a day (20 min/session) for a consecutive week after the CABG (hospital admission). Functional capacity was assessed by 6-MWT and endothelial function was assessed through the technique of FMD, before and after (~7 days) admission to CABG. The doppler ultrasound videos were analyzed by Cardiovascular Suite® software (Quipu, Pisa, Italy) to measure %FMD. Statistics: Generalized estimation equation, followed by Bonferroni post hoc (p < 0.05). Results: Systolic, diastolic and mean arterial pressure (SBP/DBP/MAP, respectively) were 133, 76 and 95 mmHg. The groups presented walking meters (m) distance before and after intervention of: IGbasal 357.80 ± 47.15 m vs. IGpost 306.20 ± 61.63 m, p = 0.401 (+51 m); VGbasal 261.50 ± 19.91 m vs. VGpost 300.75 ± 26.29 m, p = 0.052 (+39 m); CG basal 487.83 ± 83.23 m vs. CGpost 318.00 ± 31.08, p = 0.006 (−169 m). %FMD before and after intervention was IGbasal 10.4 ± 4.8% vs. IGpost 2.8 ± 2.5%, p = 0.152; VGbasal 9.8 ± 5.1% vs. VGpost 11.0 ± 6.1%, p = 0.825; CGbasal 9.2 ± 15.8% vs. CGpost 2.7 ± 2.6%, p = 0.710 and resting mean basal blood flow was IGbasal 162.0 ± 55.0 mL/min vs. IGpost 129.9 ± 63.7 mL/min, p = 0.662; VGbasal 83.74 ± 12.4 mL/min vs. VGpost 58.7 ± 17.1 mL/min, p = 0.041; CGbasal 375.6 ± 183.7 mL/min vs. CGpost 192.8 ± 115.0 mL/min, p = 0.459. Conclusions: Ventilatory muscle training for early cardiac rehabilitation improved acute functional capacity and modulated mean flow of individuals undergoing CABG.
<p>Liver fibrosis is a complex disease that is caused by inappropriate tissue repair due to the deposition of connective tissue. When a chronic lesion affects the liver, regenerative response fails and hepatocytes are replaced with abundant extracellular matrix (ECM). The imbalance between production and degradation of ECM will result in the accumulation of proteins that change normal liver architecture, and thus its functionality. The main source of ECM is the activated hepatic stellate cell (HSC). In order, to clarify possible therapeutic approaches to the disease, this work aimed to evaluate the possible antifibrotic action of <em>Pluchea sagitallis </em>(Lam.) Cabrera on an activated HSC immortalized lineage (GRX).</p><p>Our results demonstrated that the <em>P. sagittalis</em> aqueous extract at 0.039 and 0.078 mg/mL concentrations was able to reduce cell growth and proliferation. Regarding to oxidative stress evaluation, there was no statistically significant difference between the treated group and the control. Staining with OilRed-O (ORO) showed a statistically significant increase in intracellular lipid content after 5 days of treatment, exerting <em>in vitro</em> effect on the GRX phenotypic change of activated towards the quiescent state. These results were confirmed by colorimetric quantification of lipid content. Regarding the TGF-β1 and collagen production, there were no statistically significant differences observed between the groups.</p><p>In conclusion, the <em>P. sagittalis</em> aqueous extract reduces the growth and proliferation of GRX cells and induces the reversal of activated towards a quiescent phenotype. There was no decrease in cell proliferation either by necrosis or by apoptosis via activation of the senescence. Thus, our data suggest that the extract showed an antifibrotic effect, possibly by activating phenotype reversal.</p>
Background Doxorubicin (DOX) antineoplastic is considered the prototype of cardiotoxicity for inducing direct damage to the myocardium. Pharmacological blockage of Angiotensin (Ang) II action is one of the main strategies to manage DOX‐induced cardiomyopathy. The effects are also mediated by the activation of the Mas receptor (MasR)/Ang‐(1‐7) axis, which is the counter‐regulatory axis of Ang II. The modulation of MasR/Ang‐(1‐7) axis is Ang‐(1‐7) (agonist) and A779 (antagonist) and may be a potential strategy in the context of cardiotoxicity. Objective Evaluate the influence of pharmacological modulation of MasR/Ang‐(1‐7) axis on DOX‐induced cardiotoxicity in cardiomyoblast cells. Methods Murine cardiomyoblasts (H9c2) were treated with A779 (10μM) for 30′ followed by Ang‐(1‐7) (100nM) for 30′ previous to expose with 0.1μM and 0.35μM (IC50) of DOX for 24h. Cell viability (Neutral Red and Trypan Blue), cell death profile (Annexin/7AAD), DNA damage induction (Comet Assay) and mitochondrial membrane integrity (Rhodamine 123) were evaluated after treatment protocol. The experiments were performed in triplicate, and data were analyzed by ANOVA followed by Dunnet, considering p <0.05. Results MasR modulation did not prevent the reduction of viability of cardiomyoblasts by DOX, neither altered the pattern of cell death. Both concentrations of DOX induced DNA strand breaks (C: 27.5 ± 13.4; DOX 0.1μM: 53.5 ± 9.1; DOX IC50: 109.5 ± 17.6 U.A.). Pretreatment with peptides suggested a reduction of the frequency of nucleus damage (DOX 0.1μM + Ang‐(1‐7): 36.5 ± 6.3; DOX 0.1μM +A779: 36.5 ± 0.7 U.A.) only at 0.1 μM DOX concentration, while pretreatment with A779 or Ang‐(1‐7) preserved the mitochondrial membrane integrity. Conclusion Modulation by agonism or antagonism of MasR in H9c2 cells reduces the DNA damage and the mitochondrial integrity. These results seem to be independent of MasR modulation, pointing to the involvement of other receptors and their crosstalk. Support or Funding Information CAPES, CNPq and FAPICC/ICFUC
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