CASP3 ELISA kit
- Known as:
- CASP3 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CASP3-b
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CASP3 ELISA kit
Related genes to: CASP3 ELISA kit
- Gene:
- CASP3 NIH gene
- Name:
- caspase 3
- Previous symbol:
- -
- Synonyms:
- CPP32, CPP32B, Yama, apopain
- Chromosome:
- 4q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-22
- Date modifiied:
- 2016-10-05
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- The progressive deterioration of human male reproductive capacity has paralleled the mounting global dispersal of persistent organic pollutants (POPs) and plastic-associated contaminants. Nevertheless, the collective consequences of simultaneous exposure to these ubiquitous environmental stressors on spermatozoal function remain inadequately characterized. This study undertook a comprehensive evaluation of the interactive reproductive harm posed by 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) and 25nm polystyrene nanoplastics (PS-NPs) on human spermatozoa. Whereas isolated challenges with ecologically pertinent doses of either BDE-47 or PS-NPs yielded negligible alterations in sperm viability and motility parameters, concurrent administration provoked a marked superadditive compromise of multiple functional attributes indispensable for successful fertilization. Co-treatment substantially attenuated both total and progressive motility, diminished the penetrative capacity through a cervical mucus surrogate, and abrogated the induction of capacitation and progesterone-induced acrosome reaction. Mechanistic elucidation uncovered that dual exposure synergistically intensified intracellular reactive oxygen species accumulation and profoundly destabilized mitochondrial membrane potential, culminating in a robust augmentation of apoptotic rates. Furthermore, convergent network pharmacology assessments pinpointed pivotal signaling hubs governing apoptosis, including Caspase-3 and constituents of the BCL-2 family members, as principal mediators of the combined toxic insult. Collectively, these findings provide direct evidence that PS-NPs function as potent vectors capable of amplifying the spermatotoxicity of BDE-47 via a cascade of oxidative imbalance, mitochondrial dysfunction and programmed cell death initiation. This work highlights the imperative for adopting mixture centric frameworks in environmental contaminant hazard evaluation and yields novel mechanistic perspectives regarding the plausible etiological role of pollutant co-exposure to idiopathic male infertility. - Source: PubMed
Publication date: 2026/09/18
Yang YuanWang YujieQian RuiruiLuo TaoLiu Shimin - Nephrotic syndrome, characterised by proteinuria and hypoalbuminaemia, is caused by the dysregulation of glomerular podocytes and is a significant contributor to chronic kidney disease (CKD). Sympathetic neurotransmitter noradrenaline, acting through adrenoceptor signalling, contributes to progression of various diseases, including CKD. We previously reported that treatment with yohimbine, an α2-adrenoceptor antagonist, decreased urinary protein excretion in 5/6 nephrectomy-induced CKD rat model and that α2-adrenoceptors are localised in podocytes. This suggested that noradrenaline may induce proteinuria via α2-adrenoceptors in podocytes. Therefore, this study investigated the renoprotective effects of yohimbine in puromycin aminonucleoside (PAN)-induced nephrotic syndrome. Male Sprague-Dawley rats were randomly allocated to sham-operated, PAN (50 mg/kg, i.v.), and PAN + yohimbine (3 mg/L in drinking water) groups. PAN group exhibited increased urinary protein, decreased plasma protein, and increased urinary and plasma noradrenaline levels compared to sham group. Furthermore, pronounced infiltration of CD68-positive cells was observed in the PAN group. The expression levels of the podocyte markers podocin and nephrin were lower in PAN rats than in control rats. Conversely, podocytes in PAN rats exhibited increased desmin, transforming growth factor (TGF)-β1, and cleaved caspase 3 expressions along with higher prevalence of apoptotic cells. Treatment with yohimbine reduced proteinuria and hypoalbuminemia, along with suppressing the downregulation of podocin expression. Furthermore, yohimbine suppressed the expression of desmin, TGF-β1, cleaved caspase-3, and apoptotic cells in glomeruli. Administration of yohimbine reduced the infiltration of CD68-positive cells in the kidney tissue. Collectively, these findings suggest that noradrenaline may promote podocyte injury in PAN-induced nephrotic syndrome via α2-adrenoceptors. - Source: PubMed
