Objective To investigate the effect of ambroxol pretreatment on the inflammatory response and lipid peroxidation during one-lung ventilation (OLV) .Methods Forty-five ASA I or II patients aged 37-64 yr weighing 53-65 kg undergoing thoracotomy under general anesthesia were randomly divided into 3 groups ( n = 15 each): group A two-lung ventilation (TLV); group B OLV and group C ambroxol 1 mg/kg + OLV. Anesthesia was induced with midazolam, fentanyl, propofol and atracurium and maintained with propofol infusion and intermittent iv boluses of fentanyl and atracurium. The patients were mechanically ventilated (VT8-10 ml/kg, RR 12 bpm during TLV, VT 6-7 ml/kg, RR 16 bpm during OLV, I: E 1:2, FiO2 100% ). In group C ambroxol 1 mg/kg in normal saline ( NS) 100 ml was infused at 25 min before OLV (infusion rate 4 ml/min) , while in group A and B equal volume of NS was infused instead of ambroxol. Blood samples were obtained from radial artery before induction of anesthesia and OLV (T0.1 ) and at 0.5, 1, 2 h of OLV (T2-4 ) and 1, 2 h of TLV (T5,6 ) and at 24 h after operation (T7) in group B and C for determination of serum SOD activity and TNF-α, IL-6 and IL-8 concentrations and WBC and neutrophil granulocyte counts. The same indexes were detected in group A at the corresponding time points.Results Serum SOD activity was significantly lower and serum TNF-α, IL-6 and IL-8 concentrations and WBC and neutrophil granulocyte counts were significantly higher in group B than in group A. Serum SOD activity was significantly higher and serum TNF-a, IL-6 and IL-8 concentrations and WBC and neutrophil granulocyte counts were significantly lower in group C than in group B. Conclusion Pretreatment with ambroxol 1 mg/kg can inhibit inflammatory response and lipid peroxidation during OLV.

To investigate the associations between gene polymorphisms of signal transducer and activator of transcription 3 (STAT3) and liver cirrhosis (LC) after hepatitis B virus (HBV) infection. A case-control study was conducted in 243 patients with hepatitis B cirrhosis (HBV-LC, case group) and 486 HBV-infected subjects without LC (non-LC, control group) collected from January 2018 to September 2020 at the Changsha Central Hospital Affiliated to Nanhua University. Three single nucleotide polymorphisms (SNPs) of STAT3 gene, including rs4796793C>G, rs2293152C>G, and rs1053004T>C were selected through literature and biological information database, and the genotypes were detected by real-time fluorescent quantitative PCR (RFQ-PCR). The distribution differences of STAT3 SNPs genotypes between the two groups were compared using Chi-square test and haplotype analysis was conducted by Shesis online. The proportion of HBV C genotype in HBV-LC patients was significantly higher than that in the control group (80.91% vs. 70.79%, χ²=7.109, P=0.008), while the logarithm of ALT was significantly lower than that of the control group (1.78±0.43 vs. 1.95±0.54, t=3.801, P=0.000). The genotypes distributions of rs4796793, rs2293152, and rs1053004 were not significantly different between HBV-LC and non-LC in overall analysis and stratified analysis by gender (χ²=2.610, 1.505, 0.586, 2.653, 2.685, 1.583, 0.351, 5.388, 0.339, respectively, P>0.05 for each). Among the subjects infected with HBV genotype C, rs1053004 CC (vs. TT) significantly increased the risk of HBV-LC [odds ratio (OR) = 1.40, 95% confidence interval (CI): 1.03-1.91]. Among the HBV-infected subjects with HBeAg negative, rs4796793 GG genotype (vs. CC) and G allele (vs. C) significantly increased the risks of HBV-LC (OR = 2.17, 95%CI: 1.11-4.23; OR = 1.45, 95%CI: 1.06-1.97, respectively). Haplotypes analysis showed that the frequency of haplotype C-G-T composed of rs4796793, rs2293152, and rs1053004 was significantly lower in HBV-LC than that in the control group (non-LC) (27.3% vs. 35.6%, χ²=9.949, P = 0.001). The correlation between STAT3 and HBV-LC is different in HBV-infected subjects with different infection status. The HBV-infected subjects carrying haplotype rs4796793C-rs2293152G-rs1053004T of STAT3 gene have significantly decreased risk of LC.
Carcinoma, Hepatocellular/genetics* ; Case-Control Studies ; Genetic Predisposition to Disease ; Genotype ; Hepatitis B virus/genetics* ; Hepatitis B, Chronic/genetics* ; Humans ; Liver Cirrhosis/genetics* ; Liver Neoplasms/genetics* ; Polymorphism, Single Nucleotide ; STAT3 Transcription Factor/genetics*