Introduction Botanical supplements are consumed to improve health despite the mystery of their mechanisms. One possible effect is hormesis, defined as a beneficial and stimulatory health effect at a low dose and detrimental effect at a high dose, or vice versa. Hormesis is usually discovered by manually examining the shape of dose-response curves, which is not scalable to the large number of chemical-assay combinations found in high-throughput screening (HTS) results. Methods We proposed a semi-automatic statistical testing procedure to quickly evaluate large-scale dose-response data, accompanied by an R package shorm for easy implementation. The nonparametric shape tests are more flexible with few assumptions. We also developed a new visualization method to represent the test conclusions and uncertainties simultaneously. This representation highlights both significant and ambiguous findings for efficient examination. Results We applied this method to a data set of 4860 chemical-assay pairs and identified 561 (12%) dose-response curves showing statistically significant hormesis. Conclusion Our discovery of hormetic curves is in line with estimates of hormetic behaviors in dose-response repositories like Tox21. Our proposed method has been effective in screening for hormesis from large-scale dose-response data, and the visualization method effectively facilitates the interpretation of test results.
The application of nuclear technology in energy, healthcare, and aerospace sectors is increasingly widespread, causing radiation protection to be an important topic for public health and biomedical research. Ionizing radiation causes harm by damaging cells directly or indirectly. Traditional radiation protection adopts physical barriers and pharmacological methods, which have proved to be effective but have certain limitations. The Mediterranean diet, fasting or calorie restriction, ketogenic diet, plant-based diet, and high-fiber diet are common and reliable dietary patterns. Dietary patterns contribute to regulating key molecular pathways including oxidative stress, inflammatory responses, metabolism, and gut microbiota. Enhancing the body′s resistance to radiation damage through dietary intervention represents a highly promising nutritional strategy. Understanding the mechanisms and research behind dietary interventions for radiation protection facilitates the integration of radiation protection into daily life, enabling the development of personalized, precision-based dietary intervention strategies. This review focuses exclusively on research evidence and mechanism analysis to assess the impact of dietary intervention on ionizing radiation protection and look forward to their potential and challenges for clinical radiotherapy support and radiation protection for special occupational groups.
Objectives The present study aimed to investigate the protective effect of daphnetin (dap) against high glucose and high free fatty acids (HGHF) and lipopolysaccharide(LPS)-induced injury in the aforementioned co-culture system under normal control conditions (normal glucose and no exogenous FFA supplementation), and to explore its potential molecular mechanisms. Methods Neutrophils were isolated from the peripheral blood of healthy individuals. Subsequently, HK-2 cells and a neutrophil suspension were co-cultured at 1x10 5 cells/mL to establish the experimental model. The non-cytotoxic concentration of dap for subsequent experiments was determined by Cell Counting Kit-8 (CCK-8) assay. Heparin-binding protein (HBP) concentration was measured using dry quantitative immunofluorescence assay. Inflammatory cytokines were quantified via cytometric bead array, and cell apoptotic rate was assessed by Annexin V-FITC-based flow cytometry. Results Both HGHF treatment and LPS exposure significantly elevated the levels of the inflammatory mediator HBP, cytokines (TNF-α, IFN-γ, IL-1β, IL-2, IL-6 and IL-10) and cellular apoptosis, whereas dap administration markedly attenuated these inflammatory and apoptotic alterations induced by HGHF or LPS (all P <0.05). Conclusion In this in vitro model, dap attenuated HGHF- and LPS-induced inflammatory and apoptotic responses. Further studies are needed to assess its relevance to diabetic kidney disease.
