Rice (Oryza sativa) spikelet formation is dependent on carbohydrate metabolism. High temperature inhibits young panicle growth and spikelet formation, and brassinolides (BRs) are involved in the regulation of spikelet formation. Elucidation of the mechanism by which endogenous BRs mediate carbohydrate metabolism to influence spikelet formation under high temperature may provide a theoretical and technical basis to alleviate heat injury. In this study, rice cultivar ‘IR36’ was subjected to high temperature (HT; 40 °C) or normal temperature (NT; 33 °C) for 7 days at the panicle initiation stage in conjunction with application of exogenous 2, 4-epibrassinolide (EBR) and brassinazole (BRZ) at the beginning of the treatments. HT inhibited spikelet differentiation and aggravated spikelet degeneration to reduce the number of spikelets per panicle. Exogenous EBR reduced the decrease in spikelet number induced by HT, whereas exogenous BRZ enhanced the reduction in spikelet number. Analyses of the transcript levels of genes associated with BR biosynthesis and decomposition showed that HT promoted BR decomposition to reduce the endogenous BR content. HT blocked sucrose transport from leaves to young panicles, and inhibited the activities of crucial enzymes involved in sucrose hydrolysis, glycolysis, and the tricarboxylic acid cycle to reduce sugar utilization. In addition, HT reduced the activities of antioxidant enzymes and increased the contents of hydrogen peroxide and malondialdehyde. Exogenous EBR application promoted sucrose transport to young panicles and improved sucrose utilization under NT and HT, whereas application of BRZ resulted in the opposite physiological response. These results show that inhibition of spikelet formation owing to decreased sugar utilization under HT is associated with BR decomposition.

水稻（Oryza sativa) 小穗形成取决于碳水化合物代谢。高温抑制幼穗生长和小穗形成，芸苔素内酯（BRs）参与小穗形成的调节。阐明内源性BRs介导碳水化合物代谢影响高温下小穗形成的机制可能为减轻热损伤提供理论和技术基础。在这项研究中，水稻品种 'IR36' 在穗开始阶段经受高温（HT; 40 °C）或常温（NT; 33 °C）7 天，并结合施用外源 2, 4-表油菜素内酯(EBR) 和芸苔素 (BRZ) 在治疗开始时。HT抑制小穗分化并加剧小穗退化以减少每穗的小穗数。外源 EBR 减少了 HT 诱导的小穗数减少，而外源 BRZ 增加了小穗数的减少。对与BR生物合成和分解相关的基因转录水平的分析表明，HT促进BR分解以降低内源BR含量。HT 阻断了蔗糖从叶子到幼穗的运输，并抑制了参与蔗糖水解、糖酵解和三羧酸循环的关键酶的活性，从而降低了糖的利用率。此外，HT降低了抗氧化酶的活性，增加了过氧化氢和丙二醛的含量。外源 EBR 应用促进了蔗糖向幼穗的转运，提高了 NT 和 HT 下蔗糖的利用，而 BRZ 的应用导致相反的生理反应。