Protein Information

Name caspase 3
Synonyms Apopain; CASP 3; CASP3; CPP 32; CPP32; CPP32B; Caspase 3; Caspase 3 precursor…

Compound Information

Name sodium azide
CAS sodium azide

Reference List

PubMed Abstract RScore(About this table)
10797567 Chan WH, Yu JS: Inhibition of UV irradiation-induced oxidative stress and apoptotic biochemical changes in human epidermal carcinoma A431 cells by genistein. J Cell Biochem. 2000 Apr;78(1):73-84.


We previously showed that UV irradiation can elicit caspase-3 activation and the subsequent cleavage and activation of p21-activated kinase 2 (PAK2) in human epidermal carcinoma A431 cells.
2(0,0,0,2) Details
14709344 Grammatopoulos TN, Morris K, Bachar C, Moore S, Andres R, Weyhenmeyer JA: Angiotensin II attenuates chemical hypoxia-induced caspase-3 activation in primary cortical neuronal cultures. Brain Res Bull. 2004 Jan 15;62(4):297-303.

Treatment with the caspase-3 inhibitor resulted in a dose-dependent decrease in apoptosis, suggesting that sodium azide-induced apoptosis is mediated through a caspase-3 dependent pathway.
260(2,5,5,10) Details
10879632 Kumi-Diaka J, Butler A: Caspase-3 protease activation during the process of genistein-induced apoptosis in TM4 testicular cells. Biol Cell. 2000 Apr;92(2):115-24.

The overall results from all the data demonstrated that: i) genistein exerts dose- and time-dependent effects on TM4 testis cells; ii) apoptosis is induced by lower concentrations of genistein and necrosis induced by higher concentrations of genistein; iii) genistein induced activation caspase-3 enzymatic activity; iv) genistein-induction of apoptosis and necrosis was significantly inhibited by the caspase-3 inhibitor, z-DEV-FMK; v) sodium azide induced necrosis without activation of CPP32 enzymatic activity, and induction of apoptosis; and vi) genistein-induced apoptosis was associated with activation of CPP32 enzymatic activity in the cells.
85(1,1,1,5) Details
15500948 Ding X, Xu Q, Liu F, Zhou P, Gu Y, Zeng J, An J, Dai W, Li X: Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation. Cancer Lett. 2004 Dec 8;216(1):43-54.

Sodium azide (the singlet oxygen quencher) or D-mannitol (the hydroxyl radical scavenger) could protect HeLa cells from the apoptosis and necrosis induced by HMME-PDT, showing that reactive oxygen species (ROS), such as singlet oxygen and hydroxyl radical, played a decisive role in HMME-PDT-induced HeLa cells death.
Cytochrome C (Cyto C) release from mitochondria into cytosol and Caspase-3 activation after HMME-PDT were inhibited by BAPTA/AM (an intracellular calcium chelator).
2(0,0,0,2) Details
15082229 Cho S, Liu D, Fairman D, Li P, Jenkins L, McGonigle P, Wood A: Spatiotemporal evidence of apoptosis-mediated ischemic injury in organotypic hippocampal slice cultures. Neurochem Int. 2004 Jul;45(1):117-27.

In order to ascertain the existence of the synaptic pool of glutamate, sister cultures were treated with sodium azide.
Further studies revealed a time-dependent activation of caspase 3 following OGD, shown by immunoblot analysis as well as by confocal laser scanning microscopy.
1(0,0,0,1) Details
12954857 Garnier P, Ying W, Swanson RA: Ischemic preconditioning by caspase cleavage of poly (ADP-ribose) polymerase-1. J Neurosci. 2003 Sep 3;23(22):7967-73.


Preconditioning also produced an increase in activated caspase-3 peptide and an increase in caspase-3 activity in the cortical cultures.
1(0,0,0,1) Details
10597238 Suzuki S, Higuchi M, Proske RJ, Oridate N, Hong WK, Lotan R: Implication of mitochondria-derived reactive oxygen species, cytochrome C and caspase-3 in N-(4-hydroxyphenyl) retinamide-induced apoptosis in cervical carcinoma cells. Oncogene. 1999 Nov 4;18(46):6380-7.