Background Cancer cells depend on a plentiful glucose supply to sustain rapid proliferation. When glucose becomes limited, they undergo adaptive changes to survive and metastasize, yet the underlying molecular mechanisms remain poorly defined. Methods LRRC15 expression was assessed in breast cancer cells under varying glucose concentrations. Its biological role was explored through RNA interference and neutralizing antibody experiments in vitro, as well as in mouse xenograft and metastasis models. Results Low glucose (1.0 g/L) strongly induced LRRC15 expression in a manner involving the transcription factor C/EBPα, an effect reversed by restoring high glucose (4.5 g/L). Depletion of LRRC15 inhibited cell growth and migration and attenuated the enhanced migration induced by low glucose. In vivo, LRRC15 knockdown reduced tumor burden and distant metastases, and a monoclonal antibody targeting LRRC15 significantly inhibited orthotopic tumor growth and metastasis. Conclusion These findings establish LRRC15 as a glucose-responsive gene that drives breast cancer cell growth and metastasis, underscoring its promise as a therapeutic target for metastatic breast cancer.
Objectives Acute liver injury, a lethal septic shock complication with scarce treatments, lacks research on Sesamoside’s liver-protective function. We explored its protective mechanisms against lipopolysaccharide (LPS)-induced liver injury via the nuclear factor kappa B/mitogen-activated protein kinases (NF-κB/MAPK) pathway. Methods Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and NF-κB/MAPK pathway were screened via bioinformatic analysis, and an LPS-induced mouse model was established for in vivo verification. Quantitative real-time polymerase chain reaction (qPCR) detected cytokines and vasoactive factors; Western blot measured proteins; Hematoxylin and eosin (H&E) staining and Immunohistochemistry (IHC) assessed liver pathology. Results 1-, 5-, and 10 mg/kg Sesamoside suppressed LPS- triggered excess TNF-α (∼97%, p < 0.0001), IL-6 (∼95%, p < 0.0001), IL-1β (∼91%, p = 0.0011) and nitric oxide (NO) (∼96%, p < 0.0001). It reduced NOD-like receptor family pyrin domain-containing 3 (NLRP3) by ∼25% ( p < 0.0001), and decreased nuclear factor-kappa B p65 subunit (P65), phosphorylated extracellular signal-regulated kinase/total extracellular signal-regulated kinase (p-ERK/ERK), phosphorylated c-Jun N-terminal kinase/total c-Jun N-terminal kinase (p-JNK/JNK) by 61% ( p < 0.0001), 25% ( p = 0.0066) and 49% ( p < 0.0001) respectively. Liver injury and inflammatory infiltration were markedly attenuated. Conclusion Sesamoside alleviates septic shock-related acute liver injury by inhibiting NF-κB/MAPK signaling and excessive inflammation, providing a promising natural compound for targeted therapy development.
Objectives To investigate the expression pattern, prognostic significance, immune relevance, and biological function of Dynein Light Chain Roadblock-Type 1 (DYNLRB1) in hepatocellular carcinoma (HCC). Methods Publicly available datasets and analytical platforms, including TCGA, GTEx, TIMER2.0, TISIDB, LinkedOmics, GEPIA2, CancerSEA, and the Human Protein Atlas, were utilized to evaluate DYNLRB1 expression, prognostic value, and immune infiltration characteristics. In vitro functional assays—including CCK-8, EdU incorporation, colony formation, wound-healing, and Transwell assays—were performed to validate the biological role of DYNLRB1 in HCC cells. Results DYNLRB1 was significantly upregulated in HCC tissues and cell lines. Elevated DYNLRB1 expression was consistently associated with advanced clinicopathological features and poor survival outcomes across multiple metrics (including OS, DSS, DFI, and PFI). Furthermore, high DYNLRB1 expression correlated with an immunosuppressive tumor microenvironment signature, characterized by elevated inhibitory immune checkpoints. Functional enrichment suggested involvement in ribosome biogenesis and cell-cycle-associated processes. In vitro, DYNLRB1 knockdown significantly inhibited HCC cell proliferation, migration, and invasion. Conclusion DYNLRB1 is a potential prognostic biomarker associated with tumor malignant progression and an immunosuppressive microenvironment in HCC. These findings suggest that DYNLRB1 may represent a potential therapeutic target warranting further investigation.
