A highly dispersed melamine/red phosphorus (MA/RP) composite flame retardant was prepared by means of simple mechanical grinding. After co‐thermal pretreatment with polyether polyol (PPG‐2000) at 135°C, organic–inorganic hybrid foams (MA/RP/HF) containing MA/RP flame retardant were prepared by the one‐step method using main raw materials such as polyisocyanate and sodium silicate. When 0.5 wt% MA/RP with the mass ratio of 1:5 is added, MA can realize the uniform dispersion of RP in the substrate and enhance its flame retardancy, and the obtained MA/RP/HF presents uniform and closed pores and excellent basic properties. The TG results reveal that MA/RP/HF shows good thermal stability and the corresponding char residual rate reaches 37.9% at 800°C. The flame retardant test results prove that MA/RP/HF is capable of passing the V‐0 grade, with the LOI value being 26.8%. According to the cone calorimeter analysis, its peak heat release rate and total heat release decrease by 30.1% and 51.7% compared with those of rigid polyurethane‐based foam and by 40.1% and 30.0% compared with those of pure HF, respectively. Finally, the synergistic flame retardancy mechanism of MA and RP on polyurethane‐based foam was discussed.

Background and Aims: Reducing reactive oxygen species (ROS) production has proven an effective way for alleviating oxidative stress during ischemia-reperfusion injury (IRI). Moreover, inhibition of Rac1 could reduce ROS production and prevent oxidative stress injury. Previous studies have suggested a positive interactivation feedback loop between Rac1 and hypoxia-inducible factor (HIF)-1α, the latter being up-regulated early during ischemia. The positive inter-activation between Rac1 and HIF-1α would aggravate ROS production, thereby promoting IRI. This study was designed to verify the effects of Rac1 inhibition on hepatic IRI both at animal and cellular levels and to explore the interaction between Rac1 and HIF-1α during hepatic IRI. Methods: C57B/6 mice and AML-12 cells were used for the construction of hepatic IRI animal and cell models. Rac1 inhibition was achieved by NSC23766 (a specific Rac1 inhibitor). Lentiviral vectors were used for Rac1 knockdown. At designated time points, serum and liver tissues were collected from the mice and treated cells were collected for further analysis. Results: NSC23766 treatment significantly alleviated the hepatic IRI in mice, manifesting as lower vacuolation score and less apoptosis cells, lower ROS and serum/liver alanine aminotransferase/aspartate aminotransferase levels, and fewer activated inflammatory cells. IRI of AML-12 was also alleviated by 50 µM NSC23766 or Rac1-knockdown, manifesting as reduced cell apoptosis, less extensive interruption of mitochondrial membrane potential, down-regulation of apoptosis, and effects on DNA damage-related proteins. Interestingly, Rac1 knockdown also down-regulated the expression level of HIF-1α. Conclusions: Our study supports a protective effect of Rac1 inhibition on hepatic IRI. Aside from the classic topics of reducing ROS production and oxidative stress, our study showed an interaction between Rac1 and HIF-1α signaling during hepatic IRI.