Search results for: Caspase 3 Colorimetric Assay Kit
#39167288 
2024/08/21
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2-methoxyestradiol sensitizes tamoxifen-resistant MCF-7 breast cancer cells via downregulating HIF-1α.
The clinical studies for breast cancer (BC) are now assessing the efficacy of 2-Methoxyestradiol (2-ME), a naturally occurring derivative of estradiol. Our study aimed to explore the potential of combining the 2-ME and tamoxifen (TAM) on sensitization of TAM-resistant cells using LCC2 the TAM-resistant cells as a model and comparing the results to the sensitive cells MCF-7. Sulphorhodamine-B (SRB) assay is used to examine the 2-ME chemo-sensitizing impact on the cytotoxicity of TAM on LCC2 cells. Colorimetric assay kits were used to assess the level of the apoptosis-related markers caspases 3, Bcl2, and Bax in cell lysate. Hypoxia-inducible factor 1 alpha (HIF-1α) expression was measured using western blotting. Total cholesterol and triglyceride (TG) levels were examined colorimetrically, using the BIOLABO kit. The use of 2-ME enhanced the cytotoxic effects of TAM and effectively reversed TAM resistance. This was achieved by inhibiting the expression of HIF-1α, while concurrently increasing the levels of apoptotic marker caspase-3, as well as the pro-apoptotic protein Bax. Additionally, there was a reduction in the levels of Bcl2, an anti-apoptotic protein. Furthermore, a reduction in TG and cholesterol levels was noted. Our findings show that HIF-1α plays an important role in TAM resistance and that suppression of HIF-1α by 2-ME-mediated sensitization of BC-resistant cells to TAM. Therefore, the concurrent administration of TAM/2-ME might potentially serve as a viable therapeutic approach to address TAM resistance and enhance the overall therapy efficacy for patients with BC.Yasmin M Attia, Hamada Ahmed Mokhlis, Ahmed Ismail, Ahmed S Doghish, Mohamed H Sobhy, Sherif S Hassanein, Walaa A El-Dakroury, Amr D Mariee, Salama A Salama, Marwa Sharaky
2381 related Products with: 2-methoxyestradiol sensitizes tamoxifen-resistant MCF-7 breast cancer cells via downregulating HIF-1α.
100|uI x 10 vials1 vial75мg/vial5 x 10A5 cells/vial
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#39103220 //
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Dihydromyricetin protects sevoflurane-induced mitochondrial dysfunction in HT22 hippocampal cells.
Sevoflurane (Sev) is a commonly used inhalation anaesthetic that has been shown to cause hippocampus dysfunction through multiple underlying molecular processes, including mitochondrial malfunction, oxidative stress and inflammation. Dihydromyricetin (DHM) is a 2,3-dihydroflavonoid with various biological properties, such as anti-inflammation and anti-oxidative stress. The purpose of this study was to investigate the effect of DHM on Sev-induced neuronal dysfunction. HT22 cells were incubated with 10, 20 and 30 μM of DHM for 24 h, and then stimulated with 4% Sev for 6 h. The effects and mechanism of DHM on inflammation, oxidative stress and mitochondrial dysfunction were explored in Sev-induced HT22 cells by Cell Counting Kit-8, flow cytometry, enzyme-linked immunosorbent assay, reverse transcription-quantitative polymerase chain reaction, colorimetric detections, detection of the level of reactive oxygen species (ROS), mitochondrial ROS and mitochondrial membrane potential (MMP), immunofluorescence and western blotting. Our results showed that DHM increased Sev-induced cell viability of HT22 cells. Pretreatment with DHM attenuated apoptosis, inflammation, oxidative stress and mitochondrial dysfunction in Sev-elicited HT22 cells by remedying the abnormality of the indicators involved in these progresses, including apoptosis rate, the cleaved-caspase 3 expression, as well as the level of tumour necrosis factor α, interleukin (IL)-1β, IL-6, malondialdehyde, superoxide dismutase, catalase, ROS, mitochondrial ROS and MMP. Mechanically, pretreatment with DHM restored the Sev-induced the expression of SIRT1/FOXO3a pathway in HT22 cells. Blocking of SIRT1 counteracted the mitigatory effect of DHM on apoptosis, inflammation, oxidative stress and mitochondrial dysfunction in Sev-elicited HT22 cells. Collectively, pretreatment with DHM improved inflammation, oxidative stress and mitochondrial dysfunction via SIRT1/FOXO3a pathway in Sev-induced HT22 cells.Xinyan Wang, Haoyi Li, Dongchao Qu
1940 related Products with: Dihydromyricetin protects sevoflurane-induced mitochondrial dysfunction in HT22 hippocampal cells.