Background The Linear No-Threshold (LNT) model and the As Low As Reasonably Achievable (ALARA) principle form the cornerstone of contemporary radiation protection. Although these frameworks were designed as conservative regulatory tools, their extrapolation to the low-dose and dose-rate (LDDR) range commonly encountered in diagnostic imaging remains scientifically contentious. Objective This review critically examines the scientific basis for applying the LNT model and the ALARA principle in the LDDR range (1–50 mGy) routinely encountered in diagnostic imaging, with the aim of evaluating whether current regulatory practices are proportionate to demonstrated risks. Methods We conducted a narrative review of peer-reviewed literature published between 1995 and 2025, retrieved from PubMed, Scopus, and Web of Science using the search terms “LNT model,” “low-dose radiation,” “ALARA,” “radiation hormesis,” “adaptive response,” and “diagnostic reference levels.” Priority was given to systematic reviews, large-cohort epidemiological studies, and consensus statements from professional organizations (ICRP, UNSCEAR, AAPM, HPS, IOMP). Studies were grouped thematically into radiobiological evidence, epidemiological evidence, and clinical/policy implications. We acknowledge that this is a non-systematic review and that selection bias cannot be excluded. Results Multiple lines of radiobiological evidence—including DNA repair fidelity at low doses, adaptive cellular responses, apoptotic clearance of damaged cells, and immune surveillance—suggest that the dose-response relationship for stochastic effects in the LDDR range is unlikely to be linear. Large-scale epidemiological studies, including atomic bomb survivor reanalyses, occupational cohorts, and high-background radiation populations, generally fail to demonstrate statistically significant excess cancer risk below approximately 100 mGy, although confidence intervals remain wide. Case examples in scoliosis screening, mammography, and low-dose CT lung cancer screening illustrate scenarios in which overly conservative ALARA implementation may delay or deter clinically beneficial imaging. Conclusions Within the LDDR range, the available evidence does not support a linear dose-response relationship, and the indiscriminate application of ALARA based on hypothetical risks may produce net harm through deferred imaging, radiophobia, and inefficient resource allocation. We propose that radiation protection in medical imaging shift toward an evidence-informed framework that prioritizes image quality optimization, individualized risk assessment, and the adoption of complementary principles such as ASARA (As Safe As Reasonably Achievable) and AHARA (As High As Reasonably Achievable benefits). A linear-with-threshold (LT) model and the adverse outcome pathway (AOP) framework warrant further investigation as alternatives to LNT for regulatory purposes.
Objective This study aimed to evaluate the efficacy and safety of sintilimab combined with anlotinib and chemoradiotherapy as first-line treatment for driver gene-negative oligometastatic non-small cell lung cancer (NSCLC). Methods This retrospective study included patients with driver gene-negative oligometastatic NSCLC (single organ, ≤2 lesions) treated at the Affiliated Zhangjiagang Hospital of Soochow University (7/2021–12/2023). All patients received 4 cycles of sintilimab plus albumin-bound paclitaxel/carboplatin and achieved partial response or stable disease. Subsequently, patients received concurrent radical radiotherapy with or without anlotinib, or continued the original regimen. Progression-free survival (PFS), overall survival (OS), objective response rate (ORR), disease control rate (DCR), and adverse events were analyzed. Results A total of 88 patients were included: 27 in the sintilimab plus chemotherapy (SC) group, 32 in the sintilimab plus chemoradiotherapy (SCR) group, and 29 in the anlotinib plus sintilimab and chemoradiotherapy (ASCR) group. The radiotherapy group (SCR + ASCR) showed significantly longer median PFS and OS than the non-radiotherapy group (SC) (7.7 vs. 16.5 months, P < 0.001; 20.1 vs. 31.8 months, P = 0.004). The ASCR group had significantly higher 12-month PFS, 18-month OS, and 24-month OS rates than the SCR group (P = 0.005, 0.014, and 0.046, respectively). ORR and DCR were significantly lower in the non-radiotherapy group (P < 0.001 and P = 0.007). Treatment-related adverse events were manageable. Conclusion In driver gene-negative oligometastatic NSCLC patients benefiting from first-line sintilimab plus chemotherapy, adding concurrent radical radiotherapy significantly improved survival with acceptable toxicity. The addition of anlotinib further enhanced long-term outcomes. These findings are preliminary and require prospective validation.