2(0,0,0,2) Details
10764744 Bai J, Cederbaum AI: Overexpression of catalase in the mitochondrial or cytosolic compartment increases sensitivity of HepG2 cells to tumor necrosis factor-alpha-induced apoptosis. J Biol Chem. 2000 Jun 23;275(25):19241-9.

The activities of caspase-3 and -8 were increased by TNF-alpha, with the highest activities found in mC5 cells.
Sodium azide, an inhibitor of catalase, reduced the increased sensitivity of mC5 and C33 cells to TNF-alpha to the level of toxicity found with control Hp cells.
2(0,0,0,2) Details
20032508 Endale M, Kim SD, Lee WM, Kim S, Suk K, Cho JY, Park HJ, Wagley Y, Kim S, Oh JW, Rhee MH: Ischemia induces regulator of G protein signaling 2 (RGS2) protein upregulation and enhances apoptosis in astrocytes. Am J Physiol Cell Physiol. 2010 Mar;298(3):C611-23. Epub 2009 Dec 23.

It significantly increased annexin V-positive cells, cleaved caspase-3, and enhanced DNA ladder formation and cell cycle arrest.
A marked increase in RGS2 occurred after ischemic stress induced by chemicals (sodium azide and 2-deoxyglucose) or oxygen-glucose deprivation (OGD, real ischemia).
2(0,0,0,2) Details
20036216 Hur J, Lee P, Kim MJ, Kim Y, Cho YW: Ischemia-activated microglia induces neuronal injury via activation of gp91phox NADPH oxidase. Biochem Biophys Res Commun. 2010 Jan 15;391(3):1526-30. Epub 2009 Dec 28.


MCM-treated SH-SY5Y cells showed reduced the viability, increased caspase-3 activity, decreased Bcl-2/Bax ratio, and increased cytochrome c release, increased inflammatory cytokines, and increased reactive oxygen species (ROS) generation.
1(0,0,0,1) Details
17531242 Nabata A, Kuroki M, Ueba H, Hashimoto S, Umemoto T, Wada H, Yasu T, Saito M, Momomura S, Kawakami M: C-reactive protein induces endothelial cell apoptosis and matrix metalloproteinase-9 production in human mononuclear cells: Implications for the destabilization of atherosclerotic plaque. Atherosclerosis. 2008 Jan;196(1):129-35. Epub 2007 May 24.

However, recent in vitro studies raised the possibility that the effects of CRP are caused by biologically active contaminants such as sodium azide and endotoxin.
In human endothelial cells, CRP significantly inhibited cell proliferation and increased endothelial cell apoptosis evaluated by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and caspase-3 activity assay, which is reversed by a function-blocking antibody to Fc gamma RIIIB by 78%.
1(0,0,0,1) Details
14578187 Heilig C, Brosius F, Siu B, Concepcion L, Mortensen R, Heilig K, Zhu M, Weldon R, Wu G, Conner D: Implications of glucose transporter protein type 1 (GLUT1)-haplodeficiency in embryonic stem cells for their survival in response to hypoxic stress. Am J Pathol. 2003 Nov;163(5):1873-85.


Caspase-3 activity was 76% higher in GT1 (+/-) versus GT1 (+/+) at 2 hours.
1(0,0,0,1) Details
18948185 Woo HD, Kim BM, Kim YJ, Lee YJ, Kang SJ, Cho YH, Choi JY, Chung HW: Quercetin prevents necrotic cell death induced by co-exposure to benzo (a) pyrene and UVA radiation. Toxicol In Vitro. 2008 Dec;22(8):1840-5. Epub 2008 Oct 7.


Intracellular reactive oxygen species (ROS) levels were increased significantly in the co-exposed cells, and treatment with the polyphenol quercetin, but not with sodium azide or N-acetylcysteine, decreased ROS levels and increased cell viability in BaP/UVA-treated cells.
0(0,0,0,0) Details