400 ug1.00 flask100 ul96 assays1x10e7 cells96 wells400 ug1.00 flask50 ul-2ug1x10e7 cells
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#38265681 2024/01/24
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Paeonol upregulates expression of tumor suppressors TNNC1 and SCARA5, exerting anti-tumor activity in non-small cell lung cancer cells.
Paeonol, a naturally bioactive phenolic ingredient predominantly isolated from Paeonia suffruticosa, has recently garnered significant interest as an anti-tumor agent against diverse carcinomas including non-small cell lung cancer (NSCLC). However, the anti-tumor mechanism of paeonol in NSCLC remains unclear. Cell viability, caspase-3 activity, and apoptosis were evaluated using CCK-8 assay, Caspase-3 Colorimetric Assay Kit, and flow cytometry analysis, respectively. GSE186218 was downloaded from NCBI Gene Expression Omnibus (GEO). The common genes were screened using GEO2R and Draw Venn Diagram software. Expression of troponin C type 1 (TNNC1), scavenger receptor class A member 5 (SCARA5), phosphorylated protein kinase B (AKT) (p-AKT) and AKT was examined using GEPIA database, qRT-PCR and western blot analysis. Paeonol treatment concentration-dependently inhibited cell viability and increased caspase-3 activity and apoptotic rate in NSCLC cells. Only 5 overlapping genes including TNNC1 and SCARA5 were obtained among 232 upregulated genes in GSE186218, 200 underexpressed genes in TCGA-LUAD, and 200 underexpressed genes in TCGA-LUSC according to the Venn diagram software. TNNC1 and SCARA5, two known tumor suppressors, were significantly downregulated in LUAD and LUSC tissues and NSCLC cells. Paeonol dose-dependently upregulated TNNC1 and SCARA5 expression in NSCLC cells. Paeonol suppressed the AKT pathway by upregulating TNNC1 and SCARA5 expression. AKT inhibitor attenuated the effects of TNNC1 or SCARA5 knockdown on the anti-tumor activity of paeonol. In conclusion, paeonol exhibited anti-cancer activity in NSCLC cells through inactivating the AKT pathway by upregulating TNNC1 or SCARA5.Chongnan Zhang, Jing Zhang, Kai Guo
2146 related Products with: Paeonol upregulates expression of tumor suppressors TNNC1 and SCARA5, exerting anti-tumor activity in non-small cell lung cancer cells.
100 µg
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#37402454 2023/06/26
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Wheat phytase potentially protects HT-29 cells from inflammatory nucleotides-induced cytotoxicity.
The aim of this study was to investigate the protective effect of wheat phytase as a structural decomposer of inflammatory nucleotides, extracellular adenosine triphosphate (ATP), and uridine diphosphate (UDP) on HT-29 cells.Jeongmin An, Jaiesoon Cho
1019 related Products with: Wheat phytase potentially protects HT-29 cells from inflammatory nucleotides-induced cytotoxicity.
2 x 10^6 cells96T250 mg1.5 x 10^6 cells 5 G230ml 1 kit(s) 2 mL100.00 ug1.00 flask5 g
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#37183367 2023/05/16
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Petite Integration Factor 1 knockdown enhances gemcitabine sensitivity in pancreatic cancer cells via increasing DNA damage.
