Phenolamide and flavonoid glycoside profiles of 20 types of monofloral bee pollen.

This study aimed at investigating phenolamides and flavonoid glycosides in 20 types of monofloral bee pollen. The plant origins of pollen samples were determined by DNA barcoding, with the purities to over 70 %. The 31 phenolamides and their 33 cis/trans isomers, and 25 flavonoid glycosides were identified; moreover, 19 phenolamides and 14 flavonoid glycosides as new-found compounds in bee pollen. All phenolics and flavonoids are present in the amidation or glycosylation form. The MS/MS cleavage modes of phenolamides and flavonoid glycosides were summarized. Isorhamnetin-3-O-gentiobioside presented the highest levels 23.61 mg/g in apricot pollen. Phenolamides in 11 types of pollen constituted over 1 % of the total weight, especially 3.9 % in rose and 2.8 % in pear pollen. Tri-p-coumaroyl spermidine and di-p-coumaroyl-caffeoyl spermidine respectively accounted for over 2.6 % of the total weight in pear and rose pollen. The richness in phenolamides and flavonoid glycosides can offer bee pollen more bioactivities as functional foods.

Phenolic Compounds of Propolis Alleviate Lipid Metabolism Disorder.

Lipid metabolism disorder is one of the significant risk factors for a multitude of human diseases and has become a serious threat to human health. The present study aimed to evaluate the effects of phenolics from poplar-type propolis on regulating lipid metabolism by using cell models of steatosis induced by palmitic acid (PA). Our study shows that phenolic esters have higher lipid-lowering activities than phenolic acids, especially for three caffeic acid esters, including caffeic acid phenethyl ester (CAPE), caffeic acid cinnamyl ester (CACE), and caffeic acid benzyl ester (CABE). Most notably, CACE presents prominent properties to prevent intracellular lipid accumulation and to amend extracellular adipokine secretion abnormalities. In addition, our results firstly reveal that CACE can alleviate lipid metabolism disorder through mediating protein kinase RNA-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6) signaling pathway-associated protein expression, suppressing endoplasmic reticulum (ER) stress, and activating peroxisome proliferator-activated receptors (PPARs) by distinct upregulation of PPARα and downregulation of PPARγ.