Curcumin nanoparticles alleviate brain mitochondrial dysfunction and cellular senescence in γ-irradiated rats

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Янв. 31, 2025

Despite the diverse applications of γ radiation in radiotherapy, industrial processes, and sterilization, it causes hazardous effects on living organisms, such as cellular senescence, persistent cell cycle arrest, mitochondrial dysfunction. This study evaluated efficacy curcumin nanoparticles (CNPs) mitigating dysfunction senescence induced by rat brain tissues. Four groups male Wistar albino rats (n = 8 per group) were included: (Gr1) control group; (Gr2) CNPs group (healthy receiving oral administration at a dose 10 mg/kg/day, three times week for eight weeks); (Gr3) irradiated (rats exposed to single Gy head irradiation); (Gr4) + (irradiated treated with CNPs). The data obtained demonstrated that weeks attenuated oxidative stress γ-irradiated lowering brain's lipid peroxidation level [malondialdehyde (MDA)] enhancing antioxidant markers [superoxide dismutase (SOD), reduced glutathione (GSH), total capacity (TAC)] (P < 0.05). In addition, significantly increased function improving complex I, II, ATP production levels compared group. rats, also showed anti-neuroinflammatory reducing interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), nuclear factor-kappa B (NF-ĸB) Moreover, administered β-galactosidase activity expression p53, p21, p16 genes 0.05) while concurrently inducing significant increase AMPK mRNA conclusion, ameliorated neurotoxicity hold promise novel agent delay via their combined antioxidant, anti-inflammatory, mitochondrial-enhancing properties.

Язык: Английский

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Cell enlargement modulated by GATA4 and YAP instructs the senescence-associated secretory phenotype

Nature Communications, Год журнала: 2025, Номер 16(1)

Опубликована: Фев. 17, 2025

Dynamic changes in cell size are associated with development and pathological conditions, including aging. Although enlargement is a prominent morphological feature of cellular senescence, its functional implications unknown; moreover, how senescent cells maintain their state less understood. Here we show that an extensive remodeling actin cytoskeleton necessary for establishing senescence-associated pro-inflammatory secretory phenotype (SASP). This attributed to balancing act between the SASP regulator GATA4 mechanosensor YAP on expression Rho family GTPase RHOU. Genetic or pharmacological interventions reduce attenuate minimal effect senescence growth arrest. Mechanistically, couples nuclear localization NF-κB via Linker Nucleoskeleton Cytoskeleton (LINC) complex. RhoU protein accumulates mouse adipose tissue under senescence-inducing conditions. Furthermore, RHOU correlates during human Thus, our study highlights unexpected instructive role modulating reveals mechanical branch regulatory network. Senescent accumulate aging exhibit enlargement, function which has been unclear decades. Here, authors identify antagonistic genetic circuit hypertrophy reveal SASP.

Язык: Английский

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Anti-Hair Loss Effect of Veratric Acid on Dermal Papilla Cells

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(5), С. 2240 - 2240

Опубликована: Март 2, 2025

The activation of hair follicle dermal papilla cells (HFDPCs), a critical target loss relief, can be achieved through the upregulation proliferation, stimulation inducibility, and inhibition cellular senescence. Veratric acid (VA) is major benzoic found in fruits vegetables. biological activity VA on HFDPCs remains to elucidated. In this study, we investigated capacity for mitigation. An MTT assay, Ki67 staining, quantitative RT-PCR (qRT-PCR), Western blot analysis were performed confirm proliferative effect VA. Hair inductivity was determined cell aggregation assay ALP staining. Annexin V/PI staining anti-apoptotic inhibitory senescence confirmed by β-galactosidase (β-gal) qRT-PCR using replicative oxidative stress-induced models. As result, dose-dependently upregulated proliferation HFDPCs, expression growth factors, β-catenin protein levels. also increased decreased apoptotic regulation BCL2 BAX expression. Moreover, reduced β-gal senescence-associated secretory phenotype (SASP) dose-dependent manner senescent HFDPCs. These findings suggest that may serve as potential therapeutic agent alleviating targeting multiple pathways involved HFDPC activation.

Язык: Английский

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Imbalanced Redox Dynamics Induce Fibroblast Senescence Leading to Impaired Stem Cell Pools and Skin Aging

Free Radical Biology and Medicine, Год журнала: 2025, Номер unknown

Опубликована: Март 1, 2025

Язык: Английский

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Dose-dependent effects of curcumin on 22Rv1 prostate cancer cell line

Molecular Biology Reports, Год журнала: 2025, Номер 52(1)

Опубликована: Март 26, 2025

Prostate cancer (PCa) is the second most frequent type in male population over 66 years. Curcumin a polyphenolic natural compound extract from rhizomes of Curcuma longa Linn (Zingiberaceae family) which showed important anticancer effects by inhibiting cell proliferation and inducing apoptosis several types. Recently, some studies reported that oral curcumin lowered PSA levels, but it did not modify clinical outcomes patients with prostate who received intermittent androgen deprivation (IAD). Other high concentrations were toxic for patients. In this study we low doses can induce senescence-like 22Rv1 line while higher have cytotoxic effects. Five,15 30 µM blocked cycle G2/M phase only 15 induced death. addition, an increased expression p21, known senescence marker, was detected cells treated every experimental condition. However, p16, another to curcumin. context personalized approach PCa care, suggest appropriate concentration used combination radiotherapy or therapy (ADT) could be taken into consideration.

