Ac-DEVD-CHO

Ac-DEVD-CHO
Cat. No. : CS-7676 CAS No. : 169332-60-9
M. Wt. : 502.47
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  • Data Sheet

  • Introduction

  • SDS

  • COA & Spectra

Name: Ac-DEVD-CHO; N-Acetyl-Asp-Glu-Val-Asp-al
Cat. No. : CS-7676
CAS No. : 169332-60-9
Formula: C20H30N4O11
M. Wt. : 502.47
Solubility: DMSO

Activity:

Ac-DEVD-CHO is a specific caspase-3 inhibitor with Ki of 230 pM. IC50 & Target: Ki: 230 pM (caspase-3)[1]. In Vitro: To ascertain the role of caspase-3 in SLNT-induced apoptosis, a caspase-3 inhibitor (Ac-DEVD-CHO) is used. HT-29 cells are pre-incubated with Ac-DEVD-CHO (25 μM) for 1 h before the addition of SLNT (800 μg/mL). The addition of Ac-DEVD-CHO significantly prevent SLNT-induced apoptosis (from 32.91±1.21% decreased to 15.88±1.58% while NC and Ac-DEVD-CHO group are 6.45±0.96%, 7.77±0.79%, respectively)[2]. To investigate whether apoptosis induced by hypericin-mediated PDT dependent on the activation of capases, SP2/0 cells are pretreated with the 100 μM pan-caspase inhibitor (Z-VAD-FMK) or 100 μM caspase-3 inhibitor (Ac-DEVD-CHO) for 1 h. The apoptosis rate of cells pretreate with zVAD-fmk (5.32%) or Ac-DEVD-CHO (7.43%) decrease obviously after hypericin- mediate PDT treatment[3].Remarkably, 10 μmol/L Ac-DEVD-CHO partially block the effect of SIN-induced apoptosis and reduce the number of apoptotic nuclei. These effects of SIN are blocked by the caspase-3 inhibitor Ac-DEVD-CHO. Camptothecin (4 μM), a positive control, increase caspase-3 activity, which is also blocked by Ac-DEVD-CHO [4]. In Vivo: Compare with model group, in CI group, the concentrations of serum BUN are decreased significantly at all time points after operation and those of Cr are decreased significantly at 6 hours, then restore to those of the sham group at 12 hours and 24 hours; the concentrations of serum TNF-α, IL-6 are decreased and those of IL-10 elevated significantly at all time points [TNF-α (μg/L) 6 hours: 436.2±64.2 vs. 653.6±8.9, 12 hours: 233.4±85.4 vs. 579.7±137.1, 24 hours: 151.0±90.3 vs. 551.0±119.8; IL-6 (μg/L) 6 hours: 1 033.2±345.8 vs. 1 595.3±159.4, 12 hours : 366.3±68.3 vs. 1 330.7±249.8, 24 hours: 241.2±208.4 vs. 815.3±572.7; IL-10 (μg/L) 6 hours : 33.6±10.4 vs. 26.6±4.5, 12 hours: 37.2±5.0 vs. 24.5±4.3, 24 hours: 38.3±5.5 vs. 18.2±1.6, all P<0.05]; the renal cell apoptosis rate and the expression of caspase-3 mRNA are decreased significantly at all time points [apoptosis rates 6 hours: (13.9±3.2)% vs. (18.3±1.4)%, 12 hours: (10.5±3.6)% vs. (15.9±3.5)%, 24 hours: (8.4±1.8)% vs. (12.5±2.1)%; caspase-3 mRNA 6 hours: 1.95±0.16 vs. 3.84±0.35, 12 hours: 1.89±0.19 vs. 3.97±0.73, 24 hours : 2.01±0.20 vs. 4.97±0.24, all P<0.05]. The 4-day survival rate of CI group is improved (80% vs. 20%)[5].

Protocol:

Cell Assay: [4]OCLs are incubated with RANKL and treated with 0.5 mM SIN with or without the specific caspase-3 inhibitor Ac-DEVD-CHO (10 μM) for 24 h. At the end of the treatment, the cells are washed with PBS and are stained for 15 min with 10 μM Hoechst 33258 dye. Images of the stained cells are captured with a fluorescent microscope. The differences are evaluated by counting the number of cells with apoptotic nuclear condensation in each well[4]. Animal Administration: [5]One hundred and two male C57BL/6 mice are subjected to cecal ligation and puncture (CLP, a model of polymicrobial sepsis) or sham operation. The animals are assigned into three equal groups (n=34) according to random number table: sham group, model group, and caspase-3 inhibitor (CI) group. Thirty minutes before CLP, Ac-DEVD-CHO (4 μg/g) is injected subcutaneously in CI group. The levels of blood urea nitrogen (BUN) and creatinine (Cr) are determined, and the concentrations of tumor necrosis factor-α (TNF-α), interleukins (IL-6 and IL-10) are measured by enzyme linked immunosorbent assay (ELISA), the renal cell apoptosis rate is determined by flow cytometry and the expression of caspase-3 mRNA is determined by real time reverse transcription-polymerase chain reaction (RT-PCR) at 6, 12 and 24 hours after operation. The 4-day and 7-day survival rates of three groups of mice are observed[5].

References:

Liu LX, et al. The effect of caspase-3 inhibitor on the concentrations of serum inflammatory cytokines in sepsis related acute kidney injury induced by peritoneal cavity infection in mice. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2010 Dec;22(12):736-9.

Jinglin Wang, et al. A polysaccharide from Lentinus edodes inhibits human colon cancer cell proliferation and suppresses tumor growth in athymic nude mice. Oncotarget. 2017 Jan 3; 8(1): 610–623. doi: 10.18632/oncotarget.13481

Garcia-Calvo M, et al.nhibition of human caspases by peptide-based and macromolecular inhibitors. J Biol Chem. 1998 Dec 4;273(49):32608-13.

Junping Zhang, et al. Hypericin-mediated photodynamic therapy induces apoptosis of myoloma SP2/0 cells depended on caspase activity in vitro. Cancer Cell Int. 2015; 15: 58 doi: 10.1186/s12935-015-0193-1

Long-gang He, et al. Sinomenine induces apoptosis in RAW 264.7 cell-derived osteoclasts in vitro via caspase-3 activation. Acta Pharmacol Sin. 2014 Feb; 35(2): 203–210. doi: 10.1038/aps.2013.139

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