The Effects of Foot Reflexology on Vital Signs: A Meta-Analysis of Randomized Controlled Trials.

Introduction: We evaluated the effects of foot reflexology on bodily vital signs. Methods: Randomized controlled trials (RCTs) evaluating the effects of foot reflexology on vital signs were collected for a meta-analysis. Statistical analysis was conducted using RevMan5.4 software and pooled estimates of the effects were reported as mean differences (MDs) with 95% confidence intervals (CIs). Results: Thirteen studies, including 819 patients, met our inclusion criteria. Our results showed that systolic blood pressure (SBP) (MD = -4.62, 95% CI: -5.58 to -3.66; P < 0.00001), diastolic blood pressure (DBP) (MD = -3.32, 95% CI: -4.48 to -2.17; P < 0.00001), heart rate (HR) (MD = -4.76, 95% CI: -6.49 to -3.04; P < 0.00001), respiratory rate (RR) (MD = -0.77, 95% CI: -1.50 to -0.48; P < 0.00001), and pulse oxygen saturation (SpO2) (MD = 0.95, 95% CI: 0.39 to 1.52; P = 0.0009) showed statistical significance in the foot reflexology group. Conclusions: Short-term followup results showed that foot reflexology exerted positive effects on vital signs, reduced BP, HR, and RR and increased SpO2.

MiR-106a aggravates sepsis-induced acute kidney injury by targeting THBS2 in mice model.

PURPOSE: To investigate the role and related mechanisms of miR-106a in sepsis-induced AKI. METHODS: Serum from sepsis and healthy patients was collected, sepsis mouse model was established by cecal ligation and puncture (CLP). TCMK-1 cells were treated with lipopolysaccharide (LPS) and transfected with THBS2-small interfering RNA (siTHBS2), miR-106a inhibitor, miR-106a mimics and their negative controls (NCs). The expression of miR-106a, thrombospondin 2 (THBS2), Bax, cleaved caspase-3 and Bcl-2, cell viability, relative caspase-3 activity and TNF-α, IL-1ß, IL-6 content were respectively detected by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, Cell Counting Kit-8 (CCK-8) and enzyme linked immunosorbent assay (ELISA). The relationship between miR-106a and THBS2 was confirmed by dual luciferase reporter assay. RESULTS: MiR-106a was up-regulated in serum of sepsis patients, CLP-induced mice models and LPS-induced TCMK-1 cells. LPS reduced cell viability and Bcl-2 expression, and increased caspase-3 activity, Bax expression, the content of TNF-α, IL-1ß, IL-6. THBS2 was a target of miR-106a. The decreases of caspase-3 activity, TNF-α, IL-1ß, IL-6, Bax expression and the increases of cell viability, Bcl-2 expression caused by miR-106a knockdown were reversed when THBS2 silencing in LPS-stimulated TCMK-1 cells. CONCLUSION: MiR-106a aggravated LPS-induced inflammation and apoptosis of TCMK-1 cells via regulating THBS2 expression.

Hydroxysafflor Yellow A mitigated myocardial ischemia/reperfusion injury by inhibiting the activation of the JAK2/STAT1 pathway.

Hydroxysafflor Yellow A (HSYA) may reduce ischemia/reperfusion (I/R) injury. However, the underlying molecular mechanisms remain unclear. The present study explored the effect and the mechanisms of HSYA on myocardial injury in vivo and in vitro. Myocardial infarct size was assessed by Evans blue/2,3,5­triphenyltetrazoliumchloride staining. Levels of cardiac troponin I (cTnI), interleukin­6 (IL­6), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured using commercial kits. Alteration of mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) generation was determined by fluorescent signals. Apoptosis was detected by terminal deoxynucleotidyl­transferase­mediated dUTP nick­end labeling staining, flow cytometry assay and caspase­3 activity. Expression levels of the apoptosis­associated proteins were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. In vivo, animals treated with HSYA presented less severe myocardial injury and decreased janus kinase 2 (JAK2)/signal transducer and activator of transcription 1 (STAT1) activity, improved antioxidant capacity and decreased apoptosis. In vitro, compared with the hypoxia (H)/reoxygenation (R) + HSYA group, AG490 and S1491 treatment decreased the releases of cTnI, IL­6 and LDH and enhanced the resistance to oxidative stress by maintaining MMP and decreasing ROS generation. In addition, AG490 and S1491 were also identified to alleviate the H/R­induced apoptosis by inhibiting caspase 3 activity and modulating the expression levels of cleaved caspase­3, tumor necrosis factor receptor superfamily member 6 (Fas), Fas ligand, B­cell lymphoma 2 (Bcl­2) and Bcl­2­associated X protein. These data suggested that inactivation of the JAK2/STAT1 pathway strengthened the HSYA­induced protective effect in H/R­induced myocardial injury. In conclusion, the treatment of HSYA was effective in decreasing IR­induced myocardial injury, and this may be largely dependent on the JAK2/STAT1 pathway. Therefore, the present study provided a potential strategy to prevent myocardial I/R injury.

