Seasonal variations in group leaf characteristics in species with red young leaves.

The leaves of many plants are red during particular stages of their lives, but the adaptive significance of leaf colouration is not yet clearly understood. In order to reveal whether anthocyanins play a similar role (i.e. antioxidants) in different seasonal contexts, this study investigated species with red young leaves in the subtropical forest of Dinghushan biosphere reserve (South China) during summer and winter and compared group leaf characteristics between the two seasons. Of 62 total species, 33 exhibited red young leaves in summer only, 6 in winter only, and 23 in both seasons. The anthocyanins extracted from most of these species had an absorption peak at ~530 nm. Frequency distribution analysis showed that the species containing anthocyanins at levels ranging from 0.02 to 0.04 µmol cm-2 occurred most frequently in summer or winter. Based on conditional grouping of the species, no significant variation was observed in the average anthocyanin contents and antioxidant abilities between summer and winter; the flavonoid content in summer was 2-fold that in winter, whereas the anthocyanin:flavonoid ratio in summer was only half that in winter. Moreover, a positive correlation between anthocyanins and flavonoids was found in summer. Therefore, it is less likely for anthocyanins to serve as antioxidants in summer than winter, because such a function in summer leaves is readily replaced by other flavonoids.

Functional characteristics of phenolic compounds accumulated in young leaves of two subtropical forest tree species of different successional stages.

The abundance of phenolic compounds (including anthocyanins) in leaves is associated with photosynthetic performance, but the regulatory mechanism is unclear. Schima superba Gardn. et Champ. and Cryptocarya concinna Hance., which exhibit distinct anthocyanin accumulation patterns, are dominant tree species in the early- and late-successional stages, respectively, of subtropical forests in China. RNA-seq and analyses of phenolic concentrations, antioxidant capacity and photosynthetic characteristics were performed on young and mature leaves of these two species under contrasting light conditions. The high-light-acclimated young leaves of S. superba and C. concinna and low-light-acclimated young leaves of C. concinna were red. These red leaves had higher ratios of electron transport rate to gross photosynthesis (ETR:Pgross) and total antioxidant capacity to chlorophyll (TAC:Chl) than did the green leaves, regardless of light conditions. In addition, the red leaves had a higher expression level of the UDP-glucose:flavonoid 3-O-glucosyltransferase (UFGT) gene than did the green leaves, irrespective of light conditions. Total antioxidant capacity was positively correlated with flavonoid content in C. concinna leaves and with total phenolic content in leaves of both species under both high and low light. Consistent with the measurements of photosynthetic performance and flavonoids:Chl ratio, photosynthesis-related genes were extensively downregulated and flavonoid-pathway-related genes were extensively upregulated in young leaves relative to mature leaves. Under high and low light, both non-photochemical quenching and TAC:Chl, which serve as different types of photoprotective tools, were enhanced in young leaves of S. superba, whereas only TAC:Chl was enhanced in young leaves of C. concinna. Our results indicate that the biosynthesis of phenolic compounds in young leaves is likely enhanced by an imbalance between photosynthetic electron supply and demand and that flavonoids play a larger role in meditating photoprotection in late-successional species than in early-successional ones.

Induction of heat shock protein 27 by bicyclol attenuates d-galactosamine/lipopolysaccharide-induced liver injury.

Heat shock proteins (Hsps) are critical for cell survival under adverse environmental conditions. Bicyclol is a novel hepatoprotectant that has been shown to protect against liver injury by inducing Hsps, including Hsp27 and Hsp70. Although the role of Hsp70 in protecting against acute hepatic failure has been clearly explored, the precise function of Hsp27 in this setting is poorly defined. This study was undertaken to evaluate the role of Hsp27 in bicyclol-mediated hepatoprotection. Both primary hepatocytes and bone marrow-derived macrophages were subjected to bicyclol treatment, followed by detection of Hsp27 expression. Adenoviruses containing the mouse Hsp27 coding sequence or shRNA interference sequence targeting Hsp27 were used to manipulate Hsp27 expression in the liver before the mice were treated with bicyclol and/or confronted with D-galactosamine/lipopolysaccharide (Galn/LPS)-induced acute liver damage. Only hepatocytes increased their Hsp27 expression after bicyclol treatment and the time course of bicyclol-induced Hsp27 expression in hepatocytes was in line with the in vivo results. Although high-dose bicyclol could protect against liver failure without Hsp27, the effect of bicyclol given at a low dose was dependent on Hsp27 induction. Adenovirus-mediated transduction of Hsp27 protected against acute liver damage and partially replicated the protective effect afforded by bicyclol. These results demonstrated that bicyclol induced Hsp27 expression in hepatocytes, which was essential to bicyclol-mediated hepatoprotection. Overexpression of Hsp27 in hepatocytes could confer remarkable protection against acute liver damage.

Hepatocyte nuclear factor 4α induces a tendency of differentiation and activation of rat hepatic stellate cells.

AIM: To investigate the effect of hepatocyte nuclear factor 4α (HNF4α) on the differentiation and transformation of hepatic stellate cells (HSCs). METHODS: By constructing the recombinant adenovirus vector expressing HNF4α and HNF4α shRNA vector, and manipulating HNF4α expression in HSC-T6 cells, we explored the influence of HNF4α and its induction capacity in the differentiation of rat HSCs into hepatocytes. RESULTS: With increased expression of HNF4α mediated by AdHNF4α, the relative expression of Nanog was downregulated in HSC-T6 cells (98.33 ± 12.33 vs 41.33 ± 5.67, P < 0.001). Consequently, the expression of G-P-6 and PEPCK was upregulated (G-P-6: 14.34 ± 3.33 vs 42.53 ± 5.87, P < 0.01; PEPCK: 10.10 ± 4.67 vs 56.56 ± 5.25, P < 0.001), the expression of AFP and ALB was positive, and the expression of Nanog, Type I collagen, α-SMA, and TIMP-1 was significantly decreased. HNF4α also downregulated vimentin expression and enhanced E-cadherin expression. The ultrastructure of HNF4α-induced cells had more mitochondria and ribosomes compared with the parental cells. After silencing HNF4α expression, EPCK, E-cadherin, AFP, and ALB were downregulated and α-SMA and vimentin were upregulated. CONCLUSION: HNF4α can induce a tendency of differentiation of HSCs into hepatocyte-like cells. These findings may provide an effective way for the treatment of liver diseases.