Princen's modification of Vonnegut's rotating drop procedure for measuring inter‐facial tension between low viscosity liquids has been adapted for use with pairs of liquid polymers with viscosities up to 5000 poise. Extrapolation to infinite time of results obtained with 10–20 min of rotation provided steady state data as indicated by its corre‐spondence with results reported from other techniques. An adaptation of this procedure was also found useful for determining surface tension values of molten polymers at temperatures up to 290°C. Reductions of 60–70% in interfacial tension between viscous samples of a polydimethylsiloxane and a copolyether were accomplished by addition of 1–2% of amphi‐pathic or polar compounds such as polydimethylsiloxane‐polyoxyethylene copolymers and carboxyl‐substituted polydimethylsiloxanes. A linear reduction in interfacial tension with a logarithmic increase of additive concentration was noted.

Ferroptosis, an iron-dependent cell death form, has recently been observed in the development of non-alcoholic fatty liver disease (NAFLD). Melatonin (Mel) shows potential benefits for preventing and treating liver diseases. Whether and how Mel ameliorates hepatic ferroptosis in NAFLD is not fully understood. Here we established a mouse model of NAFLD induced by long-term high-fat diet (HFD) feeding. We found that Mel treatment ameliorated global metabolic abnormalities and inhibited the progression of NAFLD in mice. Most importantly, Mel supplementation significantly improved HFD-induced iron homeostasis disorders in the liver, including iron overload and ferritin transport disorders. For another, Mel ameliorated HFD-induced hepatic lipid peroxidation. The recuperative role of exogenous Mel on hepatocyte ferroptosis was also observed in PA- or Erastin-treated HepG2 cells. Mechanistically, MT2, but not MT1, was involved in the effect of Mel. Furthermore, Mel treatment inhibited HFD or Erastin-activated ER stress and activated the PKA/IRE1 signaling pathway. Co-expression of p-PKA and p-IRE1 was enhanced by the MT2 antagonist. Inhibitions of PKA and IRE1 respectively improved hepatocyte ferroptosis, and activations of cAMP/PKA reversed Mel's effect on ferroptosis. Collectively, these findings suggest that exogenous Mel inhibits hepatic ferroptosis in NAFLD by ameliorating ER stress through the MT2/cAMP/PKA/IRE1 pathway, proving that Mel is a promising candidate drug for the treatment of hepatic ferroptosis in NAFLD.

No abstract

No abstract