The effects of 24-epibrassinolide (EBR) spray application on gas-exchange, chlorophyll fluorescence characteristics, Rubisco activity, and carbohydrate metabolism were investigated in cucumber (Cucumis sativus L. cv. Jinchun No. 3) plants grown in a greenhouse. EBR significantly increased the light-saturated net CO(2) assimilation rate (A(sat)) from 3 h to 7d after spraying, with 0.1 mg l(-1) EBR proving most effective. Increased A(sat) in EBR-treated leaves was accompanied by increases in the maximum carboxylation rate of Rubisco (V(c,max)) and in the maximum rate of RuBP regeneration (J(max)). EBR-treated leaves also had a higher quantum yield of PSII electron transport (phi(PSII)) than the controls, which was mainly due to a significant increase in the photochemical quenching (q(P)), with no change in the efficiency of energy capture by open PSII reaction centres (F'(v)/F'(m)). EBR did not influence photorespiration. In addition, significant increases in the initial activity of Rubisco and in the sucrose, soluble sugars, and starch contents were observed followed by substantial increases in sucrose phosphate synthase (SPS), sucrose synthase (SS), and acid invertase (AI) activities after EBR treatment. It was concluded that EBR increases the capacity of CO(2) assimilation in the Calvin cycle, which was mainly attributed to an increase in the initial activity of Rubisco.

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Brassinosteroids (BRs) are essential for many biological processes in plants, however, little is known about their roles in early fruit development. To address this, BR levels were manipulated through the application of exogenous BRs (24-epibrassinolide, EBR) or a BR biosynthesis inhibitor (brassinazole, Brz) and their effects on early fruit development, cell division, and expression of cyclin and cyclin-dependent kinases (CDKs) genes were examined in two cucumber cultivars that differ in parthenocarpic capacity. The application of EBR induced parthenocarpic growth accompanied by active cell division in Jinchun No. 4, a cultivar without parthenocarpic capacity, whereas Brz treatment inhibited fruit set and, subsequently, fruit growth in Jinchun No. 2, a cultivar with natural parthenocarpic capacity, and this inhibitory effect could be rescued by the application of EBR. RT-PCR analysis showed both pollination and EBR induced expression of cell cycle-related genes (CycA, CycB, CycD3;1, CycD3;2, and CDKB) after anthesis. cDNA sequences for CsCycD3;1 and CsCycD3;2 were isolated through PCR amplification. Both CsCycD3;1 and CsCycD3;2 transcripts were up-regulated by EBR treatment and pollination but strongly repressed by Brz treatment. Meanwhile, BR6ox1 and SMT transcripts, two genes involved in BR synthesis, exhibited feedback regulation. These results strongly suggest that BRs play an important role during early fruit development in cucumber.

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Binge drinking is associated with increased cardiac autophagy, and often triggers heart injury. Given the essential role of autophagy in various cardiac diseases, this study was designed to investigate the role of autophagy in ethanol-induced cardiac injury and the underlying mechanism. Our study showed that ethanol exposure enhanced the levels of LC3-II and LC3-II positive puncta and promoted cardiomyocyte apoptosis in vivo and in vitro. In addition, we found that ethanol induced autophagy and cardiac injury largely via the sequential triggering of reactive oxygen species (ROS) accumulation, activation of c-Jun NH2-terminal kinase (JNK), phosphorylation of Bcl-2, and dissociation of the Beclin 1/Bcl-2 complex. By contrast, inhibition of ethanol-induced autophagic flux with pharmacologic agents in the hearts of mice and cultured cells significantly alleviated ethanol-induced cardiomyocyte apoptosis and heart injury. Elimination of ROS with the antioxidant N-acetyl cysteine (NAC) or inhibition of JNK with the JNK inhibitor SP600125 reduced ethanol-induced autophagy and subsequent autophagy-mediated apoptosis. Moreover, metallothionein (MT), which can scavenge reactive oxygen and nitrogen species, also attenuated ethanol-induced autophagy and cell apoptosis in MT-TG mice. In conclusion, our findings suggest that acute ethanol exposure induced autophagy-mediated heart toxicity and injury mainly through the ROS-JNK-Bcl-2 signaling pathway.

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