Abstract. The aim of the present study was to investigate the in vitro effects of ulinastatin (UTI) on the proliferation, invasion, apoptosis, expression and distribution of high mobility group box 1 (HMGB1) and the expression of nuclear factor κB (NF-κB) in human colon carcinoma LoVo cells. The cells were divided into control (untreated), UTI1 (400 U/ml UTI), UTI2 (800 U/ml UTI) and UTI3 (1,600 U/ml UTI) groups. The cell proliferation, invasion, apoptosis and the gene and protein expression of HMGB1 and NF-κB were detected using a tetrazolium assay, Transwell cell invasion assays, a caspase-3 activity assay, western blot analysis and reverse transcription quantitative polymerase chain reaction, respectively. The distribution of HMGB1 was detected using immunofluorescence. LoVo cell proilferation decreased the most in the UTI3 group followed, in order, by the UTI2, UTI1 and control groups. UTI inhibited invasion in LoVo cells and the inhibitory effect was enhanced as the UTI concentration increased. The activity of caspase-3 increased the least in the control group followed, in order, by the UTI1, UTI2 and UTI3 groups. UTI inhibited the expression of HMGB1 and NF-κB, and decreased the cytoplasmic distribution of HMGB1. Thus, UTI inhibited LoVo cell proliferation and induced LoVo cell apoptosis, the mechanism of which may be associated with a decreased in the expression of HMGB1 and NF-κB, and the cytoplasmic distribution of HMGB1.

Pain tolerance had a significant relationship with stress response during intubation and skin incision. We may initially use pain tolerance to direct opioid usage in the future.

At present, the timing of glutamine administration remains controversial. The aim of the present study was to confirm the early protective mechanisms of alanyl‑glutamine (Ala‑Gln) against lipopolysaccharide (LPS)‑induced lung injury, as well as to detect the best time for Ala‑Gln usage. A total of 60 adult Wistar rats were randomly divided into 6 groups: The control group (C), the LPS‑induced shock group (LPS), the pre‑Ala‑Gln treated group (A1) and the pre‑Gln treated group (G1), which separately received 4.5% Dipeptiven and 3% glutamine just before LPS administration; the post‑Ala‑Gln treated group (A2) and the post‑Gln treated group (G2), which was respectively infused with 4.5% Dipeptiven and 3% glutamine at 1 h following LPS. Survival rates were observed at 6 h following the LPS injection. Blood samples were drawn for analysis of cytokine levels 1 h prior to (T0) and 6 h following (T1) LPS injection. All rats were killed at T1 and the pulmonary samples were collected. Plasma concentrations of tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑8 at T0 and T1, apoptosis in lung epithelial cells and the expression of heat shock protein (HSP)70 were detected. The lung wet/dry weight ratio (W/D) and the content of protein in the bronchoalveolar lavage fluid (BALF) were also determined. Survival rates at 6 h following (T1) LPS administration were both 100% in groups A1 and G2, but 70% in A2 and G2 groups. The W/D, the content of protein in BALF and cytokine levels were significantly lower in groups A1 and G1 than that in group LPS (P<0.05) at T1. The apoptosis index of both alveolar and bronchial epithelial cells was obviously lower in A1 and G1 groups than that in the LPS group (P<0.05). Gray gradients of HSP70 in the A1 and G1 groups were dramatically higher than those of group LPS (P<0.05). In conclusion, pre‑administration of Ala‑Gln just before LPS can effectively protect the lung by enhancing HSP70 expression, but delayed administration cannot protect LPS‑induced lung injury.