Human Bcl2 Associated Death Promoter ELISA , BAD
- Known as:
- Human Bcl2 Associated Death Promoter Enzyme-linked immunosorbent assay test , BAD
- Catalog number:
- E01B0633
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Bcl2 Associated Death Promoter ELISA BAD
Related genes to: Human Bcl2 Associated Death Promoter ELISA , BAD
- Gene:
- BCL2 NIH gene
- Name:
- BCL2 apoptosis regulator
- Previous symbol:
- -
- Synonyms:
- Bcl-2, PPP1R50
- Chromosome:
- 18q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: Human Bcl2 Associated Death Promoter ELISA , BAD
Related articles to: Human Bcl2 Associated Death Promoter ELISA , BAD
- Colorectal cancer (CRC) remains the main cause of cancer-related mortality worldwide, highlighting the need for effective therapy. Cerium oxide nanoparticles (Cer-NPs) and Ferula latisecta have anticancer properties. This study aimed to green-synthesize of Cer-NPs using Ferula latisecta to assess oxidative stress, apoptosis, and autophagy signaling in CRC cells. The seed extract of Ferula latisecta was combined with cerium salt, synthesized the Cer-NPs, and investigated anticancer effects on human CRC cells with a focus on oxidative stress, apoptosis, and autophagy pathways. XRD, FTIR, and FESEM techniques were utilized to characterize Cer-NPs. HT29 and SW480 CRC cells were treated with a serial dilution of Cer-NPs for cell viability for 24 h and 48 h. Caspase-3 activity assay, AO/PI staining, and real-time PCR method were employed to assess the apoptosis rate and autophagy in cells. Besides, oxidative stress measurements, including intracellular ROS, MDA, LDH, and GSH, were performed. The protein levels of p53 were measured through ELISA. The synthesized Cer-NPs showed a fluorite cubic structure, a crystalline construction, and a spherical morphology with sizes of 20-50 nm. Cer-NPs significantly reduced cell viability in a dose- and time-dependent manner and increased caspase-3 activity (P < 0.05). IC50 values were 0.68 mM and 0.88 mM for HT29 and SW480 cells after 48 h. The number of AO/PI-positive cells was increased alongside ROS production within cells. The levels of MDA and LDH were increased, while the level of GSH was decreased significantly in treated cells (P < 0.05). Furthermore, Cer-NPs could significantly increase Bax, Bcl-2, Beclin-1, P62, Bax/Bcl-2, LC3 II/I ratio as well as up-regulate p53 protein level (P < 0.05). The green-synthesized Cer-NPs could directly induce oxidative stress and apoptosis, and indirectly mediate apoptosis by impairing autophagy. - Source: PubMed
Publication date: 2026/06/08
Alizade AresDaemi AminBasarali Mustafa KemalHosseini Seyyedeh TouranTahiraga Ruhiyya GuliyevaÖzbolat GülüzarYönden Zafer - Contrast agents are widely used in medical imaging to improve tissue differentiation, but they can cause serious inflammatory responses, including contrast-induced nephropathy (CIN). Dexpanthenol (DEX) is known for its antioxidant, anti-inflammatory, and anti-apoptotic properties. This study aimed to investigate the potential protective effects of dexpanthenol in a rat model of diatrizoate-induced CIN. In this study, 32 Wistar albino rats were randomly divided into four groups: control, Urografin (URO; 10 mL/kg, intraperitoneal [i.p.]), URO + DEX (500 mg/kg, i.p. for 3 days), and DEX alone. Renal function markers (serum urea and creatinine), total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) were measured. Histopathological evaluation and immunohistochemical analysis of tumor necrosis factor-alpha (TNF-α) and caspase-3 (Cas-3) were performed. Additionally, SIRT1, Bcl-2, Bax, and p53 mRNA expression levels were assessed. URO administration increased TOS and OSI values and caused significant renal histopathological damage. TNF-α and Cas-3 immunoreactivity, along with Bax and p53 gene expression, were significantly elevated, while Bcl-2 and SIRT1 expression was suppressed. DEX treatment provided partial improvement in these changes, contributed to the preservation of renal architecture, and was associated with improvements in biochemical and molecular parameters approaching those of the control levels. In conclusion, DEX may exert nephroprotective effects against CIN by reducing oxidative stress, inhibiting pro-inflammatory and apoptotic pathways, and increasing anti-apoptotic gene expression. These findings provide a preclinical basis supporting the idea that dexpanthenol is a promising candidate for further translational and clinical studies in contrast-induced renal injury. - Source: PubMed
Publication date: 2026/06/08