Because the existence of linear no-threshold (LNT) hypothesis in the low-dose region has not been confirmed, we previously proposed the “hormesis-coupled LNT theory.” Because this theory does not consider the effect of dose-rate, we applied our theory to different dose-rates using data from the previous reference (Yoshida et al. 2008). As a result, we calculated that the biological benefit via radiation can be observed at a dose-rate of <1 mGy/h. In the future, biologically beneficial factors may be identified by exploring the exposure region with cumulative doses of >350 mGy at this low-dose-rates.
Background:Pyogenic liver abscess (PLA) has been reported as a potential clinical marker for colorectal cancer (CRC). Patients with type 2 diabetes mellitus (T2DM) are generally considered at elevated risk for infections and cancers due to impaired immune function. However, the specific relationship between T2DM and CRC among individuals with PLA remains unclear. Methods:This retrospective cohort study was conducted using the TriNetX Global Collaborative Network. Adult patients (≥20 years) with PLA between 2010 and 2024 were identified and stratified by the presence of T2DM. Patients with amebic liver abscess were excluded. A 1:1 propensity score matching was performed to balance baseline characteristics between T2DM and non-T2DM groups, with standardized mean differences (SMD) <0.1 indicating adequate balance. The primary outcome was incident colon cancer (C18). The site-specific composite outcomes were right-sided colon and appendix cancer (C18.0-C18.4) and distal colorectal and anal cancer (C18.5-C21). The secondary outcome was all-cause mortality. Kaplan-Meier analyses with log-rank tests were used to compare cumulative incidence and survival between groups, and hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated using Cox proportional hazards models across multiple follow-up periods. Results:In this TriNetX-based retrospective cohort, 52,440 adults with PLA were identified, including 16,149 with T2DM. After 1:1 propensity score matching, 11,757 patients remained in each group with balanced characteristics (SMD <0.1). T2DM was not associated with an increased risk of overall colon cancer. Similar null associations were observed for the right-sided colon and appendix cancer composite and the distal colorectal and anal cancer composite., including at 3 months (HR 1.059, 95% CI 0.738-1.519), and remained non-significant at 5 years (HR 1.000, 95% CI 0.808-1.237). Findings were consistent across tumor locations. In contrast, T2DM was associated with higher all-cause mortality from 30 days (HR 1.181, 95% CI 1.051-1.326) to 5 years (HR 1.152, 95% CI 1.093-1.213). Conclusion:In patients with PLA, T2DM was not associated with an increased risk of overall colon cancer or either site-specific cancer composite. However, T2DM was consistently linked to significantly higher short- and long-term mortality, highlighting its adverse prognostic impact in this population.
Background Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with limited disease-modifying therapies. Aluminium chloride (AlCl 3 )-induced neurotoxicity mimics key pathological features of AD, including oxidative stress, neuroinflammation, and cholinergic dysfunction. Objective This study aimed to evaluate the neuroprotective effect of cnicin in an AlCl 3 -induced rat model of Alzheimer-like neurodegeneration. Methods Rats were divided into five groups: normal control, AlCl 3 control (75 mg/kg/day, p.o.), AlCl 3 with cnicin (20 and 40 mg/kg/day, p.o.), and AlCl 3 with donepezil (5 mg/kg/day, p.o.) for 30 days. Behavioral performance was assessed using hanging wire and beam walking tests. Biochemical parameters, including acetylcholinesterase (AChE), antioxidant enzymes (SOD, CAT, GSH), malondialdehyde (MDA), and inflammatory cytokines (TNF-α, IL-1β) were analyzed, along with histopathology. Results AlCl 3 administration induced significant behavioral deficits, increased AChE activity, oxidative stress, neuroinflammation, and neuronal damage. Cnicin treatment dose-dependently improved motor function, reduced AChE activity, restored antioxidant levels, decreased lipid peroxidation, and suppressed inflammatory markers. Histological analysis confirmed preservation of neuronal architecture, comparable to that of donepezil. Conclusion Cnicin exhibits significant neuroprotective effects against AlCl 3 -induced neurodegeneration by modulating cholinergic activity, oxidative stress, and inflammation, suggesting its potential as a therapeutic agent for AD.
