Recombinant Human PRDX3
- Known as:
- Recombinant Human PRDX3
- Catalog number:
- CG26
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Recombinant Human PRDX3
Related genes to: Recombinant Human PRDX3
- Gene:
- PRDX3 NIH gene
- Name:
- peroxiredoxin 3
- Previous symbol:
- AOP1
- Synonyms:
- MER5, AOP-1, SP-22
- Chromosome:
- 10q26.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-12
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human PRDX3
Related articles to: Recombinant Human PRDX3
- In this study, Dehydroepiandrosterone (DHEA-induced Polycystic Ovary Syndrome (PCOS) mice were used as models to evaluate the improvement effect of Vitexin (Vit) on ovarian fibrosis and explore the mechanism of action of the NR4A1/NLRP3 signaling pathway. Sixty 4-week-old female ICR mice of the same batch number were selected and their systems were divided into 6 groups ( = 10): normal (Control, Ctrl) group, model (Polycystic Ovary Syndrome, PCOS) group, treatment (Vitexin, The Vit group, normal gene silencing group (Ctrl ), gene silencing model group (PCOS ), and gene silencing treatment group (Vit ). Silencing gene modeling was performed by tail vein injection of adeno-associated virus (serotype AAV-8), and the mouse genotypes were detected by qRT-PCR technology 14 days after injection. After the genotype was determined, the PCOS group and the PCOS group were administered dehydroepandrosterone (6 mg/100 g/d) by gavage for 28 consecutive days for modeling, while the Vit group and the Vit group were treated with dehydroepandrosterone + vitexin (10 mg/kg/d) by gavage for 28 consecutive days. All mice were raised with pure water and regular maintenance food. After 4 weeks of drug intervention, the mice were euthanized and samples were collected. The pathological changes in ovarian tissue were observed by H&E staining, and the degree of ovarian tissue fibrosis was observed by Masson staining. The levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in mouse serum were detected by biochemical kits. The levels of inflammatory factors (IL-1β, IL-6, IL-18, TNF-α) in mouse serum were determined by enzyme-linked immunosorbent assay. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect oxidative kinase (, , , , ), inflammatory factors (, , , , , ) and fibrotic pathway-related genes (, , , , , , and ) in ovarian tissues. The levels of inflammatory factors (NLRP3, Caspase-1, ASC, IL-1β, IL-18, TNF-α, IκBα) and fibrosis in mice were determined by Western blot method, and statistical description and analysis were performed using SPSS software. In the wild-type genotype group, compared with the PCOS group, Vit treatment could effectively regulate the metabolic abnormalities of PCOS mice, including inhibiting excessive weight gain, restoring normal glucose tolerance, and reducing body fat content. After Vit treatment, the levels of MDA, TC, TG, LDL, IL-1β, IL-6, IL-18 and TNF-α in the serum of PCOS mice were significantly reduced, while the levels of SOD and HDL in the serum of PCOS mice were increased. The staining results indicated that Vit treatment could significantly inhibit the process of ovarian fibrosis in PCOS mice. The results of WB and PCR demonstrated that after Vit gavage treatment in mice, inflammatory and fibrotic factors such as Nlrp3, Caspase-1, Asc, Il-1β, Il-18, Tgf-β1, Smad3, Collagen1, CTGF, and α-SMA in ovarian tissues could be significantly down-regulated, and the fibrotic level of ovarian tissues could be reduced. Among the same measurement indicators, the silenced NR4A1 group showed a certain degree of increase compared with the wild genotype group, but there was no significant difference. Vit intervention can restore the sex hormone levels and follicular development in ovarian tissues of PCOS mice, regulate reproductive endocrine disorders and abnormal lipid metabolism levels, and regulate the expression of Collagen I, a-SMA and CTGF in the ovaries by inhibiting the NR4A1/NLRP3 signaling pathway, thereby improving the ovarian fibrosis level of PCOS mice. It is suggested that it may play a key role in the treatment of PCOS and the prevention and delay of its long-term complications. - Source: PubMed
Publication date: 2026/05/15
Sun HaoranXu JiejingPan ChengxueSong Jia-LeZhou Yanyuan - To investigate the role of peroxiredoxin isoforms (Prdx) in the radioresistance of cancer cells, the expression of Prdx1-6, DNA repair genes, and apoptosis regulators was studied in human cancer cell lines with varying radiosensitivities (A549, Caco-2, and MCF-7) after exposure to ionizing radiation. A correlation was found between high constitutive Prdx1-6 expression levels and increased radioresistance. Predominantly cytosolic isoforms Prdx2 and Prdx6 demonstrated pronounced induction after irradiation, indicating their critical role in protecting against radiation-induced oxidative stress. Most radiosensitive A549 cells exhibited the lowest baseline Prdx expression and the most pronounced transcriptional changes after irradiation, whereas MCF-7 and Caco-2 cells had higher constitutive expression and a weaker response to radiation. Mitochondrial Prdx3 and Prdx5, as well as ER-localized Prdx4, exhibited