Havabulut Cenk MustafaGündüz DemetSarman Emineİlhan İlterTepebaşı Muhammet YusufGülal AbdurrahmanSavran MehtapAşcı Halil - Oxaliplatin (OXI), a platinum-based chemotherapeutic agent commonly used in colorectal Cancer treatment, has been linked to significant nephrotoxicity involving apoptosis, endoplasmic reticulum (ER) stress, inflammation, oxidative stress, and autophagy. This study investigated the potential mechanisms involved in kidney damage caused by OXI and explored the renoprotective effects of lycopene (LP) in renal tissues of rats. Biochemical analyses revealed that OXI administration led to elevated serum urea and creatinine levels, increased lipid peroxidation (MDA), and decreased antioxidant defense (SOD, CAT, GPx, GSH), accompanied by suppression of the Nrf-2/HO-1 pathway. Inflammatory markers such as NF-κB, IL-1β, COX-2, TNF-α, and iNOS were significantly upregulated, along with ER stress-related genes (GRP78, ATF6), apoptotic markers (p53, Bax, Bcl-2), and key mediators of autophagy (Beclin-1, JNK). Additionally, Western blot and immunohistochemistry results indicated increased expression of AKT, mTOR, and PI3K proteins in the OXI group, suggesting altered survival signaling. LP treatment ameliorated these pathological alterations by restoring antioxidant enzyme activities, downregulating proinflammatory and proapoptotic signals, mitigating ER stress and autophagy activation, and reducing PI3K/AKT/mTOR protein expression. These findings demonstrate that LP exerts a renoprotective effect against OXI-induced kidney injury through multi-targeted molecular mechanisms, including modulation of inflammation, oxidative stress, autophagy, apoptosis, and survival signaling pathways. - Source: PubMed
Kandemir ÖzgeKüçükler SefaÇomaklı SelimÖzdemir SelçukDalkılınç ElifAydın ŞeymaBayav İbrahimCaglayan CuneytKandemir Fatih Mehmet - Diabetic nephropathy (DN) is a major complication of diabetes, largely driven by chronic hyperglycaemia and oxidative stress. This study investigated the dose-dependent effects of protocatechuic acid (PCA) on DN, focusing on its potential to attenuate ferroptosis and apoptosis in a streptozotocin-induced type 1 diabetes rat model.Thirty-two Wistar Albino rats were divided into four groups (n = 8): Control, Diabetes, Diabetes + PCA 50 mg/kg, and Diabetes + PCA 100 mg/kg. After 12 weeks, kidney tissues were evaluated histologically (Perls' Prussian blue, PAS), immunohistochemically (Bax, Bcl-2, Caspase-3, Caspase-9, ACSL4, GPx4, TFR-1), and by TUNEL assay.Diabetic rats exhibited iron accumulation, tubular dilatation, intracellular vacuolisation, sclerotic glomeruli, and mesangial expansion (p < 0.05), while tubular atrophy, hyaline deposition, and mononuclear infiltration were unchanged (p > 0.05). Apoptotic and ferroptotic markers (Bax, Caspase-3, Caspase-9, ACSL4, TFR-1) increased, and Bcl-2 and GPx4 decreased (p < 0.001). PCA treatment, particularly at the 100 mg/kg dose, significantly attenuated the expression of apoptotic and ferroptotic markers and reduced the number of TUNEL-positive cells (p < 0.001). These findings suggest that PCA modulates cell death by upregulating Bcl-2 and GPx4 while downregulating Bax, Caspase-3, Caspase-9, ACSL4, and TFR-1 in renal tissues. While PCA effectively suppressed these molecular markers of injury, it did not lead to significant improvements in systemic renal function parameters such as serum creatinine and BUN. Thus, PCA may serve as a potential agent for mitigating cellular damage in diabetic kidney injury by targeting specific cell death pathways. - Source: PubMed
Publication date: 2026/06/08
Kaya Muhammed TahaGuvenc Tolga - Primary cutaneous follicle center lymphomas (PCFCLs) are indolent B-cell neoplasms limited to the skin and effectively managed with local therapies. Distinguishing PCFCL from systemic follicular lymphoma (sFL) with cutaneous involvement (FL_CI) is challenging due to overlapping features. We performed an integrated pathological and genetic analysis of skin samples of 24 PCFCL and 10 FL_CI, which showed subtle pathological changes (decreased BCL2 and CD10, increased CD23 expression in PCFCL), but markedly distinct mutational landscapes. FL_CI exhibited recurrent mutations in chromatin-modifying genes ( 90%, 90%, and 30%), closely resembling sFL. In contrast, PCFCL displayed a more heterogeneous profile, with mutations affecting B-cell development, cell adhesion, and immune evasion. These molecular alterations identified three distinct PCFCL subgroups. Group 1 (44%) harbored mutations in immune evasion genes (, , , and ) and was associated with CD10 negativity, diffuse architecture, and localization in non-photoexposed areas. Group 2 (20%) showed activating and mutations, consistent CD23 and CD10 positivity, and exclusive presentation in sun-exposed sites. Group 3 (20%) shared a similar clinicopathological profile to Group 2 but was defined by mutations. Clonal origin and mutational evolution were studied in five patients, one with synchronous PCFCL and four with sequential samples from two PCFCL and 2 FL_CI. This analysis supports a model of PCFCL oncogenesis driven by circulating progenitors following complex evolutionary patterns, including convergent evolution and greater clonal diversity at relapse. Overall, our study refines the mechanisms driving PCFCL pathogenesis, while providing a framework for PCFCL differential diagnosis and clinical management. - Source: PubMed
Publication date: 2026/05/29
Combalia AndreaVidal-Robau NuriaNadeu FerranLópez CristinaFrigola GerardLopez-Oreja IreneGarcia NoeliaBashiri MelikaMozas PabloLopez-Guillermo ArmandoSalaverria ItziarEstrach TeresaCampo EliasGarcia-Herrera AdrianaAlbero Robert