Propolis is a honeybee product with broad clinical applications. Current literature describes that propolis is collected from plant resins. From a systematic database search, 241 compounds were identified in propolis for the first time between 2000 and 2012; and they belong to such diverse chemical classes as flavonoids, phenylpropanoids, terpenenes, stilbenes, lignans, coumarins, and their prenylated derivatives, showing a pattern consistent with around 300 previously reported compounds. The chemical characteristics of propolis are linked to the diversity of geographical location, plant sources and bee species.

The major environmental determinants of honeybee caste development come from larval nutrients: royal jelly stimulates the differentiation of larvae into queens, whereas beebread leads to worker bee fate. However, these determinants are not fully characterized. Here we report that plant RNAs, particularly miRNAs, which are more enriched in beebread than in royal jelly, delay development and decrease body and ovary size in honeybees, thereby preventing larval differentiation into queens and inducing development into worker bees. Mechanistic studies reveal that amTOR, a stimulatory gene in caste differentiation, is the direct target of miR162a. Interestingly, the same effect also exists in non-social Drosophila. When such plant RNAs and miRNAs are fed to Drosophila larvae, they cause extended developmental times and reductions in body weight and length, ovary size and fecundity. This study identifies an uncharacterized function of plant miRNAs that fine-tunes honeybee caste development, offering hints for understanding cross-kingdom interaction and co-evolution. How caste has formed in honeybees is an enduring puzzle. The prevailing view is that royal jelly stimulates the differentiation of larvae into queen. Here, we uncover a new mechanism that plant miRNAs in worker bee’s food postpone larval development, thereby inducing sterile worker bees. Thus, the theories about honeybee caste formation need to be re-examined from a new angle besides the traditional focus on royal jelly and its components. Furthermore, since miRNAs are transmitted between species of different kingdoms and can contribute to the phenotype regulation, this new model of horizontal miRNA transfer may open up a new avenue to further study the molecular mechanisms underlying cross-kingdom interaction and co-evolution.

Summary: There is growing number of studies demonstrating a close relationship between insect gut microbiota and insecticide resistance. However, the contribution of the honey bee gut microbiota to host detoxification ability has yet to be investigated. In order to address this question, we compared the expression of cytochrome P450s (P450s) genes between gut microbiota deficient (GD) workers and conventional gut community (CV) workers and compared the mortality rates and the pesticide residue levels of GD and CV workers treated with thiacloprid or tau ‐fluvalinate. Our results showed that gut microbiota promotes the expression of P450 enzymes in the midgut, and the mortality rate and pesticide residue levels of GD workers are significantly higher than those of CV workers. Further comparisons between tetracycline‐treated workers and untreated workers demonstrated that antibiotic‐induced gut dysbiosis leads to attenuated expression of P450s in the midgut. The co‐treatment of antibiotics and pesticides leads to reduced survival rate and a significantly higher amount of pesticide residues in honey bees. Taken together, our results demonstrated that honey bee gut symbiont could contribute to bee health through the modification of the host xenobiotics detoxification pathways and revealed a potential negative impact of antibiotics to honey bee detoxification ability and health.

Chinese propolis has been reported to possess various biological activities such as antitumor. In present study, anticancer activity of ethanol extract of Chinese propolis (EECP) at 25, 50, 100, and 200 μg/mL was explored by testing the cytotoxicity in MCF‐7 (human breast cancer ER(+)) and MDA‐MB‐231 (human breast cancer ER(−)) cells. EECP revealed a dose‐ and time‐dependent cytotoxic effect. Furthermore, annexin A7 (ANXA7), p53, nuclear factor‐κB p65 (NF‐κB p65), reactive oxygen species (ROS) levels, and mitochondrial membrane potential were investigated. Our data indicated that treatment of EECP for 24 and 48 h induced both cells apoptosis obviously. Exposure to EECP significantly increased ANXA7 expression and ROS level, and NF‐κB p65 level and mitochondrial membrane potential were depressed by EECP dramatically. The effects of EECP on p53 level were different in MCF‐7 and MDA‐MB‐231 cells, which indicated that EECP exerted its antitumor effects in MCF‐7 and MDA‐MB‐231 cells by inducing apoptosis, regulating the levels of ANXA7, p53, and NF‐κB p65, upregulating intracellular ROS, and decreasing mitochondrial membrane potential. Interestingly, EECP had little or small cytotoxicity on normal human umbilical vein endothelial cells (HUVECs). These results suggest that EECP is a potential alternative agent on breast cancer treatment.