包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
5mg | 电议 |
25mg | 电议 |
100mg | 电议 |
500mg | 电议 |
1g | 电议 |
Cell lines | ONL-93 oligodendrocytes |
Preparation Method | Cells were cultured and expanded in DMEM/nutrient mixture F-12, supplemented with 10% FBS and 1% penicillin-streptomycin at 37℃ and 5% CO2. The culture medium was changed every 2 days. The oligodendrocyte (OLN-93 cell line) model of ferroptosis was established using RSL-3 (7.89 μM). |
Reaction Conditions | The cell viability after the treatment with 0, 0.5, 1.5, 2.0, 2.5, 3.0 nM Liproxstatin-1 and the treatment with 0, 0.5, 1.0, 1.5, 2.0 μM were used for the determination of EC50. |
Applications | Liproxstatin-1 could suppress ferroptosis, with an EC50 of 115.3 nM. Liproxstatin-1 displayed the lowest EC50 among these compounds. |
Animal models | Specific-pathogen-free 8-week-old male C57BL/6 mice |
Preparation Method | To establish the animal model, first, the left ureter of mice was exposed and ligated with 4-0 silk sutures, and the ligatures were dissected to prevent retrograde urinary tract infections. The sham operation was executed in a similar manner, but without ureter ligation. Twenty-four C57BL/6 mice were randomly divided into four groups: (1) sham group, (2) Liproxstatin-1 group, (3) UUO group, and (4) UUO + Liproxstatin-1 group. The mice in the Liproxstatin-1 and UUO + Liproxstatin-1 groups were intraperitoneally injected with Liproxstatin-1 for 14 consecutive days after surgery. The mice in the sham and UUO groups were intraperitoneally injected with equal volumes of 0.9% NaCl solution. |
Dosage form | 200 μL Liproxstatin-1 (10 mg/kg/d, dissolved in DMSO and then diluted with 0.9% NaCl) |
Applications | Liproxstatin-1 could reduce the levels of renal iron in the UUO mice. In addition, Liproxstatin-1 treatment could significantly reduce the number of iron-positive cells in the UUO + Liproxstatin-1 group compared with the UUO group. Liproxstatin-1 treatment significantly decreased the GSSG/ GSH ratio in the UUO group. |
文献引用 | |
产品描述 | Liproxstatin-1 is a potent inhibitor of ferroptosis and can protect against ferroptosis-inducing agents, such as buthionine sulfoxamine (BSO), erastin, and (1S,3R)-RSL3 (RSL3). Moreover, Liproxstatin-1 does not interfere with other classical types of cell death, such as TNFα-induced apoptosis and H2O2-induced necrosis. Recently, Liproxstatin-1 has attracted the attentions as it exhibits various kinds of pharmacological activities. For example, Liproxstatin-1 can protect mouse myocardium against ischemia/reperfusion injury; Liproxstatin-1 could alleviate iron overload and attenuates morphine tolerance; Liproxstatin-1 could prevent both RSL3-induced death of primary human renal proximal TECs and GPX4 deletion-induced acute renal failure. Therefore, Liproxstatin-1 inhibits ferroptosis and promotes cell survival.[1]. The in vitro experiment demonstrated that Liproxstatin-1 could suppress ferroptosis, with an EC50 of 115.3 nM. The percentage of PI-positive cells was lower in the Liproxstatin-1 group further proving the anti-ferroptotic effect of Liproxstatin-1 (P < 0.0001). Furthermore, Liproxstatin-1 suppressed mitochondrial lipid peroxidation and increased the levels of GSH compared with the RSL-3 group (P < 0.0001). GPX4 was restored to normal levels by Liproxstatin-1 treatment.[2]. The in vivo experiment indicated that ferroptosis occurred in TECs during UUO-induced renal fibrosis and that Liproxstatin-1 was able to inhibit the ferroptosis. In addition, Liproxstatin-1 was able to prevent the morphological changes and renal function impairment that were induced by UUO in vivo.[1]. References: |