Purpose This study aims to systematically explore the molecular mechanism underlying ibrutinib-induced cardiotoxicity. Methods Network toxicology was applied using DrugBank, PharmMapper, GeneCards, OMIM, and TTD databases to identify overlapping targets between ibrutinib and myocardial injury, followed by PPI network construction (STRING; confidence ≥0.7) and GO/KEGG enrichment analyses (Metascape). Molecular docking (AutoDock Vina) verified ibrutinib’s binding affinity to core targets. In vitro, H9C2 cardiomyocytes were exposed to ibrutinib (0, 10, 20, 40, and 80 μM) for 24 h; CCK-8, DCFH-DA, EdU, and Calcein-AM/PI assays were performed to assess cell viability, ROS levels, proliferation, and cell death, respectively. Western blot analyzed phosphorylation of EGFR/PI3K/Akt/mTOR pathway proteins. Results A total of 42 overlapping targets were screened from 337 ibrutinib-related targets and 471 myocardial injury-related genes. PPI network analysis identified EGFR, AKT1, SRC, ESR1, and CASP3 as hub genes, and KEGG enrichment analysis identified the PI3K-Akt pathway as the most significantly enriched cascade. Molecular docking confirmed that ibrutinib stably bound BTK and EGFR with a binding energy of -30.2 kcal/mol and formed multiple hydrogen bonds and salt bridges (2.2–3.2 Å). In H9C2 cells, ibrutinib dose-dependently reduced viability (IC50 = 119.49 μM), increased ROS production (40 and 80 μM), inhibited proliferation (10 and 20 μM), and promoted cell death (5 and 10 μM). Western blot confirmed that ibrutinib significantly downregulated phosphorylation of PI3K p85, Akt (Ser473), mTOR (Ser2448), and p70S6K (Thr389) without altering total protein expression. Conclusion Ibrutinib induces cardiotoxicity by targeting BTK/EGFR and inhibiting the downstream EGFR/PI3K/Akt/mTOR pathway, providing a mechanistic framework for clinical safety management of BTK inhibitors.
Accurate dose estimation following radiation accidents remains challenging, particularly when personal dosimeter data are unavailable. This study presents a practical post-accident dose reconstruction approach based on minute-rate thermoluminescent dosimeter (TLD) measurements combined with exposure scenario reconstruction, demonstrated through a wavelength-dispersive X-ray fluorescence (WD‒XRF) spectrometer accident. The exposure scenario was reconstructed by placing LiF(Mg,Cu,P) TLDs at seven representative positions corresponding to head and hand locations, with the spectrometer operated under the recorded technical parameters (40 kV, 7 mA). Minute personal dose equivalent rates, H p ′(10), were measured and combined with reconstructed retention times to calculate cumulative doses, from which skin absorbed doses were derived. The measured dose rates ranged from 0.13 to 358.38 mSv/min for the head and from 0.07 to 620.24 mSv/min for the hands. The resulting cumulative skin absorbed doses were 7.58 Gy for the head and 12.52 Gy for the hands, consistent with reported dose ranges associated with localized radiation injury. This approach provides a feasible supplementary strategy for retrospective dose reconstruction under emergency or resource-limited conditions when conventional dosimetric information is unavailable.
