Catechin (EC) is a natural plant extract and has great health benefits. EC interacts with the starch isolated from Chinese chestnut to form complexes. The effect of EC addition on the structure and retrogradation properties of chestnut starch (CS) is investigated in this study. Compared with CS, when the addition of EC is 10%, the peak viscosity (PV), trough viscosity(TV), and setback (SB) of CS decreased by 45.65%, 39.95%, and 47.38% (2185.62, 922.35, and 445.42 cp), respectively. Thermogravimetric shows that the EC addition can decrease the degradation temperature of starch. Scanning electron microscope shows that EC can cause a looser gel structure of CS. The results of Fourier transform infrared show that the absorption peak of the complex at 3000-3600 cm −1 is enhanced to a high wavenumber. X-ray diffraction results in a reduction in the relative crystallinity with the increase of EC addition. In summary, the overall results suggest CS interacted with EC to form the non-inclusive complex, resulting in changes in starch structure. These results indicate that EC is a promising ingredient to restrain the retrogradation of starchy food and provides new insights for the application of other starch and polyphenols.
Random skin flap grafting is the most common skin grafting technique in reconstructive surgery. Despite progress in techniques, the incidence of distal flap necrosis still exceeds 3%, which limits its use in clinical practice. Current methods for treating distal flap necrosis are still lacking. Pinocembrin (Pino) can inhibit reactive oxygen species (ROS) and cell death in a variety of diseases, such as cardiovascular diseases, but the role of Pino in random flaps has not been explored. Therefore, we explore how Pino can enhance flap survival and its specific upstream mechanisms via macroscopic examination, Doppler, immunohistochemistry, and western blot. The results suggested that Pino can enhance the viability of random flaps by inhibiting ROS, pyroptosis and apoptosis. The above effects were reversed by co‐administration of Pino with adeno‐associated virus‐silencing information regulator 2 homolog 3 (SIRT3) shRNA, proving the beneficial effect of Pino on the flaps relied on SIRT3. In addition, we also found that Pino up‐regulates SIRT3 expression by activating the AMP‐activated protein kinase (AMPK) pathway. This study proved that Pino can improve random flap viability by eliminating ROS, and ROS‐induced cell death through the activation of SIRT3, which are triggered by the AMPK/PGC‐1α signaling pathway.
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