Publication date: 2026/09/18
Shimokawa TakaomiIwamoto AkariTamura Yasuhisa - Ketamine (KTM) is widely used in clinical settings for its anesthetic, analgesic, and antidepressant properties. However, prolonged or repeated KTM exposure can induce neurotoxicity through oxidative stress, neuroinflammation, and apoptotic mechanisms. This study investigated the neuroprotective effects of Chrysin (CHR), a natural flavonoid with potent antioxidant and anti-inflammatory properties, against KTM-induced neurotoxicity in rats. - Source: PubMed
Publication date: 2026/09/18
Karaca OnurKandemir ÖzgeŞimşek HasanAkaras NurhanKaraca Şeyda ÖteKandemir Fatih Mehmet - Silver nanoparticles (AgNPs) are among the most widely studied nanomaterials for anticancer applications. Their ability to induce selective cytotoxicity in cancer cells relative to normal cells has attracted significant scientific interest. This study compared the toxicological responses of human breast cancer cells (MCF-7) and non-tumorigenic mammary epithelial cells (MCF-10A) to biologically synthesized AgNPs (mean diameter 18 ± 3 nm). Cell viability, reactive oxygen species (ROS) generation, antioxidant enzyme activity, DNA damage parameters, mitochondrial membrane potential, and apoptosis markers were evaluated across a concentration range of 5 to 160 μg/mL. AgNPs reduced MCF-7 viability with an IC50 of ~35 μg/mL, while MCF-10A cells required ~170 μg/mL for equivalent inhibition, yielding a selectivity index of 4.1 at 72 h. ROS levels in MCF-7 cells increased 9.2-fold at 80 μg/mL versus 3.9-fold in MCF-10A. Comet assay confirmed greater DNA strand breaks in MCF-7 cells (74% tail DNA) than MCF-10A (38.5%). Antioxidant enzymes were markedly depleted in cancer cells but partially retained in normal cells. Apoptosis analysis revealed caspase-3 activation 2.5-fold higher in MCF-7 than MCF-10A. Mechanistically, diminished antioxidant capacity and defective DNA repair in cancer cells underlie differential sensitivity. These findings support AgNPs as a selective anticancer agent and provide a mechanistic framework for nanoparticle-based therapeutic development. - Source: PubMed
Publication date: 2026/09/18
Zhang JieLiu Wang - Endemic fluorosis from high-fluoride groundwater is a global concern. While fluoride exposure is linked to male infertility, the mechanisms remain unclear. This study utilized male Sprague-Dawley (SD) rats and in vitro immortalized human testicular Sertoli (iHTS) cells to investigate the potential mechanisms underlying sodium fluoride (NaF)-induced testicular damage. In vivo, three-month NaF exposure caused testicular tissue disorganization, decreased sperm viability and motility, and increased sperm abnormalities. Furthermore, NaF exposure significantly altered the oxidative stress status in the rat testis, evidenced by decreased total antioxidant capacity (T-AOC), total superoxide dismutase (T-SOD), and glutathione (GSH) levels, along with increased malondialdehyde (MDA) content. Meanwhile, levels of pyroptosis-related proteins (AIM2, Cleaved Caspase-3, GSDME, and GSDME-N), as well as LDH, interleukin (IL)-1β, and IL-18, were significantly increased. Similar results were observed in vitro. Interestingly, knocking down AIM2 in NaF-treated iHTS cells significantly decreased the levels of Cleaved Caspase-3, GSDME, GSDME-N, IL-1β, IL-18, and LDH. Furthermore, inhibiting NaF-induced oxidative stress with N-acetylcysteine (NAC) effectively mitigated these NaF-induced protein and biochemical alterations. These findings suggest that excessive fluoride exposure induces oxidative stress in testicular tissue and cells, subsequently activating the AIM2/Caspase-3/GSDME pyroptotic axis, thereby leading to testicular damage. - Source: PubMed
Publication date: 2026/09/18
Wang GuoqingBa RuijieLiu BinWang YanNiu ShuWan HedanDu YuhuiYu FangfangZhou GuoyuZhu JingyuanBa Yue