Ask about this productRelated genes to: PRDX1 antibody
- Gene:
- PRDX1 NIH gene
- Name:
- peroxiredoxin 1
- Previous symbol:
- PAGA
- Synonyms:
- NKEFA
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-01
- Date modifiied:
- 2014-11-19
Related products to: PRDX1 antibody
Related articles to: PRDX1 antibody
- To explore the role and molecular mechanism of peroxiredoxin 1 (PRDX1) in hypertension-induced endothelial dysfunction. (1) Bioinformatics analysis: A total of 40 C57BL/6J mice aged 8-10 weeks (20-25 g) were randomly divided into the saline group and angiotensin Ⅱ (AngⅡ, 0.8 mg·kg⁻¹·d⁻¹) group, with 20 mice in each group. After 4 consecutive weeks of intervention, mice were sacrificed, and thoracic aortic tissues were collected for transcriptome sequencing. Gene Ontology functional annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed on differentially expressed genes. (2) Cell experiments: Human umbilical vein endothelial cells (HUVECs) were divided into the control group (endothelial cell culture medium) and the AngⅡ intervention group (medium containing 10⁶ mol/L AngⅡ). Wound healing assay, cell adhesion assay, and Transwell assay were used to assess cell migration and adhesion. Lentiviral or small interfering RNA (siRNA) transfection was performed to achieve PRDX1 overexpression and knockdown, respectively. The overexpression experiment was divided into the LV-NC (negative control lentivirus) group, Ang Ⅱ+LV-NC group, LV-PRDX1 (PRDX1 overexpression lentivirus) group and Ang Ⅱ+LV-PRDX1 group. The knockdown experiment was divided into the NC-siRNA (negative control siRNA) group, si-PRDX1 group, NC-siRNA+rapamycin (50 nmol/L) group and si-PRDX1+rapamycin group. Immunofluorescence staining was applied to detect intracellular reactive oxygen species level. Quantitative reverse transcription-polymerase chain reaction was used to detect the mRNA expression levels of PRDX1 and mammalian target of rapamycin (mTOR). Western blot was adopted to determine the total protein and phosphorylation levels of PRDX1, mTOR, p70 ribosomal S6 kinase (p70S6K) 1 and endothelial nitric oxide synthase (eNOS). Co-immunoprecipitation assay was used to verify the protein interaction between PRDX1 and mTOR. Nitrate reductase method was used to measure cellular nitric oxide (NO) content. (3) Animal experiments: Forty C57BL/6J mice aged 8-10 weeks (20-25 g) were used to construct the PRDX1 overexpression model via adeno-associated virus serotype 9 (AAV9) vector. Mice were assigned into 4 groups with 10 animals per group: saline+AAV9-GFP (empty vector) group, saline+AAV9-PRDX1 (recombinant virus) group, AngⅡ+AAV9-GFP group, and AngⅡ+AAV9-PRDX1 group. Systolic blood pressure and diastolic blood pressure of mice in each group were dynamically monitored at day 0, 7, 14, 21 and 28 after modeling. Plasma NO level was detected by the nitrate reductase method. After sacrifice, isolated thoracic aortic tissues were subjected to morphological and pathological staining analysis, and a microvascular tension measurement system was used to evaluate the acetylcholine-mediated endothelium-dependent vasodilation function. (1) Bioinformatics analysis: Transcriptome sequencing revealed that numerous differentially expressed genes were identified in the thoracic aorta of mice in the AngⅡ group compared with the saline group. These genes were mainly enriched in biological processes closely associated with oxidative stress, such as reactive oxygen species metabolism and oxidative phosphorylation regulation. (2) Cell experiments: Compared with the control group, HUVECs in the AngⅡ intervention group presented decreased protein and mRNA levels of PRDX1, as well as elevated phosphorylation levels of mTOR and p70S6K1 (all <0.05). Compared with the LV-NC group, the LV-PRDX1 group showed higher PRDX1 mRNA expression, lower reactive oxygen species levels, enhanced cell migration and adhesion capacities, and increased NO content (all <0.05). In