Search results for: Caspase 4 Fluorometric Assay Kit
#36549173 2022/12/19 To Up
Acute ATP loss during irreversible electroporation mediates caspase independent cell death.
Irreversible electroporation (IRE) has been reported to variably cause apoptosis, necrosis, oncosis or pyroptosis. Intracellular ATP is a key substrate for apoptosis which is rapidly depleted during IRE, we sought to understand whether intracellular ATP levels is a determinant of the mode of cell death following IRE. A mouse bladder cancer cell line (MB49) was treated with electric fields while increasing the number of pulses at a fixed electric field strength, and pulse width. Cell proliferation and viability and ATP levels were measured at different timepoints post-treatment. Cell death was quantified with Annexin-V/Propidium Iodide staining. Caspase activity was measure with a fluorometric kit and western blotting. A pan-caspase (Z-VAD-FMK) inhibitor was used to assess the impact of signal inhibition. We found cell death following IRE was insensitive to caspase inhibition and was correlated with ATP loss. These findings were confirmed by cell death assays and measurement of changes in caspase expression on immunoblotting. This effect could not be rescued by ATP supplementation. Rapid and acute ATP loss during IRE interferes with caspase signaling, promoting necrosis. Cell necrosis from IRE is expected to be immunostimulatory and may be effective in cancer cells that carry mutated or defective apoptosis genes.Leo Razakamanantsoa, Neeraj R Rajagopalan, Yasushi Kimura, Michele Sabbah, Isabelle Thomassin-Naggara, François H Cornelis, Govindarajan Srimathveeravalli
1879 related Products with: Acute ATP loss during irreversible electroporation mediates caspase independent cell death.
100ug Lyophilized1 kit100 Tests100 tests100ug Lyophilized1 kit25 Tests100ug Lyophilized100ug Lyophilized1 kit1 kit100 testsRelated Pathways
#33999319 2021/05/17 To Up
Debio-0932, a second generation oral Hsp90 inhibitor, induces apoptosis in MCF-7 and MDA-MB-231 cell lines.
Heat shock protein 90 (Hsp90) is a key chaperone that is abnormally expressed in cancer cells, and therefore, designing novel compounds to inhibit chaperone activities of the Hsp90 is a promising therapeutic approach for cancer drug discovery. Debio-0932 is a second-generation Hsp90 inhibitor that exhibited promising anticancer activity against a wide variety of cancer types with a strong binding affinity for Hsp90 and high oral bioavailability. Anticancer activities of the Debio-0932 were tested in MCF-7 and MDA-MB-231 cell lines. Molecular docking results indicated that Debio-0932 was selectively bound to the ATP binding pocket of the Hsp90 with an estimated free energy of binding - 7.24 kcal/mol. Antiproliferative activity of Debio-0932 was determined by XTT assay and Debio-0932 exhibited a cytotoxic effect on MCF-7 and MDA-MB-231 cells in a time and dose-depended manner. Apoptosis inducer role of Debio-0932 was evaluated in MCF-7 and MDA-MB-231 cells with fluorometric apoptosis/necrosis detection kit. Treatment with Debio-0932 stimulated apoptosis in both breast cancer cell lines. mRNA and protein expression levels of Bax, Bcl-2 and Casp-9 were determined in MCF-7 and MDA-MB-231 cells by RT-PCR and Western blotting respectively. Debio-0932 stimulated the down-regulation of anti-apoptotic protein Bcl-2 and the up-regulation of apoptotic protein Bax and cleavage of Casp-9 in cancer cells. Moreover, the anti-invasive potential of Debio-0932 was evaluated in endothelial cells (HUVEC) by wound-healing assay. Debio-0932 decreased the migration of HUVEC cells as compared to the control group. These results indicate that Debio-0932 is a promising compound to treat triple-negative breast cancer and hormone receptor-positive breast cancer, and their metastases.Aykut Özgür, Altan Kara, Nazan Gökşen Tosun, Şaban Tekin, İsa Gökçe
1399 related Products with: Debio-0932, a second generation oral Hsp90 inhibitor, induces apoptosis in MCF-7 and MDA-MB-231 cell lines.
100 5mg100ug Lyophilized100 assays20 ul100 ug5 mg100 assays25 mg1 SetRelated Pathways
#32322173 2020/04/16 To Up
Herbal melanin inhibits colorectal cancer cell proliferation by altering redox balance, inducing apoptosis, and modulating MAPK signaling.