Chemoresistance is still a vital obstacle in various tumors chemotherapy. This study aimed to explore the role of Petite Integration Factor 1 (PIF1) in the sensitivity of gemcitabine response to pancreatic cancer cells. Gene Expression Profiling Interactive Analysis (GEPIA) database was employed for evaluating the level of PIF1 in pancreatic cancer tissues and normal tissues. The mRNA level of PIF1 was detected via reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. The relative protein expression of PIF1, cleaved caspase-3, and phosphorylated histone H2Ax (γH2Ax) was assessed through western blot. Cell viability and apoptosis were assessed via Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. Moreover, lactate dehydrogenase (LDH) release and caspase-3 activity were determined via the corresponding LDH Cytotoxicity Assay Kit and caspase-3 colorimetric assay kit. PIF1 expression was upregulated in pancreatic cancer tissues and cells. Knockdown of PIF1 exhibited the repressive impact on the viability of AsPC-1 and PANC-1 cells. PIF1 knockdown enhanced LDH release and apoptosis in both AsPC-1 and PANC-1 cells. PIF1 downregulation could augment the sensitivity of gemcitabine in pancreatic cancer cells, as evidenced by lower cell viability and higher LDH release and apoptosis rate after knocking down PIF1 in gemcitabine-treated pancreatic cancer cells relative to pancreatic cancer cells treated with gemcitabine alone. Moreover, PIF1 knockdown increased γH2Ax protein expression and DNA damage, and gemcitabine treatment-induced DNA damage in AsPC-1 and PANC-1 cells was exacerbated by PIF1 silencing. Furthermore, gemcitabine treatment-caused increase of DNA damage was alleviated by PIF1 overexpression; whereas, this effect of PIF1 upregulation was reversed by thymidine, a DNA synthesis inhibitor. In addition, the decreased gemcitabine sensitivity response to pancreatic cancer cells caused by PIF1 upregulation was also hindered by thymidine treatment. In conclusion, PIF1 silencing enhanced gemcitabine sensitivity response to pancreatic cancer cells through aggrandizing DNA damage.Kun Wang, Xiangdong Hua, Xibo Fu, Zhiqiang Hao, Ao Jiao, Siyuan Li
1528 related Products with: Petite Integration Factor 1 knockdown enhances gemcitabine sensitivity in pancreatic cancer cells via increasing DNA damage.
10 ug100ìl x 10 vials1x10e7 cells100ul1x10e7 cells10ug100ul10ug
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#37069938 2023/04/11
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Tectorigenin alleviates the apoptosis and inflammation in spinal cord injury cell model through inhibiting insulin-like growth factor-binding protein 6.
Since tectorigenin has been reported to possess anti-inflammation, redox balance restoration, and anti-apoptosis properties, we determine to unravel whether tectorigenin has potential in alleviating spinal cord injury (SCI). Herein, PC12 cells were induced by lipopolysaccharide (LPS) to establish SCI models. The cell viability and apoptosis were detected through cell counting kit-8 and flow cytometry assays. The caspase-3/8/9 content was measured by colorimetric method. Western blot was conducted to quantify the expressions of cleaved caspse-3/8/9, IGFBP6, TLR4, IκBα, p-IκBα, RELA proto-oncogene, p65, and p-p65. Enzyme-linked immunosorbent assay and real-time quantitative polymerase chain reaction were carried out to quantitate expressions of IGFBP6, interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). SwissTargetPrediction and GSE21497 database were utilized to predict the potential therapeutic targets of tectorigenin. Comparison of IGFBP6 expression in SCI tissues and normal tissues was analyzed by GEO2R. Our study found that LPS induced the declined cell viability, elevated cell apoptosis, upregulation of caspase-3/8/9, cleaved caspase-3/8/9, IL-1β, IL-6, TNF-α, IGFBP6, and TLR4, and the activation of IκBα and p65 in PC12 cells. Tectorigenin reversed the above effects of LPS. IGFBP6 was predicted to be the potential therapeutic target of tectorigenin and was overexpressed in SCI tissues. Notably, IGFBP6 overexpression offset the effects of tectorigenin on PC12 cells. In conclusion, tectorigenin could alleviate the LPS-induced apoptosis, inflammation, and activation of NF-κB signaling in SCI cell models via inhibiting IGFBP6.Liqiang Zhou, Kui Yan, Shuxing Xing, Jun Cheng
1076 related Products with: Tectorigenin alleviates the apoptosis and inflammation in spinal cord injury cell model through inhibiting insulin-like growth factor-binding protein 6.
100.00 ug100.00 ug100.00 ug100.00 ug100.00 ugProtein1 kit(96 Wells)10ug100.00 ug10ug10ug0.1ml (1mg/ml)
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#36974531 2023/03/01
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Punica granatum Seed Essential Oil Suppressed Methadone-Induced Cell Death by Natural Antioxidant Activity.
