Zhu Xiangjie, Cao Mingjie, Li Chenyang, Zhu Chenyu, Li Han, Tian Yuanmingyue, Shang Jiaqi, Sun Jiaqi, Zhou Bingfeng, Wu Xianda, Zhou Shujing, Xu Xinjian
College of Bee Science and Biomedicine, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Honeybee Research Institute, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Insects. 2025 Mar 1;16(3):250. doi: 10.3390/insects16030250.
Exposure to low temperatures during honeybee development has been shown to impede brain development and affect cognitive function in adult bees. On the other hand, neuronal damage due to oxidative stress has been reported in many cases. Hence, biochemical parameters related to oxidative stress in honeybee pupae brain were determined. The levels of GSH in the pupal brain decreased after 24 h and 48 h of exposure to low temperatures; there were also reduced activities of SOD and CAT enzymes following 48 h of low-temperature treatment compared to the control group. Furthermore, analysis of transcriptome data post-24 h and -48 h low-temperature stress revealed the suppression of the glutathione metabolism and peroxisome pathways in pupal brains. Additionally, expression pattern clustering analysis and KEGG enrichment showed that 10 differentially expressed genes with down-regulated expression trends post-low-temperature treatment were significantly enriched in the peroxisome pathway, including , highlighting their connection to peroxisome function. RT-qPCR validation was conducted on 11 core enriched genes in pathways identified via GSEA, and all these genes exhibited a downregulated expression pattern, confirming the inhibition of glutathione metabolism and peroxisome function under low-temperature stress. The present study showed that exposing honeybee pupae to low temperatures suppressed both the glutathione metabolism and peroxisome pathways, resulting in increased oxidative stress. This research enhances our understanding of how the pupal brain reacts to cold stress and illuminates the neural damage associated with low temperatures during honeybee capped brood development.
研究表明，蜜蜂发育过程中暴露于低温环境会阻碍其大脑发育，并影响成年蜜蜂的认知功能。另一方面，许多案例报道了氧化应激导致的神经元损伤。因此，本研究测定了蜜蜂蛹脑内与氧化应激相关的生化参数。在暴露于低温环境24小时和48小时后，蛹脑内谷胱甘肽（GSH）水平下降；与对照组相比，低温处理48小时后，超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性也有所降低。此外，对低温胁迫24小时和48小时后的转录组数据进行分析，结果显示蛹脑内谷胱甘肽代谢和过氧化物酶体途径受到抑制。另外，表达模式聚类分析和KEGG富集分析表明，低温处理后表达趋势下调的10个差异表达基因在过氧化物酶体途径中显著富集，这突出了它们与过氧化物酶体功能的联系。对通过基因集富集分析（GSEA）确定的途径中的11个核心富集基因进行了RT-qPCR验证，所有这些基因均呈现下调的表达模式，证实了低温胁迫下谷胱甘肽代谢和过氧化物酶体功能受到抑制。本研究表明，将蜜蜂蛹暴露于低温环境会抑制谷胱甘肽代谢和过氧化物酶体途径，从而导致氧化应激增加。该研究增进了我们对蛹脑如何应对冷应激的理解，并揭示了蜜蜂封盖子发育期间与低温相关的神经损伤。
