Abstract
Tanshinone IIA (Tan IIA) is a major compound extracted from a traditional herbal medicine Salvia miltiorrhiza BUNGE, which is used to treat cardiovascular diseases, cerebrovascular diseases and postmenopausal syndrome. It has also been shown to possess anti-inflammatory activity. Since Tan IIA has a similar structure to that of 17β-estradiol (E2), the present study was undertaken to characterize the estrogenic activity of Tan IIA and to demonstrate a functional role of this activity in RAW 264.7 cells. In transient transfection assay, Tan IIA (10 μM) increases ERE-luciferase activity in an estrogen receptor (ER) subtype-dependent manner when either ERα or ERβ were co-expressed in Hela cells. In LPS-induced RAW 264.7 cells, Tan IIA exerts anti-inflammatory effects by inhibition of iNOS gene expression and NO production, as well as inhibition of inflammatory cytokine (IL-1β, IL-6, and TNF-α) expression via ER-dependent pathway. Therefore, it could serve as a potential selective estrogen receptor modulator (SERM) to treat inflammation-associated neurodegenerative and cardiovascular diseases without increasing the risk of breast cancer.
บทคัดย่อTanshinone นอกจากนี้ยังได้รับการแสดงที่จะมีการต่อต้าน- กิจกรรมการอักเสบ ตั้งแต่ตาลไอไอเอมีโครงสร้างคล้ายกับที่ของ β - estradiol (E2) Abstract
Tanshinone IIA (Tan IIA) is a major compound extracted from a traditional herbal medicine Salvia miltiorrhiza BUNGE, which is used to treat cardiovascular diseases, cerebrovascular diseases and postmenopausal syndrome. It has also been shown to possess anti-inflammatory activity. Since Tan IIA has a similar structure to that of 17β-estradiol (E2), the present study was undertaken to characterize the estrogenic activity of Tan IIA and to demonstrate a functional role of this activity in RAW 264.7 cells. In transient transfection assay, Tan IIA (10 μM) increases ERE-luciferase activity in an estrogen receptor (ER) subtype-dependent manner when either ERα or ERβ were co-expressed in Hela cells. In LPS-induced RAW 264.7 cells, Tan IIA exerts anti-inflammatory effects by inhibition of iNOS gene expression and NO production, as well as inhibition of inflammatory cytokine (IL-1β, IL-6, and TNF-α) expression via ER-dependent pathway. Therefore, it could serve as a potential selective estrogen receptor modulator (SERM) to treat inflammation-associated neurodegenerative and cardiovascular diseases without increasing the risk of breast cancer.
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