relatively stable expression. A549 cells demonstrated the highest induction of DNA repair genes, which may indicate more severe DNA damage. In contrast, MCF-7 cells were characterized by high basal expression of repair genes and elevated γH2AX levels before irradiation, which may reflect their "readiness" for repair and explain their higher radioresistance. Furthermore, radioresistant MCF-7 cells had increased expression of anti-apoptotic genes (BCL2, MCL1, BIRC5), suppressing the mitochondrial apoptotic pathway. Meanwhile, A549 cells showed higher induction of pro-apoptotic genes (PUMA, NOXA, BAK1) and activation of caspase-3, which correlates with their increased radiosensitivity. Therefore, peroxiredoxins protect cells from radiation exposure, either by being constitutively expressed or by being highly inducible in response to radiation, and promote cell survival after irradiation. This makes them attractive targets for overcoming cancer cell radioresistance. - Source: PubMed
Publication date: 2026/05/22
Sharapov M GGoncharov R GKarmanova E EParfenyuk S BGlushkova O VLunin S M - Lung cancer remains the malignant tumor with the highest global incidence and mortality, posing a severe threat to public health. Peroxiredoxin 3 (PRDX3), a well-characterized ferroptosis biomarker, has been implicated in lung cancer progression. Accumulating evidence suggests that PRDX3 may serve as a core gene and potential biomarker, which is critical for elucidating pathogenesis, improving diagnostic accuracy, and developing targeted therapeutic strategies for lung cancer. - Source: PubMed
Publication date: 2026/05/06
Kong QiZhang LeiGong ShuangWu YueWang Jue - Ferroptosis is a regulated form of cell death driven by iron-dependent lipid peroxidation. Although its biological and clinical relevance is increasingly clear, routine and specific detection of ferroptosis remains challenging, especially in tissues and clinical specimens. Indirect measurements of ferroptosis such as lipophilic fluorescent probes (C11-BODIPY581/591), reactive aldehydes (MDA/4-HNE), and pharmacological rescue either lack specificity for ferroptosis, or are impractical for in vivo analysis. Recent work has identified hyperoxidized peroxiredoxin 3 (PRDX3), also known as SO-PRDX3, as a ferroptosis-specific biomarker: Under ferroptotic stress, mitochondrial PRDX3 undergoes selective and irreversible hyperoxidation at its catalytic cysteine residue to generate sulfinic/sulfonic derivatives, a reaction facilitating ferroptosis. Building on this biology, here we outline a method that detects ferroptosis in cells and tissues using 5H7c, a rabbit monoclonal antibody recognizing hyperoxidized but not unmodified PRDX3. The approach offers high specificity, broad sample compatibility (cell lines, animal tissues), and platform flexibility (Western blotting, immunohistochemistry, immunofluorescence). - Source: PubMed
Publication date: 2026/03/26
Sun PeihaoYin WeinanSheng MengmengMeng YawenHan KaiwenLi ZhihaoXu YanchaoCui ShaojieYe Jin - Equus caballus is a species of considerable economic and cultural significance. However, the regulatory networks involved in equine sexual maturation remain unclear and eventually limit its reproduction and utilization. In this study, testicular tissues from eight Kazakh horses at two developmental stages (2 years, representing pre-maturation, and 3 years, representing post-maturation) were analyzed using whole transcriptome sequencing, data-independent acquisition (DIA) proteomics, and untargeted metabolomics. An integrated regulatory network was constructed encompassing ceRNA, mRNA, protein, and metabolite interactions. Transcriptome analysis revealed that significantly changes circRNAs, LncRNAs, including eca-miR-34-5p, eca-miR-34c, eca-miR-449a, eca-miR-486-3p, and target genes such as TRAF1, TRAF3, ALPK3, SLC29A4 and CPNE3. A total of 277 differentially expressed genes were identified at both the mRNA and protein levels, which are primarily involved in biological processes including PI3K-AKT signaling, focal adhesion, extracellular matrix (ECM) receptor interactions, phospholipase D signaling, and ovarian steroidogenesis. LncRNAs and circRNA were found to modulate COL1A1 expression by competitively binding to miR-7844-x and regulating SPARC through interactions with eca-miR-146-5p and eca-miR-328. Integrated proteomic and metabolomic analyses highlighted TAP1, COL14A1, PRDX3, and SEBENP1 central proteins, along with key metabolites such as guanosine, Austocystin B, methanone, and glycerophosphocholine. These molecules were mainly enriched in pathways related to ovarian steroidogenesis, steroid hormone biosynthesis, and propionate metabolism. In conclusion, this study presents a comprehensive regulatory network involving LncRNA, circRNA, miRNA, mRNA, proteins, and metabolites during equine testicular development. The findings provide novel insights into the molecular basis of equine sexual maturation and offer a valuable foundation for improving reproductive regulation and breeding efficiency in horses. - Source: PubMed
Publication date: 2026/04/02
Yang XixiWen LiuxiangWen MingyueYao XinkuiMeng JunZeng YaqiRen Wanlu