Background The current study investigates the suitability of encapsulating the Artemisinin-plant-originated lipophilic drug molecule into polyethylene glycol-coated mesoporous silica nanoparticles in a suitable dose regimen for the specific targeting of the drug in colorectal cancer. Methodology Mesoporous silica nanoparticles (MSNPs) were synthesized through the sol-gel method, and Artemisinin was loaded. Then characterization of Artemisinin-loaded mesoporous silica nanoparticles coated with polyethylene glycol (MSN-PEG@Artemisinin) was performed by Fourier transform infrared spectroscopy (FTIR), Zeta analysis, Polydispersity index (PDI) and X-Ray diffraction (XRD) techniques and compared with the standard drug Gemcitabine. The in vivo analysis of 1,2-dimethylhydrazine (DMH) was used to induce colorectal tumors in the colon of inbred male Wistar rats. The treatment group of rats was administered MSN-PEG@Artemisinin through intraperitoneal injection. Hematoxylin and eosin staining were performed to the histopathological examination of tumors. Results The average size of MSN-PEG@Artemisinin was 203.6 ± 64.78 nm with a zeta potential of -10.9mV. PDI was measured at 0.106. FTIR analysis also supported the successful loading of Artemisinin in mesoporous silica nanoparticles with PEG coating without showing interactions. The encapsulation efficiency (EE) and Drug loading (DL) percentages were 82.75% and 33.10%, respectively. XRD indicated a uniform mesoporous structure with a proper hexagonal symmetry. The in-vitro release was carried out in phosphate buffer with 7.4 pH following biphasic system with 26% drug release during the first 2.5 hours and 57% in 24 hours, indicating a good controlled release rate. In-vivo study revealed DMH-induced colorectal rats showed the increased tumor weight (34.8±0.75mg) tumor length (8.2±0.6) and tumor width (6.0±0.5) at a dose level of 0.5 ml/kg. Artemisinin loaded MSNPs significantly (p < .005) suppressed tumor weight (15.6±1.56), tumor length (5.7±0.23) and tumor width (2.3±0.8) at a dose level of 100 mg/kg body weight. Overexpression of 8-OHdG, MMP-7, CA-19-9, KRAS, IL-8, Caspase-8, PD-1 and PDL-1 in CRC, which were successfully treated with MSN-PEG@Artemisinin and standard Gemicitabine ((p≥0.056). MSNPs-PEG@Artemisinin suppressed DMH-induced colorectal carcinogenesis by targeting oxidative stress, KRAS/MMP-7/IL-8 inflammatory signaling, PD-1/PD-L1-mediated immune evasion, and Caspase-8-associated apoptotic dysregulation. Conclusion These results highlight the potential of modified MSNPs as a versatile drug delivery system for colorectal cancer, providing a viable approach to enhance the therapeutic window of Artemisinin by controlling the dose while reducing the adverse effects of cancer therapies. This research contributes to advancements in pre-clinical studies and to improvements in targeted colorectal cancer therapies by providing insights into the development and use of mesoporous silica nanoparticles as a promising drug delivery system.
Introduction:Children are highly susceptible to radiation's carcinogenic effects. Lifestyle, in particular, diet-induced obesity (DIO) is closely linked to cancer risk factors. Most prior studies, however, have concentrated on the impact of long-term lifestyle factors. Objective:We assessed the impact of a short-term, high-fat diet (HFD) during young or adult on lifespan shortening and tumor development after infant radiation exposure. Methodology:B6C3F1 male mice were irradiated at 1 week of age with 4 Gy of gamma rays or did not undergo irradiation (0 Gy). After weaning, they were assigned to HFD or normal-fat diet (NFD) for four weeks during young (4-8 weeks old) or adult (20-24 weeks old) stages. Body weight measurement, plasma biochemical analysis, lifespan analysis, and histopathological analysis for tumor diagnosis were carried out. Results:A temporary gain of body weight and hyperlipidemia were observed in mice fed the HFD. Although short-term HFD intake had limited impact on lifespan shortening and tumor development, a short-term HFD at a young age significantly increased spontaneous hepatocellular carcinoma (HCC) risk. Conclusion:The influence of a short-term HFD on DIO-associated cancer, such as HCC, should be specifically noted. Lifestyle normalization has potential for reducing cancer risk.