MiR-106a aggravates sepsis-induced acute kidney injury by targeting THBS2 in mice model

Abstract Purpose To investigate the role and related mechanisms of miR-106a in sepsis-induced AKI. Methods Serum from sepsis and healthy patients was collected, sepsis mouse model was established by cecal ligation and puncture (CLP). TCMK-1 cells were treated with lipopolysaccharide (LPS) and transfected with THBS2-small interfering RNA (siTHBS2), miR-106a inhibitor, miR-106a mimics and their negative controls (NCs). The expression of miR-106a, thrombospondin 2 (THBS2), Bax, cleaved caspase-3 and Bcl-2, cell viability, relative caspase-3 activity and TNF-α, IL-1β, IL-6 content were respectively detected by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, Cell Counting Kit-8 (CCK-8) and enzyme linked immunosorbent assay (ELISA). The relationship between miR-106a and THBS2 was confirmed by dual luciferase reporter assay. Results MiR-106a was up-regulated in serum of sepsis patients, CLP-induced mice models and LPS-induced TCMK-1 cells. LPS reduced cell viability and Bcl-2 expression, and increased caspase-3 activity, Bax expression, the content of TNF-α, IL-1β, IL-6. THBS2 was a target of miR-106a. The decreases of caspase-3 activity, TNF-α, IL-1β, IL-6, Bax expression and the increases of cell viability, Bcl-2 expression caused by miR-106a knockdown were reversed when THBS2 silencing in LPS-stimulated TCMK-1 cells. Conclusion MiR-106a aggravated LPS-induced inflammation and apoptosis of TCMK-1 cells via regulating THBS2 expression.

Hydroxysafflor yellow A protects against angiotensin II­induced hypertrophy.

Myocardial infarction (MI) is life­threatening and is generally accompanied by myocardial hypertrophy. Notably, Hydroxysafflor yellow A (HSYA) can prevent tissue injuries. The objective of this study was to investigate the effect of HSYA on hypertrophy after MI. Hematoxylin and eosin (H&E) staining assays were performed to measure cell area. The protein synthesis rate was assessed using the 3H Leucine incorporation assay. Reverse transcription­quantitative polymerase chain reaction (RT­qPCR), western blot analysis and the immunohistochemical assay were used to detect the expression of target genes. The activity of superoxide dismutase (SOD), malondialdehyde (MDA) and the reactive oxygen species (ROS) generation were examined using commercial kits. Decreased myocardial hypertrophy was observed in animals treated with HSYA. Furthermore, the expression of nuclear factor (erythroid­derived 2)­like 2 (Nrf2) was higher in HSYA administration groups compared with that in the MI model group. In H9c2 cardiomyocytes, the pretreatment with HSYA increased the cell viability, however, it reduced protein synthesis rate, mitigated cell surface area and decreased the expression of Brain natriuretic factor (BNP) and ß­myosin heavy chain (ß­MHC). By contrast, the downregulation of Nrf2 deteriorated and reversed the effect of Ang II and HSYA. Furthermore, oxidative stress was alleviated by HSYA via inhibiting ROS generation, modulating the activities of SOD and MDA. In addition, the expression of NAD(P)H:quinone oxidoreductase 1 (NQO1) and heme oxygenase­1 (HO­1) were recovered by the pretreatment of HSYA that was combated by siNrf2. In conclusion, HSYA exerted anti­hypertrophic effects, which was pertinent with the activation of Nrf2/NQO­1/HO­1 signaling pathway. The findings of this study may inspire a novel strategy to combat MI.

Efficacy and safety of ticagrelor in patients with acute coronary syndrome: A meta-analysis of randomized controlled trials.

Acute coronary syndrome (ACS) is a dangerous and urgent clinical pattern of coronary artery disease. Aspirin and adenosine diphosphate P2Y12 receptor antagonists are the standard dual anti-platelet therapy for patients with ACS. Ticagrelor is a new oral antagonist of the adenosine diphosphate P2Y12 receptor. Randomized controlled trials (RCTs) have evaluated the efficacy and safety of ticagrelor compared to clopidogrel or prasugrel in patients with ACS, obtaining conflicting results. Thus, we conducted a meta-analysis of these RCTs to determine the efficacy and safety of ticagrelor in patients with ACS. Results of the meta-analysis indicate that ticagrelor decreased the risk of major adverse cardiovascular events (MACE) and all-cause death, but increased the risk of bleeding events. In Asiatic patients, analysis indicates that ticagrelor did not decrease the risk of MACE and all-cause death, while increasing the risk of bleeding events. Together, this meta-analysis suggests that ticagrelor was more effective, but less safe than clopidogrel and prasugrel in patients with ACS. Subgroup analysis indicates that ticagrelor was not more effective, although less safe than clopidogrel in Asiatic patients, thus more evidence is needed to further evaluate the efficacy and safety of ticagrelor in Asiatic patients.

Does Anterior Fat Pad Removal Reduce the Incidence of Atrial Fibrillation after CABG? A Meta-Analysis of Randomized Controlled Trials.

BACKGROUND: Atrial fibrillation (AF) is a common complication after coronary artery bypass grafting (CABG). Several prospective randomized controlled trials (RCTs) have evaluated the effect of intact and removed anterior fat pads on the incidence of AF after CABG with conflicting results. We collected these RCTs and conducted a meta-analysis to determine whether anterior fat pad removal is effective in preventing the new onset of AF after CABG. METHODS AND RESULTS: Prospective RCTs were collected for analysis and the main outcomes include the occurrence of AF after CABG, total hospital stay, and major complications. Statistical analysis was conducted using RevMan 5.0.18 software (The Cochrane Collaboration), and pooled estimates of the effect were reported as risk ratios (RRs) or mean differences (MDs) with their 95% confidence intervals (CIs). The results of this meta-analysis indicate that anterior fat pad removal was not associated with a decreased risk of occurrence of AF after CABG (RR = 1.34, 95% CI: 0.88-2.03; P = 0.18), and it also did not increase the risk of major complications (RR = 1.05, 95% CI: 0.75-1.47; P = 0.79) or lengthen total hospital stay (MD = 0.06, 95% CI: -0.46 to 0.58; P = 0.83) compared with the control group. CONCLUSION: Anterior fat pad removal did not decrease the risk of the occurrence of AF after CABG despite its safety and convenience, and it should not be used to prevent new-onset AF after CABG unless new evidence is provided.