AKBA (3-acetyl-11-keto-β-Boswellic Acid) is a pentacyclic triterpene acid that effectively and non-competitively inhibits 5-lipoxygenase (5-LOX), exhibiting various biological activities including anti-inflammatory, antitumor, and neuroprotective effects[1, 2]. AKBA can inhibit the NF-κB signaling pathway and also acts as an Nrf2/HO-1 activator[3, 4].
In vitro, pretreatment of human lens epithelial cells (HLECs) with AKBA (2, 8μM) for 1h significantly reduced H2O2-induced apoptosis and oxidative damage, significantly decreased intracellular caspase-3 and Bax expression, and increased Bcl-2 expression[5]. Treatment of MCF-7 cells with AKBA (50, 100, 200µg/mL) for 24h dose-dependently inhibited cell viability, reduced cell colony formation ability, and induced apoptosis and cell cycle arrest[6].
In vivo, AKBA (100mg/kg) significantly reduced the volume and weight of subcutaneous xenograft tumors in mice after oral treatment for 14 days with U87-MG glioblastoma cells[7].
References:
[1] Gong Y, Jiang X, Yang S, et al. The biological activity of 3-O-acetyl-11-keto-β-boswellic acid in nervous system diseases[J]. Neuromolecular medicine, 2022, 24(4): 374-384.
[2] Park Y S, Lee J H, Harwalkar J A, et al. Acetyl-11-Keto-ß-Boswellic acid (Akba) is cytotoxic for meningioma cells and inhibits phosphorylation of the extracellular-signal regulated kinase 1 and 2[M]//Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 5. Boston, MA: Springer US, 2002: 387-393.
[3] Lv M, Shao S, Zhang Q, et al. Acetyl-11-Keto-β-Boswellic acid exerts the anti-cancer effects via cell cycle arrest, apoptosis induction and autophagy suppression in non-small cell lung cancer cells[J]. OncoTargets and therapy, 2020: 733-744.
[4] Minj E, Upadhayay S, Mehan S. Nrf2/HO-1 signaling activator acetyl-11-keto-beta boswellic acid (AKBA)-mediated neuroprotection in methyl mercury-induced experimental model of ALS[J]. Neurochemical research, 2021, 46(11): 2867-2884.
[5] Yang T, Lin X, Li H, et al. Acetyl-11-keto-beta boswellic acid (AKBA) protects lens epithelial cells against H2O2-induced oxidative injury and attenuates cataract progression by activating Keap1/Nrf2/HO-1 signaling[J]. Frontiers in Pharmacology, 2022, 13: 927871.
[6] Ahmed S A, Al-Shanon A F, Al-Saffar A Z, et al. Antiproliferative and cell cycle arrest potentials of 3-O-acetyl-11-keto-β-boswellic acid against MCF-7 cells in vitro[J]. Journal of Genetic Engineering and Biotechnology, 2023, 21(1): 75.
[7] Li W, Liu J, Fu W, et al. 3-O-acetyl-11-keto-β-boswellic acid exerts anti-tumor effects in glioblastoma by arresting cell cycle at G2/M phase[J]. Journal of Experimental & Clinical Cancer Research, 2018, 37(1): 132.
AKBA (3-acetyl-11-keto-β-Boswellic Acid)是一种五环三萜酸，能够有效地非竞争性地抑制5-脂氧合酶（5-lipoxygenase, 5-LOX），具有抗炎、抗肿瘤、神经保护等多种生物活性[1, 2]。AKBA能够抑制NF-κB信号通路，还能够作为一种Nrf2/HO-1激活剂[3, 4]。
在体外，AKBA（2, 8μM）预处理人晶状体上皮细胞（HLECs）1h，显著减轻了H2O2诱导的细胞凋亡和氧化损伤，显著降低了细胞内caspase-3和Bax的表达，升高了Bcl-2的表达[5]。AKBA（50, 100, 200µg/mL）处理MCF-7细胞24h，以剂量依赖性方式抑制了细胞活力，降低了细胞克隆形成能力，诱导了细胞凋亡和细胞周期阻滞[6]。
在体内，AKBA（100mg/kg）通过口服治疗U87-MG胶质母细胞瘤细胞异种移植小鼠14天，显著降低了小鼠皮下异种移植瘤的体积和重量[7]。