Methadone is an opioid used in treating chronic and acute pains as well as opioid dependence. It induces death in neural cells. This study investigates Punica granatum oil's effects as a natural antioxidant on methadone-induced cell death.Hossein Zhaleh, Hamed Mahdizadeh, Shahab Khoshkhoy
1068 related Products with: Punica granatum Seed Essential Oil Suppressed Methadone-Induced Cell Death by Natural Antioxidant Activity.
1 kit100ug Lyophilized96 assays100ug Lyophilized1 kit100ug Lyophilized200 Tests1 kit
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#36916093 2023/03/01
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CHAC1 exacerbates LPS-induced ferroptosis and apoptosis in HK-2 cells by promoting oxidative stress.
Sepsis-induced acute kidney injury (AKI) is a singularly grievous and life-threatening syndrome. Its pathogenesis is closely related to inflammatory response, apoptosis, oxidative stress, and ferroptosis. Cation transport regulator-like protein 1 (CHAC1), as a proapoptic factor, may be involved in apoptosis, oxidative stress, and ferroptosis. This study aimed to explore the role of CHAC1 in the lipopolysaccharide (LPS)-induced the human renal proximal tubular epithelial (HK-2) cells.Zhihui Zhou, Hongwei Zhang
2083 related Products with: CHAC1 exacerbates LPS-induced ferroptosis and apoptosis in HK-2 cells by promoting oxidative stress.
-100 ug1x10e7 cells2000 Units200ul1.00 flask5mg1 mg20x50 ug
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#36889691 2023/03/09
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In vitro chondrotoxicity of bupivacaine, levobupivacaine and ropivacaine and their effects on caspase activity in cultured canine articular chondrocytes.
Bupivacaine, levobupivacaine and ropivacaine are potent, long acting, amide-type local anesthetics that have several clinical applications including intra-articular administration. The objectives of this study were to evaluate their in vitro effects on cell viability and caspase activity to elucidate whether they activate the extrinsic or intrinsic pathways of apoptosis in canine articular chondrocytes. Chondrocytes in monolayer culture were treated with culture medium as the control, or with 0.062% (0.62 mg/mL) bupivacaine, 0.062% levobupivacaine, and 0.062% ropivacaine for 24 hr. Cell viability was evaluated using the live/dead, 3-(4,5-dimehylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT), and Cell Counting Kit-8 (CCK-8) assays. Evaluation of caspase-3, caspase-8, and caspase-9 activity was performed using colorimetric assays. The MTT and CCK-8 assays were used to evaluate the effect of caspase inhibitors on local anesthetic chondrotoxicity. All three local anesthetics decreased chondrocyte viability after 24 hr (P<0.001). Apoptosis was induced through both the extrinsic and intrinsic pathways. Bupivacaine increased caspase-3, caspase-8, and caspase-9 activity (P<0.001). Levobupivacaine increased caspase-3 (P=0.03) while ropivacaine did not significantly upregulate activity for all three caspases. Caspase inhibition did not suppress bupivacaine chondrotoxicity whereas inhibition of caspase-8 and caspase-9 decreased ropivacaine chondrotoxicity and mildly attenuated levobupivacaine chondrotoxicity. In summary, the level of chondrotoxicity, the type of caspase activated, the level of caspase activation, and the response to caspase inhibitors was dependent on the type of local anesthetic. Therefore, ropivacaine may be a safer choice for intra-articular administration compared to levobupivacaine and bupivacaine.Carol Mwale, Takafumi Sunaga, Yanlin Wang, Eugene C Bwalya, H M Suranji Wijekoon, Sangho Kim, Masahiro Okumura
2268 related Products with: In vitro chondrotoxicity of bupivacaine, levobupivacaine and ropivacaine and their effects on caspase activity in cultured canine articular chondrocytes.
100 µl (2 mM)20 µl5 mg20 µl100 µl (2 mM)5x25 µl100 48 assays 100
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#36467371 //
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Astragaloside IV ameliorates spinal cord injury through controlling ferroptosis in HO-damaged PC12 cells .
Spinal cord injury (SCI) is associated with significant paralysis and high fatality. Recent research has revealed that ferroptosis participates in the pathogenesis of SCI. Astragaloside IV (AS-IV), the main active ingredient of the plant , has been reported to promote motor function recovery in rats with SCI. This study explored the effects of AS-IV in HO-treated PC12 pheochromocytoma cells.Yifei Zhou, Lin Li, Chenghuang Mao, Dongsheng Zhou