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Additional file 1. Supplementary table 1. General characteristics of the studied groups. Supplementary table 2. Univariate and multivariate logistic regression evaluating factors associated with HCC in ALD, HCV and ALD+HCV patients. Supplementary table 3. Univariate and multivariate logistic regression evaluating factors associated with EGVB in ALD, HCV and ALD+HCV patients. Supplementary table 4. Relation between alcohol abstinence and risk of EGVB in ALD, ALD+HBV and ALD+HCV. Supplementary table 5. Relation between alcohol abstinence and risk of HCC in ALD patients (detailed). Supplementary table 6. Relation between alcohol abstinence and risk of EGVB in ALD patients (detailed). Supplementary table 7. Relation between alcohol abstinence and risk of HCC in ALD+HBV patients (detailed). Supplementary table 8. Relation between alcohol abstinence and risk of EGVB in ALD+HBV patients (detailed). Supplementary table 9. Relation between alcohol abstinence and risk of HCC in ALD+HCVpatients (detailed). Supplementary table 10. Relation between alcohol abstinence and risk of EGVB in ALD+HCV patients (detailed). Supplementary figure 1. Changing trend in the proportion of various liver cirrhosis etiology over the years. Supplementary figure 2. Age-sex distribution of the studied population. Supplementary figure 3. Proportion of HCC (fig A) and EGVB (fig B) in ALD, ALD+HBV and ALD+HCV patients according to the duration of alcohol abstinence.

Objective: To investigate the therapeutic effect of 2,3,5,4ʹ-tetrahydroxystilbene-2-O-β-D-glucoside (TSG) on the expression of 5-hydroxytryptamine (5-HT)/5-HT receptor 2A (5-HT2A), 5-HT transporter (5-HTT), and uncoupling protein 4 (UCP4) after cerebral ischemia/reperfusion (I/R) injury. Methods: Sprague–Dawley rats were randomly divided into control, model and 125 (low-dose), 250 (middle-dose), and 500 (high-dose) mg/mL TSG groups. Rat cerebral I/R injury model was established by middle cerebral artery occlusion (MCAO). After successful establishment of rat MCAO model, rats in control and model groups were decapitated immediately. Rats in TSG group were orally administered 125, 250, and 500 mg/mL TSG in corresponding groups at a dose of 1 mL/100 g per day for 7 continuous days, and then the rats were decapitated. The infarct size was determined using triphenyl tetrazolium chloride staining and the expression of UCP4 and 5-HT2A in the hippocampus and thalamic nucleus was detected using immunohistochemistry and western blot assay. The expression of 5-HTT in brain tissue was detected using western blot assay. Serum 5-HT levels were detected using ELISA. Results: After treatment, the infarct size due to cerebral I/R injury decreased with increased concentrations of TSG. Synchronous reduction of 5-HT in the blood and 5-HTT in the brain was observed, and 5-HT2A was expressed in normal brain tissue but its level was increased in rats after cerebral I/R injury. A high level of UCP4 was found in normal brain tissue, which rose by 6 hrs after cerebral I/R injury but reduced to minimal levels 24 hrs after injury. With increasing TSG concentration, the levels of 5-HT, 5HTT, and UCP4 were increased, while the level of 5-HT2A was decreased. Conclusion: TSG is effective in treating cerebral I/R injury in rats, and its mechanism may be implemented through the 5-HT/5-HTR pathway, by increasing 5-HT release, enhancing the activity of 5-HTT, increasing expression of UCP4, and inhibiting 5-HT2A activity.

Additional file 1: Figure S1. Cell surface markers on MSC were detected by flow cytometry. Table S1. Primer sequences of Gapdh, Nos2, Ptgs2, Il6, Ifnb1 and Jag1 genes used in the RT-PCR. Figure S2. Different mRNA expression of MSCs pretreated with IFN-γ or TLR2/4 ligand alone or their combinations. Figure S3. A representative result from control group showed the gating strategy in Fig. 3.