ABSTRACT
Objective To learn the effects on improving mental anxiety and depression in empty-nest elderly with hip replacement by accompany care work, and the factors influencing psychological anxiety and depression after hip replacement in empty-nest eldly. Then to explore comprehensive nursing strategies for hip arthroplasty in empty-nest eldly. Methods We investigated empty-nest elderly with hip arthroplasty by using homemade questionnaire, SAS and SDS scale between november 2015 and october 2017. Different nursing methods were used to treat empty-nesters in different groups, and the influencing factors of anxiety and depression were analyzed.Results It is not statistically significant in demographic characteristics (χ2＜3.84, P＞0.05) and anxiety (t = 1.2037, P=0.2308) and depression (t =1.0094, P=0.3142) at the time of entering the hospital, etc. Patients anxiety is statistically significant at time of discharge (t =-5.0159, P≤0.001) and one month after discharge (t =-9.5160, P ＜ 0.001), Patients depression is statistically significant at time of discharge (t =-2.9271, P = 0.0039) and one month after discharge (t =-8.2383, P＜0.001).The factors causing anxiety is nursing mode, number of chronic diseases and postoperative complications. The factors causing depression are economic income, nursing mode, and number of chronic diseases.Conclusion Accompany care work can improve the problems of anxiety and depression in an empty-nest eldly man after hip replacement. It is related to anxiety in nursing patterns, chronic diseases, postoperative complications.Meanhiwle while depression is related to economic income, nursing patterns, and types of chronic diseases, etc.
ABSTRACT
Acetaminophen (APAP) overdose is the most frequent cause of acute liver failure and is primarily caused by cytochrome P450 (CYP) 2E1-driven conversion of APAP into hepatotoxic metabolites. Several reports showed that melatonin attenuated APAP-induced acute liver failure. Nevertheless, the exact mechanism remains obscure. In the present study, we investigated the effects of melatonin on apoptosis-inducing factor (AIF)-dependent cell death in APAP-induced acute liver failure. Mice were intraperitoneally (i.p.) injected with different doses of melatonin (1.25, 5, 20 mg/kg) 30 min before APAP (300 mg/kg, i.p.). As expected, melatonin significantly alleviated APAP-induced cell death, as determined by TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay. Further analysis showed that melatonin significantly attenuated APAP-induced activation of the serine/threonine kinase receptor interacting protein 1 (RIP1). In addition, melatonin inhibited APAP-induced hepatic c-Jun N-terminal kinase (JNK) phosphorylation and mitochondrial Bax translocation. Correspondingly, melatonin inhibited APAP-induced translocation of AIF from mitochondria to nuclei. Interestingly, no changes were induced by melatonin on hepatic CYP2E1 expression. In addition, melatonin had little effect on APAP-induced hepatic glutathione (GSH) depletion. In conclusion, melatonin protects against AIF-dependent cell death during APAP-induced acute liver failure through its direct inhibition of hepatic RIP1 and subsequent JNK phosphorylation and mitochondrial Bax translocation.
Subject(s)
Antioxidants/pharmacology , Apoptosis Inducing Factor/metabolism , Liver Failure, Acute/metabolism , Liver Failure, Acute/prevention & control , Melatonin/pharmacology , Acetaminophen/adverse effects , Animals , Antioxidants/administration & dosage , Cell Death/drug effects , Cytochrome P-450 CYP2E1/metabolism , Cytochromes c/metabolism , Enzyme Activation/drug effects , GTPase-Activating Proteins/metabolism , Glutathione/metabolism , Hepatocytes/drug effects , Hepatocytes/metabolism , JNK Mitogen-Activated Protein Kinases/metabolism , Liver Failure, Acute/chemically induced , Liver Failure, Acute/pathology , Male , Melatonin/administration & dosage , Mice , Phosphorylation/drug effects , Protein TransportABSTRACT
Increasing evidence demonstrates that melatonin has an anti-inflammatory effect. Nevertheless, the molecular mechanisms remain obscure. In this study, we investigated the effect of melatonin on toll-like receptor 4 (TLR4)-mediated molecule myeloid differentiation factor 88 (MyD88)-dependent and TRIF-dependent signaling pathways in lipopolysaccharide (LPS)-stimulated macrophages. RAW264.7 cells were incubated with LPS (2.0 µg/mL) in the absence or presence of melatonin (10, 100, 1000 µm). As expected, melatonin inhibited TLR4-mediated tumor necrosis factor alpha (TNF-α), interleukin (IL)-1ß, IL-6, IL-8, and IL-10 in LPS-stimulated macrophages. In addition, melatonin significantly attenuated LPS-induced upregulation of cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) in macrophages. Further analysis showed that melatonin inhibited the expression of MyD88 in LPS-stimulated macrophages. Although it had no effect on TLR4-mediated phosphorylation of c-Jun N-terminal kinase (JNK), p38, and extracellular regulated protein kinase (ERK), melatonin significantly attenuated the activation of nuclear factor kappa B (NF-κB) in LPS-stimulated macrophages. In addition, melatonin inhibited TLR4-mediated Akt phosphorylation in LPS-stimulated macrophages. Moreover, melatonin significantly attenuated the elevation of interferon (IFN)-regulated factor-3 (IRF3), which was involved in TLR4-mediated TRIF-dependent signaling pathway, in LPS-stimulated macrophages. Correspondingly, melatonin significantly alleviated LPS-induced IFN-ß in macrophages. In conclusion, melatonin modulates TLR4-mediated inflammatory genes through MyD88-dependent and TRIF-dependent signaling pathways.
