The pathogenesis underlying alcoholic liver disease (ALD), which is often a result of alcohol abuse, currently remains unclear. Previous studies have reported that enteric dysbiosis serves an important role in the pathogenesis of ALD. The present study aimed to investigate the effects of glutamine and probiotics on a rat model of alcoholic liver disease (ALD). Sixty male Sprague-Dawley rats were randomly divided into 6 groups including control (C), alcohol (M), alcohol + Golden Bifido (T), alcohol + glutamine (G), alcohol + Medilac-S® (N) and alcohol + Golden Bifido + glutamine (L). Histology, body weight (BW), triglycerides (TG), serum aspartate transaminase (AST), alanine aminotransferase (ALT), tumor necrosis factor (TNF-α), interleukin-6 (IL-6), diamine oxidase (DAO), occludin, endotoxin and D-lactate levels were assessed whilst changes in the gut flora were evaluated and compared. Results determined that all probiotic and glutamine treatments elevated the abnormally decreased BW and occludin levels whilst the abnormal elevated serum AST, ALT, TG, IL-6, TNF-α, DAO, endotoxin and D-lactate levels were significantly reduced following chronic ethanol consumption. Histopathological observation of the liver demonstrated that probiotic and glutamine treatments attenuated liver damage induced by alcohol. Moreover, sequencing determined that there was a reduction in Firmicutes as well as an increase in Actinobacteria, Proteobacteria and Porphyromonadaceae abundance in the ALD group compared with the healthy controls. However, these changes were prevented by glutamine and probiotic therapy. In conclusion, the present results suggested that probiotics and glutamine ameliorated ALD by suppressing inflammation and regulating the gut microbiota. Therefore, probiotic and glutamine treatments can potentially serve as therapies for the prevention and treatment of ALD.

G protein-coupled receptors (GPCRs) are important signal transduction mediators and pharmacological therapeutic targets. G protein-coupled receptor 137 (GPR137) was initially reported as a novel orphan GPCR around 10 years ago. Some orphan GPCRs have been implicated in cancer cell proliferation and migration. The aim of this study is to investigate the role of GPR137 in hepatocellular carcinoma (HCC). GPR137 is widely expressed in several human HCC cell lines, as determined by real-time PCR. We then applied lentivirus mediated RNA interference (RNAi) to knock down GPR137 expression in two HCC cell lines HepG2 and Bel7404. Depletion of GPR137 remarkably inhibited cell proliferation and colony formation capacity. Knockdown of GPR137 in HepG2 cells led to cell cycle arrest at G0/G1 phase and G2/M phase, and induced cell apoptosis, as determined by flow cytometry analysis, which contributed to cell growth inhibition. Our findings suggested that GPR137 could facilitate HCC cell proliferation and thus promote hepatocarcinogenesis.

BackgroundSudden sensorineural hearing loss (SSNHL) can cause great panic in patients. Whether it is advantageous to add intravenous batroxobin in the treatment of SSNHL remains to be determined. This study aimed to compare the short-term efficacy of therapy combined with intravenous batroxobin and that without intravenous batroxobin in SSNHL patients.MethodsThis retrospective study harvested the data of SSNHL patients hospitalized in our department from January 2008 to April 2021. The hearing levels on the admitted day (before treatment) and the discharge day were considered pre-treatment hearing and post-treatment hearing, respectively. The hearing gain was the difference value of pre-treatment hearing and post-treatment hearing. We used Siegel's criteria and the Chinese Medical Association of Otolaryngology (CMAO) criteria to evaluate hearing recovery. The complete recovery rate, overall effective rate, and hearing gain at each frequency were considered outcomes. Propensity score matching (PSM) was conducted to balance the baseline characteristics between the batroxobin group and the non-batroxobin group. Sensitivity analysis was carried out in flat-type and total-deafness SSNHL patients.ResultsDuring the study period, 657 patients with SSNHL were admitted to our department. Among them, a total of 274 patients met the enrolled criteria of our study. After PSM, 162 patients (81 in each group) were included in the analysis. Once the hospitalized treatment was completed, the patients would be discharged the next day. Logistic regression analysis of the propensity score-matched cohort indicated that both the complete recovery rates [Siegel's criteria, OR: 0.734, 95% CI: 0.368–1.466, p = 0.381; CMAO criteria, OR: 0.879, 95% CI: 0.435–1.777, p = 0.720] and the overall effective rates [Siegel's criteria and CMAO criteria, OR: 0.741, 95% CI: 0.399–1.378, p = 0.344] were not significantly different between the two treatment groups. Sensitivity analysis has shown similar results. For flat-type and total-deafness SSNHL patients, no significant difference was found in post-treatment hearing gain at each frequency between the two groups after PSM.ConclusionThere was no significant difference in short-term hearing outcomes between treatment with batroxobin and treatment without batroxobin in SSNHL patients by Siegel's and CMAO criteria after PSM. Future studies for better therapy regimens of SSNHL are still needed.

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