D-Allose is an ultra-low-calorie aldohexose that exhibits cryoprotective function on cell survival during freezing [1]. D-Allose protects mouse hippocampal HT-22 cells from oxygen-glucose deprivation and reperfusion (OGD/R) -induced injury by inhibiting the Gal-3/TLR4 signalling pathway [2]. D-Allose has been widely used to inhibit the proliferation of a variety of cancer cells and prevent cancer cells from taking up glucose[3].
In vitro, D-Allose treatment for 48 hours significantly inhibited the viability of MIA PaCa-2 cells with an IC50 value of 53.25mM[4]. Treatment of cells with 40mM D-Allose for 48 hours inhibited the growth of PC-3 cells, induced apoptosis, and caused cell cycle arrest[5]. Treatment of RT112 cells with 50mM D-Allose for 24h inhibited cell viability, induced intracellular reactive oxygen species (ROS) production, and stimulated TXNIP expression[6].
In vivo, D-Allose treatment via intraperitoneal injection at a dose of 100mg/kg/day for 28 days significantly reduced tumor volume in a subcutaneous U87MG cell xenograft mouse model [7]. Intravenous administration of 0.4mg/g D-Allose 1 hour before ischemia significantly inhibited apoptosis, reduced blood brain barrier (BBB) permeability, and decreased inflammatory cytokine levels in the mice model of middle cerebral artery occlusion and reperfusion (MCAO/Rep) [8].
References:
[1] Chen Z, Chen J, Zhang W, et al. Recent research on the physiological functions, applications, and biotechnological production of D-allose[J]. Applied microbiology and biotechnology, 2018, 102(10): 4269-4278.
[2] Huang Y, Thonusin C, Tokuda M, et al. The beneficial effects of D-allose and D-allulose on the brain under ischemic stroke and obese-insulin resistant conditions: evidence from in vitro to clinical studies[J]. Metabolic Brain Disease, 2025, 40(4): 1-15.
[3] Noguchi C, Kamitori K, Hossain A, et al. D-allose inhibits cancer cell growth by reducing GLUT1 expression[J]. The Tohoku journal of experimental medicine, 2016, 238(2): 131-141.
[4] Malm S W, Hanke N T, Gill A, et al. The anti-tumor efficacy of 2-deoxyglucose and D-allose are enhanced with p38 inhibition in pancreatic and ovarian cell lines[J]. Journal of Experimental & Clinical Cancer Research, 2015, 34(1): 31.
[5] Naha N, Lee H Y, Jo M J, et al. Rare sugar D-allose induces programmed cell death in hormone refractory prostate cancer cells[J]. Apoptosis, 2008, 13(9): 1121-1134.
[6] Tohi Y, Taoka R, Zhang X, et al. Antitumor effects of orally administered rare sugar D-allose in bladder cancer[J]. International Journal of Molecular Sciences, 2022, 23(12): 6771.
[7] Suzuki K, Ogawa D, Kanda T, et al. Antiproliferative effects of D-allose associated with reduced cell division frequency in glioblastoma[J]. Scientific Reports, 2023, 13(1): 19515.
[8] Huang T, Gao D, Hei Y, et al. D-allose protects the blood brain barrier through PPARγ-mediated anti-inflammatory pathway in the mice model of ischemia reperfusion injury[J]. Brain research, 2016, 1642: 478-486.
D-Allose是一种超低热量的醛己糖，在冷冻过程中对细胞存活具有冷冻保护功能[1]。D-Allose通过抑制Gal-3/TLR4信号通路，保护小鼠海马HT-22细胞免受氧糖剥夺/再灌注（OGD/R）诱导的损伤[2]。D-Allose已被广泛用于抑制多种癌细胞的增殖并阻止癌细胞摄取葡萄糖[3]。
在体外，D-Allose处理48小时显著抑制了MIA PaCa-2细胞的活力，IC50值为53.25 mM[4]。使用40 mM D-阿洛糖处理细胞48小时，抑制了PC-3细胞的生长，诱导了细胞凋亡，并引起细胞周期阻滞[5]。使用50mM的D-Allose处理RT112细胞24小时，抑制了细胞活力，诱导了细胞内活性氧（ROS）的产生，并刺激了TXNIP的表达[6]。
在体内，每日腹腔注射100mg/kg剂量的D-Allose，持续28天，显著降低了皮下U87MG细胞异种移植小鼠模型中的肿瘤体积[7]。在缺血前1小时静脉注射0.4mg/g剂量的D-Allose，显著抑制了小鼠大脑中动脉闭塞/再灌注（MCAO/Rep）模型中的细胞凋亡，降低了血脑屏障（BBB）通透性，并减少了炎症细胞因子水平[8]。