PRDX1 Pre-design Chimera RNAi
- Known as:
- PRDX1 Pre-design Chimera RNAi
- Catalog number:
- H00005052-R03
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PRDX1 Pre-design Chimera RNAi
Related genes to: PRDX1 Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: PRDX1 Pre-design Chimera RNAi
- In this study, integrated proteomic and transcriptomic analyses identified peroxiredoxin 1 (PRDX1) as a novel urinary biomarker for bladder cancer (BC). PRDX1 was significantly upregulated in BC tissues and was associated with poorer overall survival. In vitro experiments further demonstrated that PRDX1 promotes malignant phenotypes of BC cells, including proliferation, migration, and invasion. Silencing PRDX1 in BC cells significantly reduced the invasiveness and proliferation ability.To address the clinical need for rapid and non-invasive detection, we developed an innovative optical fiber biosensor based on surface plasmon resonance (SPR) technology for the quantitative detection of urinary PRDX1. The biosensor exhibited excellent analytical performance, including high sensitivity (limit of detection: 0.06 ng/mL), a wide linear range (0-25 ng/mL), rapid response (∼14 s), as well as good stability and selectivity. In clinical validation involving 97 BC patients and 30 healthy controls, the biosensor demonstrated outstanding diagnostic performance, with an area under the receiver operating characteristic curve (AUC) of 0.91 and an overall diagnostic accuracy of 86.6%, outperforming conventional enzyme-linked immunosorbent assay (ELISA). Collectively, this study not only identifies PRDX1 as a promising biomarker for non-invasive diagnosis and prognostic evaluation of BC, but also establishes an efficient SPR-based optical fiber sensing platform, providing new insights into both clinical detection and the functional role of PRDX1 in BC progression. - Source: PubMed
Publication date: 2026/06/15
Cheng KunZhang Heng-BiaoXie Hua-RongWang LiZhang TongWan ShunYang Jian-WeiHong Pan-GuanWang Xu-YanJiao Pan-PanXu Chang-HongDeng Yi-diChen Si-YuDing Li-YunYang Li - Within the scope of this investigation, two novel compounds (3a and 3b) were designed and synthesized in two steps. Compounds 3a and 3b were tested utilizing the MTT study to evaluate their in vitro cytotoxic activity against healthy human embryonic kidney, lung cancer, breast cancer, and human liver cancer cell lines. It was determined that compound 3b exhibited high levels of cytotoxic activity against both liver and breast cancer cell lines, with IC values of 10.83 and 11.55 µM, respectively. Also, to elucidate the anticancer mechanism of compounds, pro-apoptotic BAX and BiD, anti-apoptotic BCL2 and BCL-xl, oxidant enzymes PRDX1 and SOD1 levels were examined by RT-qPCR. Moreover, cellular oxidative stress levels were spectrophotometrically measured, and cellular senescence was evaluated via the senescence-associated β-galactosidase test. DFT calculations and RDG, ELF, and LOL analyses were performed to demonstrate the reactivity of these compounds. Compounds significantly down-regulated anti-apoptotic genes, whereas mRNA levels of pro-apoptotic genes were up-regulated in MCF-7 cells. Moreover, oxidative stress status was significantly increased depending on the compound treatment. Consistently, PRDX1 and SOD1 levels were also significantly up-regulated. Furthermore, cellular senescence was significantly induced by the compounds. Fluorescence spectroscopy demonstrated strong binding of both compounds with CT-DNA, characterized by static quenching mechanism and binding constants of 6.02 × 10M(for 3a) and 8.69 × 10M(for 3b), suggesting an intercalative binding mode. In contrast, moderate affinity toward BSA indicated suitable transport characteristics with reduced nonspecific protein binding. Molecular docking studies supported the experimental findings. These combined results verify the potential of the synthesized derivatives as promising candidates for further investigation as biologically active anticancer agents. - Source: PubMed
Publication date: 2026/06/23
Kundu SevgiAkkoc SenemErzurumlu YalçınAlhag Sadeq KAlkeridis Lamya AhmedFeizi-Dehnayebi Mehran - 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