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Leaf color is a key trait that determines the ornamental quality of landscape tree species such as Acer tutcheri, and anthocyanin is the main pigment for red leaf coloration. Red leaf fading significantly reduces the ornamental value of A. tutcheri leaves in the spring; however, the physiological mechanism that causes red leaf discoloration in this species is still unclear. Only the anabolic or degradative metabolism of anthocyanin has been studied in terms of leaf color changes. In this study, leaves from four color-change stages of A. tutcheri during the spring were selected by the average sampling method, which involves measuring and analyzing the pigment content and physiological factors related to anthocyanin metabolism, aiming to clarify the key physiological factors of spring leaf coloration. Our results show that the reduced anthocyanin/chlorophyll ratio was the direct cause of red leaf fading in spring. The carbohydrates synthesized during the growth of juvenile leaves were mainly used for their growth and development, whereas fewer carbon sources were used for the synthesis of anthocyanin. Phenylalanine ammonia-lyase and chalcone isomerase activities increased in the early stages of juvenile leaf development and decreased in the middle and late stages, whereas peroxidase activity continued to increase. The decrease in anthocyanin synthesis-related enzyme activity reduced the accumulation of anthocyanin, whereas the increase in anthocyanin degradation-related enzyme activity accelerated the depletion of anthocyanin. Increasing vacuole pH was a major factor in the degradation of anthocyanin. The physiological characteristics of A. tutcheri leaves during the spring season suggest that anthocyanin is a key factor affecting the presentation of color in juvenile leaves, and red leaf fading in the spring of A. tutcheri is the result of the joint effect of the decrease in anthocyanin anabolic metabolism and the increase in anthocyanin degradative metabolism. [ABSTRACT FROM AUTHOR]

Cerebral oedema is a major pathological change of acute carbon monoxide (CO) poisoning, the pathogenesis of which is still unclear. In the aquaporin (AQP) water channel family, AQP1 and AQP4 play critical roles in the progress of cerebral oedema of various neuropathological events. However, their functions in CO poisoning have not been demonstrated. In this study, we investigated the expressions of AQPs and associated mechanisms of brain injury in an acute CO poisoning rat model. Compared with the control injected intraperitoneally with equal volume of air, the dry weight/wet weight (DW/WW) ratio of brain water content, levels of AQP1, AQP4, phosph‐p38 mitogen‐activated protein kinase (p‐p38 MAPK) and astrocyte marker, glial fibrillary acidic protein (GFAP) in the frontal cortex and hippocampal CA1 of acute CO poisoning group significantly increased at 6, 12, 24 hours after CO injection. Intracerebroventricular injection with a p38 MAPK inhibitor, SB203580 (200 µmol/L/kg/d), before CO injection reduced water content in the brain tissues and significantly decreased levels of AQP1, AQP4, p‐p38 MAPK and GFAP. Therefore, our study showed that the overexpressions of AQP1 and AQP4 were involved in the development of CO poisoning‐induced cerebral oedema, which could be attenuated by inhibition of p‐p38 MAPK signalling. Manipulation of AQPs and p38 MAPK may be a new therapeutic strategy for acute CO poisoning. [ABSTRACT FROM AUTHOR]