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The corrosion behavior of E690 steel in 3.5 wt.% NaCl solution at temperatures from 20 °C to 60 °C was investigated using electrochemical test. The corrosion morphology was characterized using SEM and AFM, and the corrosion layer was characterized using EDS, Raman spectroscopy and XPS. The results showed that the corrosion rate of E690 steel improves with the increase in temperature. The corrosion layers of E690 steel are mainly composed of α-Fe2O3, α-FeOOH and γ-FeOOH. With the elevated temperature, the content of α-FeOOH in corrosion layers increases, while the content of α-Fe2O3 and γ-FeOOH decreases. The corrosion mechanisms were briefly discussed.

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Purpose: To investigate the protective role of aromadendrin in septic liver injury in mice, and  its mechanism of action.Methods: Eight-week-old male C57BL/6 mice (n=6 for each group) were administrated with aromadendrin (SMB00175, Sigma-Aldrich) at 0 mg/kg, 30 mg/kg and 60 mg/kg via a hypodermic intraperitoneal injection. HE staining was used to examine liver histopathological structural changes in the liver while DAPI/Tunel staining was employed to evaluate liver cell apoptosis. The mRNA expression levels of TNF-α, IL-1β and IL-6 were determined by quantitative reverse transcriptionpolymerase chain reaction (qRT-PCR). Moreover, enzyme-linked immunosorbent assay (ELISA)was applied to assess the levels of TNF-α, IL-1β and IL-6, as well as the activities of catalase (CAT), antioxidant glutathione (GSH), superoxide dismutase (SOD) and malondialdehyde (MDA). Moreover, the protein levels of p65, p-p65, p-IκBα and IκBα were analyzed by Western blotting.Results: The liver tissues exhibited severe structural damages, with edema, necrosis, and neutrophil infiltration, but recovered as a result of aromadendrin treatment (p < 0.05). The increased serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in CLP mice were reduced by aromadendrin, which also attenuated liver injury and cell apoptosis. Aromadendrin inhibited the levels ofu TNF-α, IL-1β and IL-6 in the mice, while the activities of GSH and antioxidant enzymes (SOD and CAT) were also significantly lowered in the mice, but attenuated by aromadendrin (p < 0.05). Aromadendrin also prevented the increased level of MDA, and suppressed the phosphorylation of p65 and IκBα (p < 0.05).Conclusion: Aromadendrin protects mouse liver from sepsis-induced injury by inhibiting NF-κB signaling in vivo, thus suggesting a potential strategy for the therapy of sepsis-induced liver injury.

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