Язык: Английский

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Phenotypic changes associated with continuous long term in vitro expansion of bone marrow-derived mesenchymal stem cells

Biochimie, Год журнала: 2025, Номер unknown

Опубликована: Апрель 1, 2025

In vitro expansion of mesenchymal stem cells is necessary to obtain a higher cell number for clinical applications. However, long-term can produce significant phenotypic changes on these cells, decreasing their therapeutic utility. Therefore, understanding the that triggers in will allow better and more consistent therapy results. Here, we evaluate caused by continuous passaging through colony forming unit-fibroblast assay, senescence beta-galactosidase staining, morphology examination, secretome analysis, surface marker expression, protein quantification, osteogenic adipogenic differentiation, CD4+ T lymphocyte immunosuppressive potential. Long-term culture decreases potential self-renewal, increases size, senescence, but does not consistently affect differentiation. Surface expression remains similar positive negative markers, while secretory phenotype shifts with decreased p14ARF, MMP-3, p21 Waf1/Cip1,ENA-78, GCP-2, GROα, IL-3, IL-7, IL-8, RANTES, TNFβ, VEGF-A increased p53, p16 INK4a, MCP-1, SDF-1 expression. Immunomodulatory unchanged. These findings help understand undergo expanded vitro.

Язык: Английский

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Targeting p53-p21 signaling to enhance mesenchymal stem cell regenerative potential

Regenerative Therapy, Год журнала: 2025, Номер 29, С. 352 - 363

Опубликована: Апрель 8, 2025

Язык: Английский

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Cellular senescence: A new perspective on the suppression of periodontitis (Review)

Molecular Medicine Reports, Год журнала: 2024, Номер 30(6)

Опубликована: Окт. 14, 2024

Cellular senescence, characterized by cell cycle arrest, can result in tissue dysfunction when senescent cells persist and accumulate. Periodontitis, a chronic inflammatory condition caused the interaction between bacteria immune system of host, primarily manifests as damage to periodontal tissues. Aging inflammation are interlinked processes that exacerbate each other. The progression localized is often accelerated conjunction with organ aging. presence release cytokines, modulators, growth factors proteases associated senescence‑associated secretory phenotype contribute deterioration present review aimed elucidate mechanisms cellular senescence its potential impact on periodontitis, offering novel insights for modulating microenvironment

Язык: Английский

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Epidermal loss of PRMT5 leads to the emergence of an atypical basal keratinocyte-like cell population and defective skin stratification

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Ноя. 8, 2024

ABSTRACT During skin development, ectoderm-derived cells undergo precisely coordinated proliferation, differentiation, and adhesion to yield stratified epidermis. Disruptions in these processes can result congenital anomalies including ectodermal dysplasia harlequin ichthyosis. Protein Arginine Methyl Transferase 5 (PRMT5)—an enzyme responsible for methylating arginine residues histones other proteins—maintains progenitor status germ limb bud cells. Similarly, vitro evidence suggests that PRMT5 prevents differentiation of basal keratinocytes, leading us hypothesize preserves the stem-cell phenotype keratinocytes vivo . To test this possibility, we generated conditional knockout (cKO) mice lacking Prmt5 early ectoderm (E7.5), impacting entire cKOs exhibited gross defects, compromised barrier function, reduced postnatal viability. Histological analyses revealed significant defects epidermal stratification, without alterations apoptosis or proliferation. Single-cell RNA ATAC-seq analysis identified an atypical population keratinocyte-like cKOs, a senescence-like program, characterized by increased Cdkn1a (p21), elevated senescence-associated secretory (SASP) molecules ( Igfbp2 ), decreased developmental transcription factor Trp63 ) expression. Our findings suggest keratinocyte senescence repressing , shedding light on epigenetic regulation maintenance disorders.

Язык: Английский

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Potential of natural senolytic compounds in eliminating senescent cells and alleviating age-related skin deterioration: a narrative review

Aging advances., Год журнала: 2024, Номер 1(2), С. 143 - 153

Опубликована: Дек. 1, 2024

Cellular senescence is one of the entirely accepted biological theories for aging process. It related to physiological limitations damaged cells, proliferation, and some diseases in old adults. This review explores mechanisms underlying skin aging, emphasizing role cellular its impact on dermal health, focusing senescence-associated secretory phenotype contribution systemic inflammation, cancer development, age-related diseases. The effects ultraviolet-induced carcinogenesis are addressed, relating oxidative damage caused by prolonged exposure ultraviolet radiation with premature acquisition senescent-like characteristics cells that ultimately lead photocarcinogenesis. In addition, this highlights potential natural senolytic compounds developing novel treatment options skin. vitro research has shown promising results applied treating together nanocarriers can better deliver these compounds. However, many aspects their use vivo still unknown. Future describing compound’s interactions an organism efficient needed if products ever be new formulations.

Язык: Английский

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