Bog blueberry anthocyanins alleviate photoaging in ultraviolet‐B irradiation‐induced human dermal fibroblasts

Abstract Fruits of bog blueberry ( Vaccinium uliginosum L.) are rich in anthocyanins that contribute pigmentation. Anthocyanins have received much attention as agents with potentials preventing chronic diseases. This study investigated the capacity of anthocyanin‐rich extract from bog blueberry (ATH‐BBe) to inhibit photoaging in UV‐B‐irradiated human dermal fibroblasts. BBe anthocyanins were detected as cyanidin‐3‐glucoside, petunidin‐3‐glucoside, malvidin‐3‐glucoside, and delphinidin3‐glucoside. ATH‐BBe attenuated UV‐B‐induced toxicity accompanying reactive oxygen species (ROS) production and the resultant DNA damage responsible for activation of p53 and Bad. Preincubation of ATH‐BBe markedly suppressed collagen degradation via blunting production of collagenolytic matrix metalloproteinases (MMP). Additionally, ATH‐BBe enhanced UV‐B‐downregulated procollagen expression at transcriptional levels. We next attempted to explore whether ATH‐BBe mitigated the MMP‐promoted collagen degradation through blocking nuclear factor κB (NF‐κB) activation and MAPK‐signaling cascades. UV‐B radiation enhanced nuclear translocation of NF‐κB, which was reversed by treatment with ATH‐BBe. The UV‐B irradiation rapidly activated apoptosis signal‐regulating kinase‐1 (ASK‐1)‐signaling cascades of JNK and p38 mitogen‐activated protein kinase (p38 MAPK), whereas ATH‐BBe hampered phosphorylation of c‐Jun, p53, and signal transducers and activators of transcription‐1 (STAT‐1) linked to these MAPK signaling pathways. ATH‐BBe diminished UV‐B augmented‐release of inflammatory interleukin (IL)‐6 and IL‐8. These results demonstrate that ATH‐BBe dampens UV‐B‐triggered collagen destruction and inflammatory responses through modulating NF‐κB‐responsive and MAPK‐dependent pathways. Therefore, anthocyanins from edible bog blueberry may be protective against UV‐induced skin photoaging.