contrast with the AngⅡ+LV-NC group, the AngⅡ+LV-PRDX1 group exhibited reduced phosphorylation levels of mTOR and p70S6K1 and increased eNOS phosphorylation level (all <0.05). In addition, relative to the NC-siRNA group, the si-PRDX1 group had higher reactive oxygen species levels and elevated phosphorylation of mTOR and p70S6K1, accompanied by decreased NO content, reduced eNOS phosphorylation, and weakened cell migration and adhesion abilities (all <0.05). Compared with the si-PRDX1 group, the above abnormal changes were partially reversed in the si-PRDX1+rapamycin group (all <0.05). Co-immunoprecipitation assay confirmed a protein interaction between PRDX1 and mTOR. (3) Animal experiments: In comparison with the saline+AAV9-GFP group, the AngⅡ+AAV9-GFP group had higher systolic and diastolic blood pressure, lower plasma NO level, thicker thoracic aortic media, increased collagen deposition, disordered arrangement of elastic fibers, and impaired endothelium-dependent vasodilation in response to acetylcholine (all <0.05). Notably, the AngⅡ+AAV9-PRDX1 group showed lower systolic and diastolic blood pressure, alleviated pathological damage of the thoracic aorta, improved endothelium-dependent vasodilation function, and higher plasma NO level than the AngⅡ+AAV9-GFP group (all <0.05). PRDX1 can inhibit the excessive activation of the mTOR/p70S6K signaling pathway by scavenging reactive oxygen species and promoting NO production, thereby regulating eNOS activity and ameliorating endothelial dysfunction and vascular injury under hypertensive conditions. Targeted regulation of the PRDX1/ROS/mTOR/p70S6K signaling axis is expected to provide a novel therapeutic target and intervention strategy for the prevention and treatment of hypertensive vascular diseases. - Source: PubMed
Liang YQiu Y MLiu Z FHe JZhou ZYan L QLu XYang YWang HWu Z ZNing Z XXia W H - As the most frequent clinical problem, intervertebral disc degeneration (IVDD) and associated inflammatory pain are still a big challenge, thus there is a need for improved and more lasting therapeutic approaches. In this study, a lipidic prodrug of diclofenac, Diclofenac Lauryl Ester (L-DCF), was synthesized and formulated into nanoparticles (Nanofenac-L) using the ethanol injection method followed by microfluidization. The encapsulation efficiency of Nanofenac-L was > 97% with sustained drug release, releasing around 65% of the diclofenac in 48 h. The therapeutic potential of Nanofenac-L was evaluated in rat intervertebral disc-derived nucleus pulposus cells. Nanofenac-L was found to be more effective than free Diclofenac Sodium (DCF-Na) in terms of anti-inflammatory activity, which was confirmed with significant suppression of COX-2 and Substance P. Furthermore, Nanofenac-L increased the expression of antioxidant genes in cells, such as SOD1, GPX1 and PRDX1. Preventive treatment was found to have shown therapeutic value whereas the curative treatment yielded a significant therapeutic effect indicating the possibility of Nanofenac-L to alleviate inflammation as well as to slow down disease progression. Altogether, these results suggest that Nanofenac-L could represent a promising long-lasting anti-inflammatory, pain relieving and antioxidant nanotherapeutic. Comprehensive preclinical and clinical evaluation is essential to translate these findings into viable therapies. - Source: PubMed
Publication date: 2026/06/18
Hussain SaadatArif AqsaBano PerveenSaleem RudabaRajput Shafiqa NaeemZhang LiangliangKhan IrfanMujeeb-Ur-Rehman - Gambogic acid (GA) is a natural bioactive compound derived from Garcinia hanburyi Hook. F, has proven anticancer activity and is currently in Phase II clinical trials for the treatment of cancer. However, the molecular mechanisms and targets underlying GA's anti-renal cell carcinoma effects remain unclear. - Source: PubMed
Publication date: 2026/06/03