Colorectal carcinoma is one of the most deadly cancers that requests effective and safe chemotherapy. Evaluation of natural product-based anticancer drugs as adjuvant treatment with fewer side effects is largely unexplored research fields. Herbal melanin (HM) is an extract of the seed coats of that modulates an inflammatory response through toll-like receptor 4 (TLR4). This TLR4 receptor is also involved in the modulation of apoptosis. We therefore explored the anticancer potential of HM and specifically its effect on the molecular mechanisms underlying adenocarcinoma and metastatic colorectal cancer (mCRC) cell death in vitro.Omar Al-Obeed, Adila Salih El-Obeid, Sabine Matou-Nasri, Mansoor-Ali Vaali-Mohammed, Yazeid AlHaidan, Mohammed Elwatidy, Hamad Al Dosary, Zeyad Alehaideb, Khayal Alkhayal, Adil Haseeb, James McKerrow, Rehan Ahmad, Maha-Hamadien Abdulla
1207 related Products with: Herbal melanin inhibits colorectal cancer cell proliferation by altering redox balance, inducing apoptosis, and modulating MAPK signaling.
100 ml.25 ml.100 ug100ug Lyophilized0.5 mg100 Tests100 Tests0.5 mg100ug LyophilizedRelated Pathways
#30417434 2018/11/11 To Up
Adenosine protects pancreatic beta cells against apoptosis induced by endoplasmic reticulum stress.
Chronic exposure to high glucose induces endoplasmic reticulum (ER) stress in pancreatic beta cells (PBCs). The previous evidence showed that adenosine modulate PBCs viability and insulin secretion. The aim of this study was to evaluate possible involvement of adenosine in protection of MIN6 β-cells from Tunicamycin (Tu)-induced ER stress. MIN6 cells were cotreated with Tu and different concentrations of adenosine. Cell viability, proliferation, and apoptosis were evaluated using 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), 5-bromo-2'-deoxyuridine (Brdu), and colony formation assays. Caspase-12 activity was assayed using the fluorometric method. Thioflavin T (ThT) staining was used for the evaluation of protein aggregation. Insulin secretion was evaluated using specific an ELISA kit. Ca mobilization assayed using Fura2/AM probe. BIP, CHOP, XBP-1, and XBP-1s expression in both messenger RNA (mRNA) and protein levels were evaluated using the reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. Bcl-2, p-eIF2α/eIF2α, and GADD34 levels also determined with Western blot analysis. Adenosine protected MIN6 cells against Tu-induced ER stress in a dose-dependent manner and increased their proliferation. Decreased caspase-12 activity and upregulated Bcl-2 protein may explain antiapoptotic effects of adenosine. ThT staining indicated an attenuated aggregation of misfolded proteins. Adenosine effectively increased insulin secretion in Tu-treated cells. BIP, CHOP, XBP1, and sXBP1 expression were decreased significantly in cotreated cells, indicating alleviation of ER stress. However, adenosine potentiated the expression of GADD34 and decreased p-eIF2α/eIF2α ratio. Adenosine increased cytosolic Ca levels, which may promote adenosine triphosphate (ATP) synthesis in mitochondria, helping ER to preserve protein hemostasis. Taken together, adenosine upregulated Bcl-2 and GADD34 to protect PBCs against Tu-induced apoptosis and increase Insulin secretion.Mohammad Keyvanloo Shahrestanaki, Fatemeh Panahi Arasi, Mahmoud Aghaei
1734 related Products with: Adenosine protects pancreatic beta cells against apoptosis induced by endoplasmic reticulum stress.
100ul250 0.25 mL96 tests1.00 flask 100ul 100 UG0.1 mg25ml 5 GRelated Pathways
#28578345 2017/06/05 To Up
Calcium Channel Opening Rather than the Release of ATP Causes the Apoptosis of Osteoblasts Induced by Overloaded Mechanical Stimulation.
Stress fracture is one of the most common overuse injuries in athletes. Overloaded mechanical stimulation is an important factor affecting stress fractures, but the mechanism is unclear.Lu Liu, Hui Li, Ying Cui, Ruixin Li, Fan Meng, Zi Ye, Xizheng Zhang
2356 related Products with: Calcium Channel Opening Rather than the Release of ATP Causes the Apoptosis of Osteoblasts Induced by Overloaded Mechanical Stimulation.
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#27434554 // To Up
[Effects of autophagy on lipopolysaccharide-induced vascular hyper-permeability].
To investigate the effects of autophagy on lipopolysaccharide (LPS)-induced vascular hyper-permeability.Shengbiao Wang, Shuang Yin, Yunfeng Li, Cuiling Li, Tao Li, Youtan Liu
1035 related Products with: [Effects of autophagy on lipopolysaccharide-induced vascular hyper-permeability].
1 mg50 ul96T 25 ml Ready-to-use 25 MG2ug96T 6 ml 2 ml 100ug400 ugRelated Pathways
#27260571 2016/04/12 To Up
The effects of the antioxidant α-tocopherol succinate on cisplatin-induced ototoxicity in HEI-OC1 auditory cells.
