ABSTRACT
BACKGROUND: and purpose: Preoperative anxiety is an important factor for postoperative complications, and many patients are using aromatherapy to relieve preoperative anxiety. This study aimed to evaluate the effect of aromatherapy on preoperative anxiety in adult patients. METHODS: An electronic search of six databases (Cochrane Library, PubMed, Embase, CINAHL, CNKI, and WanFang Data) was conducted for full-text publications of trials published from the inception of the databases to February 20, 2020. All randomized controlled trials (RCTs) where aromatherapy was used for treatment of preoperative anxiety were included. Interventions included all types of aromatherapy compared to standard care or placebo. The primary outcome was self-rated anxiety and the secondary outcome was adverse effect. Two researchers independently screened and extracted relevant data. A random-effects model was utilized to calculate the effect size as mean difference (MD). RESULTS: Our search retrieved 347 records. Thirteen trials were included for qualitative analysis, of which ten RCTs with 750 patients were included for meta-analysis. Most studies had a high or unclear selection and performance bias. Overall, aromatherapy was found to decrease preoperative anxiety significantly compared to the control group (MD = -3.95, 95%CI [-6.36, -1.53], P = 0.001). According to subgroup analysis, most subgroups showed a significant effect of aromatherapy on preoperative anxiety, except for the no treatment subgroup (MD: 5.40, 95%CI: 7.76 to 0.71) and female subgroup (MD: 3.96, 95%CI: 9.19 to 1.27). CONCLUSION: Aromatherapy may be an effective complementary treatment for preoperative anxiety. Nevertheless, due to methodological limitations of the included trials, further studies with strict control of the research design are required for firm recommendations.
Subject(s)
Aromatherapy , Adult , Anxiety/therapy , Anxiety Disorders , Female , Humans , Postoperative Complications , Randomized Controlled Trials as TopicABSTRACT
Nuclear factor-kappa B (NF-κB), which is reported to play an important role in the pathogenesis of depression, also has a central role in the genesis and progression of inflammation. Here, we have targeted the nuclear translocation of NF-κB using 4-methyl-N1-(3-phenyl-propyl)-benzene-1,2-diamine (JSH-23) to elucidate its role in depression. We investigated the antidepressant-like effects of JSH-23 in the chronic mild stress (CMS) mouse model, which is a valid, reasonably reliable, and useful model of depression. The antidepressant-like effects of JSH-23 were evaluated using the sucrose preference test (SPT) and the forced swimming test (FST). We also assessed inflammatory markers [interleukin (IL)-6 and tumor necrosis factor-α (TNF-α)] and components of antioxidant defense [superoxide dismutase (SOD) and nuclear factor erythroid-2-related factor 2 (Nrf 2)] in the hippocampus. Fluoxetine, a classical antidepressant, was used in this study as a positive control. Administration of JSH-23 significantly prevented the decreased sucrose preference in the SPT and prevented the increased immobility time in the FST caused by CMS, but had no effect on locomotor activity. Expression of NF-κB p65 protein in the hippocampus was decreased, and elevated levels of IL-6 and TNF-α were reduced, after JSH-23 administration. In addition to its anti-inflammatory effect, JSH-23 treatment increased the expression of SOD and Nrf 2 in the hippocampus, suggesting that it strengthens antioxidant defense. The current study demonstrated that inhibiting the NF-κB signaling cascade using JSH-23 prevented depressive-like behaviors by decreasing inflammation and improving antioxidant defense in the hippocampus. We concluded that NF-κB activation plays an important role in the pathophysiology of depression and that targeting NF-κB signaling may provide a novel and effective therapy for depression. Additional preclinical studies and clinical trials are, however, needed to further elucidate the effects of this therapeutic strategy.