Wang JinyanZhang WeiYang LiZhong XiaoruOu JinhuanIyaswamy AshokGu XinYang ChuanbinGuo BingShi MingjunWang Jigang - Degenerative lumbar spinal stenosis (LSS) is driven by fibrosis and hypertrophy of the ligamentum flavum (LF). Oxidative stress-an excess of reactive oxygen species (ROS) over antioxidant defenses-may underlie LF remodeling, but tissue-level evidence is limited. LF from patients with LSS (n = 180) and controls (n = 102) underwent transcriptomic microarray and microRNA (miRNA) profiling, reverse-transcription quantitative PCR (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and biochemical assays of thiobarbituric acid-reactive substances (TBARS), total glutathione (GSH), and glutathione peroxidase (GPx) activity. Protein-protein interaction (PPI) and functional enrichment analyses were performed. Among 14,130 oxidative-stress-related transcripts, 8,197 were differentially expressed (p < 0.05). Redox-sensitive inflammatory mediators were upregulated, including tumor necrosis factor (TNF), interleukin-1β (IL-1B), interleukin-6 (IL-6), and C-X-C motif chemokine ligand 8 (CXCL8), alongside mitogen-activated protein kinases (MAPK8/JNK1, MAPK14/p38α, MAPK1/ERK2) and superoxide dismutase 2 (SOD2) and peroxiredoxin-1 (PRDX1). Antioxidant defenses-catalase (CAT), superoxide dismutases SOD1/SOD3, glutathione peroxidase-1 (GPX1), and sirtuin-3 (SIRT3)-were downregulated. RT-qPCR confirmed these trends. ELISA demonstrated higher MAPK8 and IL-6 and lower SIRT3 and GPX1 in hypertrophic LF (all p < 0.05). Biochemically, LSS tissue showed increased TBARS and GPx activity and decreased GSH versus controls; oxidative imbalance intensified with greater pain and higher body mass index. Selected miRNAs (e.g., hsa-miR-3163→MAPK8, hsa-miR-4291→SIRT3) were reduced. PPI networks were highly enriched (p < 1 × 10⁻¹⁶). Notably, MAPK8, SIRT3, GPX1, and IL-6 dysregulation was independent of pain category. LF in LSS exhibits a persistent ROS-driven, MAPK-amplified inflammatory program with mitochondrial vulnerability (SIRT3 loss) and impaired peroxide detoxification (GPX1 decline). This oxidative signature likely sustains fibrosis and LF thickening and nominates MAPK8-SIRT3-GPX1-IL-6 as candidate biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/06/03
Strojny DamianSkóra KlaudiaKulpok TomaszWnuk ZygmuntNiedziałek WojciechSobański DawidStaszkiewicz RafałGrabarek Beniamin Oskar - Sirtuin 1 (SIRT1) is an important protein for maintaining cellular homeostasis, and targeting SIRT1 represents a promising strategy for alleviating osteoporosis. The discovery of highly potent and safe SIRT1 activators therefore holds significant translational value for clinical anti-osteoporosis therapies. In this study, we performed deep mining of high-throughput RNA-sequencing (RNA-seq) data from 576 young and aged skeletal stem/progenitor cells (SSPCs) and identified SIRT1 downregulation as a critical hallmark of SSPC ferroptosis during aging-related osteoporosis. In SIRT1 heterozygous deficiency (SIRT1) mice, we found that SIRT1 deficiency triggered SSPC ferroptosis and induced premature osteoporosis. Computer-aided drug design (CADD) was employed to screen 9634 compounds targeting the SIRT1 active site, leading to the identification of the natural compound Hydroxygenkwanin (HGK) as a novel SIRT1 activator. HGK treatment effectively restored SIRT1 activity, suppressed ferroptosis in SSPCs in vitro, and ameliorated osteoporosis in vivo. Through transcriptomic analysis and lactylation profiling, we further found that HGK can activate SIRT1 and reverse the lactylation-mediated suppression of the enzymatic activities of SOD1 and PRDX1. This mechanism may underlie the ability of HGK to reduce SSPC ferroptosis and alleviate osteoporosis. Overall, our findings suggest that HGK possesses translational potential for the treatment of osteoporosis through SIRT1 activation. - Source: PubMed
Publication date: 2026/05/12
Zhai YuCao LinhaiLi HaoCheng ShengwenWei JiayingLi XinhangTang WenjingZhao ChenHuang WeiLiu Minghan