MiR-125b-5p is targeted by curcumin to regulate the cellular antioxidant capacity

Lin, Lingli; Chen, Xi; Sun, Xiaoting; Xiao, Baoping; Li, Jian; Li, Jingwen; Li, Guiling

doi:10.1080/10715762.2022.2162393

Cited by 4 publications

(2 citation statements)

References 45 publications

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“…MiRNAseq revealed the top ten most enriched miRNAs: miR-125b-5p, miR-21-5p, miR-143-3p, let-7i-5p, miR-146a-5p, miR-125b-5p, miR-199b-3p, miR-16-5p, miR-221-3p and let-7c-5p (Figure .5A,B). We searched for miRNAs that were involved in oxidative stress (miR-181a-5p, miR-126, miR-146a-5p, miR-125b-5p, miR-484, and miR-27) [22][23][24][25][26][27]. MiR-125b-5p and miR-146a-5p were candidates that were abundant in MSC-sEVs and were likely associated with ferroptosis (Figure .…”

Section: Mir-125b-5p Enrichment In Msc-sevs Suppresses Ferroptosismentioning

confidence: 99%

Mesenchymal Stem Cell-derived Exosomal miR-125b-5p Suppressed Retinal Microvascular Endothelial Cell Ferroptosis by Targeting P53 in Diabetic Retinopathy

Tong,

Chen,

Xiang

et al. 2024

Preprint

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Progressive endothelial cell injury of retinal vascular is a vital factor in diabetic retinopathy (DR) pathogenesis. Mesenchymal stromal cells-derived small extracellular vesicles (MSC-sEVs) showed beneficial effects on DR. However, the effects of MSC-sEVs in endothelial dysfunction of DR and the mechanism is still unclear. In this study, MSC-sEVs mitigated retinal blood-retina barrier(BRB) impairment in rats with streptozotocin (STZ)-induced DR by reducing ferroptosis in vivo and in vitro. MSC-sEVs miRNA sequencing analysis revealed that miR-125b-5p may mediate HRMEC ferroptosis and P53 as a downstream target based on dual-luciferase reporter assays. Silencing miR-125b-5p in MSC-sEVs reversed the therapeutic effects of MSC-sEVs on rats with DR and advanced glycation end products (AGE)-treated HRMECs. Additionally, overexpression of miR-125b-5p could diminish ferroptosis in HRMECs, and this effect could be effectively reversed by overexpressing P53. This study indicated the potential therapeutic effect of MSC-sEVs on vascular endothelial function maintenance and that the delivery of sEVs carrying miR-125b-5p could prevent endothelial cell ferroptosis by inhibiting P53, thereby protecting the BRB.

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Section: Mir-125b-5p Enrichment In Msc-sevs Suppresses Ferroptosismentioning

confidence: 99%

Mesenchymal Stem Cell-derived Exosomal miR-125b-5p Suppressed Retinal Microvascular Endothelial Cell Ferroptosis by Targeting P53 in Diabetic Retinopathy

Tong,

Chen,

Xiang

et al. 2024

Preprint

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“…The 2 ′ , 7 ′ −dichlorofluorescein diacetate (DCFH − DA) was used for quantification of the intracellular ROS levels according to a previously described method. 41 Briefly, the cells were harvested and labeled with 1 μM DCFH-DA in Opti-MEM for 30 min at 37 °C. The cells were then washed three times with and finally resuspended in Opti-MEM.…”

Section: Cellular Ros Level Measurementmentioning

confidence: 99%

Curcumin Protects Pheochromocytoma Cells Against Hydrogen Peroxide-Induced Oxidative Stress

Sun,

Chen,

Lin

et al. 2023

Natural Product Communications

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Objective: Oxidative stress represents a characteristic of neurodegenerative diseases, which may be alleviated by the functional food component—curcumin. However, the underlying mechanism remains unclear. The current study aimed to address how curcumin protects variant differentiated pheochromocytoma (PC12) cells against hydrogen peroxide (H2O2)-induced cell stress, using low- and high-differentiated PC12 cells, and validated in old-aged mice. Methods: The MTT assay was first carried out to test the cell viability upon H2O2 and/or curcumin treatment and cellular lipid peroxidation was assessed as cellular damages by quantifying the amount of cellular malondialdehyde. Cellular oxidative stress was determined by measuring the cellular and mitochondrial ROS levels, and total cellular antioxidant capacities were determined as the ABTS free radical scavenging ability (ABTS) and Fe3+ reduction ability of cells. The activities and expression of major antioxidant enzymes, including glutathione peroxidase (GPx), superoxidase dismutase (SOD) and catalase (CAT), were also tested. Furthermore, oxidative phosphorylation of mitochondria was assessed by measuring the ATP level and the ADP/ATP ratio. Finally, the antioxidant activity of curcumin was determined in 6-month-old mice by measuring cellular antioxidant capacity and antioxidant enzyme activities. Results: H2O2 caused oxidative damage and decreased cell viability, which was reversed by curcumin with different dosed effects in variant differentiated PC12 cells. Moreover, curcumin's protective effect was attributed to an enhanced antioxidant enzyme system. In consistent, curcumin recovered H2O2-deteriorated oxidative phosphorylation. Further studies verified that curcumin significantly improved the antioxidant capacity of old-aged mice, which may have elevated oxidative stress. Conclusion: Taken together, curcumin improved the antioxidant capacity of variant differentiated PC12 cells and old-aged mice, which was closely associated with the modulation of mitochondrial function and antioxidant enzyme system. This study may shed light on the molecular mechanism underlying the alleviation of neurodegenerative diseases by natural polyphenols.

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Marine anticancer drugs in modulating miRNAs and antioxidant signaling

Chuang,

Yen,

Tang

et al. 2024

Chemico-Biological Interactions

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MiR-125b-5p is targeted by curcumin to regulate the cellular antioxidant capacity

Cited by 4 publications

References 45 publications

Mesenchymal Stem Cell-derived Exosomal miR-125b-5p Suppressed Retinal Microvascular Endothelial Cell Ferroptosis by Targeting P53 in Diabetic Retinopathy

Mesenchymal Stem Cell-derived Exosomal miR-125b-5p Suppressed Retinal Microvascular Endothelial Cell Ferroptosis by Targeting P53 in Diabetic Retinopathy

Curcumin Protects Pheochromocytoma Cells Against Hydrogen Peroxide-Induced Oxidative Stress

Marine anticancer drugs in modulating miRNAs and antioxidant signaling

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