D-α-tocopherol succinate significantly reduced a cisplatin-induced hair cell loss in HEI-OC1 cell lines. These effects were mediated by its scavenging activity against reactive oxygen species (ROS) and inhibition of apoptosis.Sung Kyun Kim, Gi Jung Im, Yun Suk An, Se Hee Lee, Hak Hyun Jung, Sang Yoo Park
2161 related Products with: The effects of the antioxidant α-tocopherol succinate on cisplatin-induced ototoxicity in HEI-OC1 auditory cells.
1400 ug11mgRelated Pathways
#26314451 // To Up
[Protective Effect of Ulinastatin against Activation of Tourniquet-Induced Platelet Mitochondria Apoptotic Signaling].
To investigate the protective effect of ulinastatin against the activation of tourniquet-induced platelet mitochondria apoptotic signaling.Chun-Yan Xie, Jin-Fang Xiao, Zhen-Long Zhao
2378 related Products with: [Protective Effect of Ulinastatin against Activation of Tourniquet-Induced Platelet Mitochondria Apoptotic Signaling].
100ug100ug 5 G200 1.00 flask50 ul100ug25 assays1 mg1 kit0.05 mg96 assaysRelated Pathways
#22963151 // To Up
Involvement of endoplasmic reticulum stress in isoliquiritigenin-induced SKOV-3 cell apoptosis.
Isoliquiritigenin (ISL), a licorice chalconoid, is a bioactive agent with chemopreventive potential that has been patented for tumor treatment in China. This study investigated the mechanisms of ISL-induced apoptosis in ovarian carcinoma SKOV-3 cells. Cell viability was evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. The apoptotic rate was determined via flow cytometry using an annexin V-FITC apoptosis detection kit. The intracellular reactive oxygen species (ROS) levels were assessed using a 2,7-dichlorofluorescein probe assay. Malondialdehyde (MDA) formation was determined via thiobarbituric acid reactive substance test. The expressions of growth arrest and DNA damage-inducible gene (GADD153/CHOP), 78 kDa glucose-regulated protein (GRP 78), α-subunit of eukaryotic initiation factor 2 (eIF2α) phosphorylation, activating transcription factor 6α (ATF6α), and unspliced form of X-box binding protein1 (XBP1U) were analyzed via Western blot. Caspase-3 and caspase-12 activities were assessed using a fluorometric kit. Findings indicate that ISL significantly inhibits SKOV-3 cell proliferation, increases intracellular ROS levels, and causes SKOV-3 cell apoptosis. Moreover, ISL-exposed SKOV-3 cells trigger endoplasmic reticulum (ER) stress, as indicated by the enhancement of ER stress-related molecules p-eIF2α, GADD153/CHOP, GRP78, XBP1 expression, and cleavage of ATF6α. However, caspase-12 inhibitor (Z-ATAD) effectively and partially prevents ROS and MDA formation and inhibits ISL-induced SKOV-3 cell apoptosis. ISL induces apoptosis via ER stress-triggered signaling pathways in SKOV-3 cells. ER stress-induced cancer cell apoptosis has been discussed in some patents.Xuan Yuan, Bacui Yu, Yanming Wang, Jiangtao Jiang, Liangliang Liu, Hong Zhao, Wang Qi, Qiusheng Zheng
1705 related Products with: Involvement of endoplasmic reticulum stress in isoliquiritigenin-induced SKOV-3 cell apoptosis.
96 assays400 ug 100ul400 ug1 mg1 mg25 g500 ml5 x 2 ml1 kit30ml1x10e7 cellsRelated Pathways
#22741020 2012/01/09 To Up
DMSO exhibits similar cytotoxicity effects to thalidomide in mouse breast cancer cells.
The purpose of this study was to evaluate the cytotoxic effect of thalidomide on 4T1 and 4THMpc mouse breast cancer cell lines. Mouse breast cancer cells (4T1) and cells derived from metastatic lesions (4THMpc) were treated with various doses of thalidomide [10(-2)-100 µM dissolved in dimethyl sulfoxide (DMSO) as recommended] and 1.4 µM DMSO (maximum DMSO concentration in the highest thalidomide dose) as a DMSO control against the untreated control groups. MTT was used to evaluate the cytotoxic effects of the treatments. Therefore, we investigated the role of thalidomide on apoptosis. A fluorometric EnzChek caspase-3 enzyme activity assay kit was used to evaluate the apoptotic effects of thalidomide. Thalidomide dissolved in DMSO exhibited cytotoxic effects on 4T1 and 4THMpc cells compared to the control groups incubated without any supplement. Treatment with thalidomide resulted in apoptosis of mouse breast cancer cells in a time- and dose-dependent manner as demonstrated by caspase-3 enzyme activity. However, DMSO alone suppressed cell proliferation more effectively than thalidomide. In cultured mouse breast cancer cells the inhibitory effect of thalidomide may be partially attributed to the solvent DMSO alone.Ece Simsek Oz, Esra Aydemir, Kayahan Fışkın
1867 related Products with: DMSO exhibits similar cytotoxicity effects to thalidomide in mouse breast cancer cells.
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