Objectives To determine whether hormesis can be derived from the geometry of bounded adaptive biological endpoints, and whether the derivation yields quantitative predictions independent of curve fitting. Methods Bounded endpoints were represented in rapidity coordinates using the arctanh linearisation of the adopted Möbius composition law. Repair activation and damage accumulation were modelled as opposing bounded rapidity increments with independently measurable thresholds. The molecular-to-functional attenuation factor was derived for linear pathways from the metabolic-control summation theorem and separated from a testable multi-target extension. Predictions were compared with published H 2 O 2 , CdCl 2 , and heat-shock dose-response data. Results The model predicts a biphasic response whenever repair activation precedes toxicity (D a < D t ) and high-dose damage ultimately exceeds bounded repair capacity. The exact hyperbolic model is the primary model; the product form is used only as a conservative analytical approximation. Aggregate predictions — peak-amplitude range, mean amplitude, and hormetic-zone width — matched the Calabrese hormesis database of more than 10,000 responses without parameter fitting; across three mechanistically distinct agents, independently published data confirmed the structural prediction that adaptive activation precedes toxicity, and pathway-specific attenuation distinguished linear NRF2-mediated responses (130–160%) from larger multi-target heat-shock responses (200–300%). The peak-location law is presented as a falsifiable prediction. Conclusion Within the stated scope of independently composing bounded adaptive endpoints, hormesis follows from finite repair capacity plus adaptive upregulation. The framework does not claim that all biological history is axiomatic; it identifies the conditional geometry that constrains dose-response shape once a bounded adaptive endpoint is specified.
Dietary restriction (DR) has been extensively investigated for its capacity to extend lifespan and mitigate age-associated pathologies. In the context of ionizing radiation (IR), DR—implemented through caloric reduction, selective nutrient restriction, or fasting-based regimens—has emerged as a significant modulator of both cellular and systemic responses to radiation exposure. Growing evidence suggests that DR influences radiation outcomes in a highly context-dependent manner, exerting either protective or sensitizing effects depending on tissue type, metabolic status, timing of intervention, and radiation conditions. This review synthesizes current knowledge regarding the mechanisms through which DR modulates responses to IR, with particular emphasis on oxidative stress regulation, inflammatory signaling, mitochondrial homeostasis, DNA damage responses, cellular quality-control pathways, and carcinogenic processes. We further discuss how distinct dietary paradigms interact with nutrient-sensing and stress-adaptive networks to influence radiation sensitivity and tissue recovery. Emerging evidence indicates that the timing, intensity, and composition of dietary interventions critically shape tissue responses to IR, underscoring the importance of considering nutritional status in radiation risk assessment and therapeutic planning. By integrating established findings with emerging mechanistic insights, this review highlights the translational potential of DR for improving outcomes in radiation oncology and reducing radiation-induced injury.
