Effect of short-term mindfulness-based stress reduction on sleep quality in male patients with alcohol use disorder

BackgroundSleep disturbance is one of the most prominent complaints of patients with alcohol use disorder (AUD), with more than 70% of patients with AUD reporting an inability to resolve sleep problems during abstinence. Mindfulness-based stress reduction (MBSR) has been shown to improve sleep quality and as an alternative therapy to hypnotics for sleep disorders.ObjectiveThe aim of the present study was to evaluate the effect of short-term MBSR on sleep quality in male patients with AUD after withdrawal.MethodsA total of 91 male patients with AUD after 2 weeks of routine withdrawal therapy were randomly divided into two groups using a coin toss: the treatment group (n = 50) and the control group (n = 41). The control group was received supportive therapy, and the intervention group added with MBSR for 2 weeks on the basis of supportive therapy. Objective sleep quality was measured at baseline and 2 weeks after treatment using the cardiopulmonary coupling (CPC). Indicators related to sleep quality include total sleep time, stable sleep time, unstable sleep time, rapid eye movement (REM) sleep time, wake-up time, stable sleep latency, sleep efficiency, and apnea index. These indicators were compared by an analysis of covariance (ANCOVA) between the two groups, controlling for individual differences in the respective measures at baseline.ResultsThe results showed that there were no significant differences in the age [t (89) = –0.541, P = 0.590), BMI [t (89) = –0.925, P = 0.357], educational status [t (89) = 1.802, P = 0.076], years of drinking [t (89) = –0.472, P = 0.638), daily intake [t (89) = 0.892, P = 0.376], types of alcohol [χ2 (1) = 0.071, P = 0.789], scores of CIWA-AR [t (89) = 0.595, P = 0.554], scores of SDS [t (89) = –1.151, P = 0.253), or scores of SAS [t (89) = –1.209, P = 0.230] between the two groups. Moreover, compared with the control group, the total sleep time [F (1.88) = 4.788, P = 0.031) and stable sleep time [F (1.88) = 6.975, P = 0.010] were significantly increased in the treatment group. Furthermore, the average apnea index in the patients who received MBSR was significantly decreased than in the control group [F (1.88) = 5.284, P = 0.024].ConclusionThese results suggest that short-term MBSR could improve sleep quality and may serve as an alternative treatment to hypnotics for sleep disturbance in patients with AUD after withdrawal

Network Pharmacology-Based Study on the Molecular Biological Mechanism of Action for Qingdu Decoction against Chronic Liver Injury

Background. Qingdu Decoction (QDD) is a traditional Chinese medicine formula for treating chronic liver injury (CLI). Materials and methods. A network pharmacology combining experimental validation was used to investigate potential mechanisms of QDD against CLI. We firstly screened the bioactive compounds with pharmacology analysis platform of the Chinese medicine system (TCMSP) and gathered the targets of QDD and CLI. Then, we constructed a compound-target network and a protein-protein interaction (PPI) network and enriched core targets in Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways. At last, we used a CLI rat model to confirm the effect and mechanism of QDD against CLI. Enzyme-linked immunosorbent assay (ELISA), western blot (WB), and real-time quantitative polymerase chain reaction (RT-qPCR) were used. Results. 48 bioactive compounds of QDD passed the virtual screening criteria, and 53 overlapping targets were identified as core targets of QDD against CLI. A compound-CLI related target network containing 94 nodes and 263 edges was constructed. KEGG enrichment of core targets contained some pathways related to CLI, such as hepatitis B, tumor necrosis factor (TNF) signaling pathway, apoptosis, hepatitis C, interleukin-17 (IL-17) signaling pathway, and hypoxia-inducible factor (HIF)-1 signaling pathway. Three PPI clusters were identified and enriched in hepatitis B and tumor necrosis factor (TNF) signaling pathway, apoptosis and hepatitis B pathway, and peroxisome pathway, respectively. Animal experiment indicated that QDD decreased serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), endotoxin (ET), and IL-17 and increased prothrombin time activity (PTA) level. WB and RT-qPCR analyses indicated that, compared with the model group, the expression of cysteinyl aspartate specific proteinase-9 (caspase-9) protein, caspase-3 protein, B-cell lymphoma-2 associated X protein (Bax) mRNA, and cytochrome c (Cyt c) mRNA was inhibited and the expression of B-cell lymphoma-2 (Bcl-2) mRNA was enhanced in the QDD group. Conclusions. QDD has protective effect against CLI, which may be related to the regulation of hepatocyte apoptosis. This study provides novel insights into exploring potential biological basis and mechanisms of clinically effective formula systematically

The association between hypertension and nonalcoholic fatty liver disease (NAFLD): literature evidence and systems biology analysis

Nonalcoholic fatty liver disease (NAFLD) has become a major public health issue as its progression increases risks of multisystem morbidity and mortality. Recent evidence indicates a more complex relationship between hypertension and NAFLD than previously thought. In this study, a comprehensive literature search was used to gather information supporting the comorbidity phenomenon of hypertension and NAFLD. Then, systems biology approach was applied to identify the potential genes and mechanisms simultaneously associated with hypertension and NAFLD. With the help of protein-protein interaction network-based algorithm, we found that the distance between hypertension and NAFLD was much less than random ones. Sixty-four shared genes of hypertension and NAFLD modules were identified as core genes. Kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment analysis indicated that some inflammatory, metabolic and endocrine signals were related to the potential biological functions of core genes. More importantly, drugs used to treat cardiovascular diseases, hypertension, hyperlipidemia, inflammatory diseases and depression could be potential therapeutics against hypertension-NAFLD co-occurrence. After analyzing public OMICs data, ALDH1A1 was identified as a potential therapeutic target, without being affected by reverse causality. These findings give a clue for the potential mechanisms of comorbidity of hypertension and NAFLD and highlight the multiple target-therapeutic strategy of NAFLD for future clinical research