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The anti‐osteoclastic effect of rosemary ethanol extract is due to the down‐regulation of ROS level via NADPH oxidase1 and Nrf2 signal pathway by carnosic acid
Author(s) -
Lee SangHyun,
Lee DaeKun,
Jang HaeDong
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.03397
Subject(s) - carnosic acid , chemistry , rankl , rosmarinus , osteoclast , bone resorption , acid phosphatase , officinalis , biochemistry , viability assay , antioxidant , pharmacology , apoptosis , endocrinology , botany , biology , activator (genetics) , enzyme , essential oil , in vitro , gene , chromatography
Rosmarinus officinalis , commonly known as rosemary, is a woody, perennial herb which belongs to the mint family and wildly used in the fields of medicine and daily‐use chemical industry. The anti‐osteoclastic effect of rosemary ethanol extract (REE) was investigated using tartrate acid resistant phosphatase (TRAP) activity, bone resorption assay and western blot analysis in RANKL‐induced RAW264.7 cell. REE dose‐dependently inhibited TRAP‐positive multinucleated osteoclasts formation and bone resorption between 1 µg/mL and 20 µg/mL. In addition, REE attenuated RANKL‐induced cathepsin K and NFATc1 expression in a dose‐dependent manner. The major bioactive constituents of REE are carnosol and carnosic acid(CA). The anti‐osteoclastic effect of CA was stronger than that of carnosol and the potent suppressive effect of CA on ROS was shown by only carnosic acid. The suppressive effect of CA on ROS and O 2 • level was dose‐dependently increased between 1 and 20 μM. Furthermore, CA attenuated the translocation of Nox1 activated factor, p47phox, to the membrane and abolished RANKL‐induced ROS generation by activating Nrf2 and its transcriptional targets. These results indicate that the inhibitory effect of REE on RANKL‐induced osteoclastogenesis may be attributed to the maintenance of redox homeostasis by CA through regulation of ROS production and scavenging.