3-O-Acetyl-α-boswellic acid (Aαba) is a pentacyclic triterpene extracted from the gum resin of genus Boswellia and has been shown to have analgesic, anti-arthritic, anti-inflammatory, and anti-cancer effects. A 2-day exposure of young human skin fibroblasts (passage 8) with 1 µM Aαba significantly increased cell survival and metabolic activity compared to non-treated cells. However, Aαba at the doses of 50 - 100 µM resulted in a dose-dependent inhibitory effect on MTT activity and reached almost 100% toxicity at 100 µM. In near-senescent cells (passage 51), Aαba at high concentration (75 and 100 µM) suppressed the MTT activity to a lesser extent compared with the young cells. In replicatively senescent cells (passage 58), treatment with 1 μM Aαba morphologically rejuvenated late passage cells. The exposure of early passage cells (passage 14) with 1 µM Aαba for 24 h resulted in downregulated the expressions of CCNH, CDKN1B, CDKN2A, E2F3, CCNE1, HDAC1, cyclin D1, CDKN1A, cyclin dependent kinase 7, and transforming growth factor beta 2, and upregulated CDKN2C and CDKN1A levels as compared to cells at late passage[1]. Treatment of monocytes with AαBA (1 - 10µM) inhibited LPS-induced expression of TNF-α in a dose-dependent manner. In HEK293 cells transiently transfected with pNFκB-Luc vector and stimulated with TNF-α (100 ng/mL), a pretreatment with AαBA at 10 µM inhibited NF-κB activation by 40.9 ± 9.8%. AαBA at 10 µM also significantly abolished the nuclear localization of p65 in LPS-stimulated monocytes[2].
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