Gastric cancer (GC) ranks third globally in cancer mortality. It develops via a well-defined pathological sequence: normal gastric mucosa progresses sequentially to superficial gastritis, chronic atrophic gastritis (CAG), intestinal metaplasia, dysplasia, and ultimately invasive carcinoma. Given this stepwise carcinogenic cascade, early intervention during the precancerous stage, particularly in CAG, is paramount for secondary GC prevention. Emerging evidence underscores that microRNAs (miRNAs), a major subclass of non-coding RNAs (ncRNAs), exert crucial regulatory effects on gastric carcinogenesis. Dysregulated miRNAs are frequently detected in Helicobacter pylori-infected gastric mucosa, driving chronic inflammation, epithelial-mesenchymal transition (EMT), and subsequent malignant transformation. Recently, traditional Chinese medicine (TCM) has gained increasing recognition as a promising therapeutic approach for precancerous lesions of gastric cancer (PLGC). Classical TCM formulations and bioactive herbal compounds have been shown to exert multi-targeted and multi-pathway efficacy in inhibiting the progression of this disease. This review integrates available evidence and indicates that TCM interventions, including herbal prescriptions and acupuncture, exert anti-inflammatory, anti-fibrotic and anti-metastatic effects by regulating microRNA expression profiles, thereby alleviating chronic inflammation, pathological remodeling and tumor cell invasion. Collectively, these findings demonstrate TCM’s adjunctive potential in CAG treatment and GC prevention, providing a novel mechanistic approach to halt precancerous gastric carcinogenesis.
Objectives This study aims to valorize Fagonia arabica (Dhamasa booti) herbal waste by synthesizing bioactive iron oxide (FeO) and zinc oxide (ZnO) nanoparticles for anticancer applications. Methods Aqueous extracts of F. arabica were utilized to green-synthesize FeO and ZnO NPs. The nanoparticles were characterized for morphology, size, crystallinity and zeta potential. Their antioxidant activity, brine shrimp lethality, and hemolytic assays were performed to determine bioactivity and cyto-compatibility. Results FeO and ZnO NPs were spherical, monodispersed and polycrystalline with particle sizes of 28.8 nm and 30.4 nm, respectively. ZnO NPs showed stronger antioxidant activity (80.81% scavenging at 150 μg/mL) and higher cytotoxicity in the brine shrimp assay (LC 50 = 0.98 μg/mL), compared to FeO NPs and the crude extract. Minimal hemolytic activity, confirmed their favorable biocompatibility. Zeta potential values of -36 mV (FeO) and +33.6 mV (ZnO) indicate moderate colloidal stability. In vitro anticancer analysis revealed superior performance of ZnO NPs with IC 50 values of 43.79 µg/mL (HepG2) and 66.71 µg/mL (HT-29). Conclusion Fagonia Arabica- derived ZnO NPs exhibit potent antioxidant, cytotoxic and anticancer activities, along with favorable biocompatibility. Their significant therapeutic performance highlights their role as effective plant-mediated antineoplastic agents and supports the value-added utilization of F . arabica herbal waste.
Objectives Ferroptosis is a distinct form of programmed cell death characterized by iron (Fe)-dependent oxidative stress and the accumulation of intracellular reactive oxygen species. Cisplatin (CPT), a chemotherapeutic agent, can induce ferroptosis in glioma cells and act synergistically with erastin (EST). The total extract of the fungus Sanghuangporus vaninii (TSV) has anticancer and antioxidant activities. This investigation aimed to assess the properties of TSV on CPT-induced inflammatory response and ferroptosis-related changes in glioma cells. Methods LNZ308 glioma cells were exposed to CPT and EST, followed by treatment with different TSV concentrations. Cell viability was assessed. Intracellular reactive oxygen species (ROS), glutathione peroxidase 4 (GPX4), glutathione (GSH), labile iron pool (LIP), LPO, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were examined, and cell migration was assessed using a scratch assay. Results TSV (25 µg/mL) exhibited limited toxicity to LNZ308 cells but failed to reverse the CPT-induced loss of cell viability. TSV markedly reduced ROS levels, LIP, and LPO, while restoring GSH and GPX4 levels. Moreover, it diminished IL-1β, TNF-α, and IL-6 in CPT-treated LNZ308 cells in a dose-responsive manner. L-ascorbic acid diminished ROS levels during oxidative stress. TSV also promoted scratch closure in both untreated and CPT-treated LNZ308 cells. Conclusion The results indicate that TSV modulates CPT-induced oxidative, inflammatory, and ferroptotic responses in LNZ308 glioma cells in vitro, supporting further investigation of its potential as an adjunct to chemotherapy.
