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The fundamental purpose of this work is to determine the anti‐inflammatory/antioxidant activity of stem cell conditioned medium enhanced by mono‐ or dual‐doped TiO2 nanoparticles. The transmission electron microscope, X‐ray diffraction, and energy‐dispersive X‐ray analyses are used to characterize the nanoparticles. Isolation/characterization of adipose tissue mesenchymal stem cells (AD‐MSCs) is done. In vitro assays reveal that protein denaturation and proteinase induction are significantly increased with lipopolysaccharide (LPS) comparable to control, while treatments significantly decrease the induction compared to LPS. In vitro assays reveal decreasing in hydroxyl radical scavenging and DPPH radical scavenging activities with LPS, while treatments significantly increase the activity compared to LPS. Induction with LPS decreases in vitro catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) expression levels and enzyme activities are significantly compared to controls, while treatments significantly increase the CAT expression compared to LPS. Induction with LPS increases the in vitro interleukin 4 (IL4), IL6, IL10, and tumor necrosis factor α expression levels, and their activities significantly decline with treatment compared to controls, while treatments significantly decline expression compared to LPS. The anti‐inflammatory and antioxidant properties of AD‐MSC‐conditioned medium enhanced with mono‐ or dual‐doped TiO2 nanoparticles are identified in this investigation. To sum up, the work has shown that mono‐ and dual‐doped TiO2 can inhibit the inflammation caused by LPS in vitro. The PI3K/AKT pathway is triggered when lipopolysaccharide (LPS) binds to TLR4 on the cell membrane. This causes the NF‐κB complex to get phosphorylated and IKB to degrade, allowing NF‐κB to go into the nucleus. Pro‐inflammatory genes including interleukin‐4 (IL‐4), IL‐6, and tumor necrosis factor α are triggered by this. NF‐κB activation is further enhanced by LPS's simultaneous induction of oxidative stress, which produces reactive oxygen species (ROS) and byproducts like MDA. By breaking down the Keap1‐Nrf2 complex, ROS releases Nrf2, which moves to the nucleus and attaches to the antioxidant response element to promote the production of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). This activates the Nrf2 pathway to combat oxidative. The addition of TiO2 nanoparticles (mono‐ and dual‐doped) and adipose tissue mesenchymal stem cell (AD‐MSC)‐conditioned media modulates these pathways by reducing oxidative and inflammation, with AD‐MSC bioactive factors and TiO2 nanoparticles (NPs) synergistically enhancing the anti‐inflammatory and antioxidant responses to restore cellular balance.

Globally, colorectal cancer ranks second in women and third in men. Hydrophilic anticancer agents have limited use in lipid systems due to their weak solubility. Therefore, this study aimed to develop oleogels based on pumpkin seed oil (R1) and hydrophilic bioactive canola extract (BCE or R2) that were extracted from canola meal by-products. BCE was effectively dispersed in oleogels through the encapsulation of BCE with various concentrations (0.08, 0.2, and 0.4%) in soy lecithin to form BCE gelling agents. Four formulations (F1 as plain, F2-F4 with different concentrations of BCE) were produced using two gelators (BCE gelling agent and beeswax). The oxidative stability, microstructure, FTIR, antioxidant activity, and time-dependent experiment were investigated. The cytotoxicity against colorectal HCT116 and Caco-2 cancer cell lines in vitro was evaluated. The anti-apoptotic PI3k and COX-2 protein expressions were also assessed. The peroxide, p-anisidine, and total oxidation values of F4 were 7.85, 26.66, and 42.35, respectively, during 60 days at 60 ± 2 °C. The antioxidant activity values of F4 were 74.40% for DPPH, 54.28% for ABTS, and 5.77 mg/g for FRAP. F4 demonstrated the highest significant cytotoxic effects on cancerous cells, particularly in the Caco-2 cells with 1.40- and 1.41-fold increases compared to R2 and the positive control doxorubicin, respectively. PI3k and COX-2 expression levels were down-regulated while iNOS activity was up-regulated in both cells, with very high down-regulation recorded for F4 in Caco-2 cells. This study developed a method for producing stable lipid products loaded with hydrophilic antioxidants that may be used as an anti-colorectal platform.

Hepatocellular carcinoma (HCC) is a global health problem with regional differences in epidemiological statistics. Co-assembling the drug nanoparticles and targeting moieties could improve the therapeutic delivery of anti-cancer drugs. In this attempt, we tracked the extrinsic and intrinsic apoptotic pathways in HCC cells using viramidine (VRM)-loaded aptamer (APT) nanoparticles. In these NPs, both APT and VRM act as targeted ligands/drugs to HCC cells. The NPs were characterized using TEM, ESI–MS, FTIR, and 1 H NMR. The results showed uniform particles with round and smooth shapes on the nano-scale. SRB-based cytotoxicity was performed and IC 50 values were measured for HCC versus normal cells upon the proposed treatments. The flow cytometry technique was applied to determine apoptosis, then confirmed using genetic and protein analyses. In addition, nitric oxide (NO) and its enzyme (iNOS) were analyzed to examine the effect of reactive nitrogen species (RNS) on apoptosis induction. The present findings indicated that Huh-7 cells were more sensitive to APT-VRM NPs than HepG2 cells, recording the lowest IC 50 values (11.23 ± 0.23 µM and 16.69 ± 1.12 µM), as well as the highest significant increase in the apoptotic cells (61.5% and 42%), respectively. Intriguingely, normal BHK-21 cells recorded undetectable IC 50 values in the applied NPs, confirming their targeted delivery ability. The genetic expression and protein levels of c-FLIP, Bcl-2, and TNF-α were down-regulated, while FADD, caspase 8, caspase 3, caspase 9, and Bax were up-regulated upon treatment with APT-VRM NPs. The prepared VRM NPs labeled with APT could significantly elevate NO via activation of iNOS. In conclusion, APT-VRM NPs bioconjugate interferes with HCC cells through NO-mediated extrinsic and intrinsic apoptosis.

This study aimed at targeting hepatic cancer stem cells (CSCs) with quercetin (Q) or kaempferol (K) loaded into poly(lactide-co-glycolide) (PLGA) nanoparticles (NPs) decorated with CD133 antibody. For this purpose, the formulated Q NPs and K NPs and their free forms were evaluated for their cytotoxic potential, apoptotic activity, and anti-migratory effect against CD133 + CSCs isolated from the Huh7 cell line. Moreover, their influence on the hepatic CSCs-relevant molecular pathways was evaluated through analyzing several related gene expression levels. Interestingly, the in vitro study revealed that the Q NPs and K NPs and their free forms exhibit significant cytotoxic potential against CSCs isolated from the Huh7 cell line. The flow cytometric analysis revealed that Q NPs recorded the highest induction of apoptosis (77.8%) relative to the control (1.8%). The migration of hepatic CSCs is restrained by treatment with the suggested NPs and their free forms, but the most pronounced effect was observed after treatment with Q NPs. Both Q NPs and K NPs triggered significant down-regulation in the expression level of ABCG2, survivin, vimentin, cyclin D1, c-Myc, MMP-7, and VEGF genes in hepatic CSCs. The treatment with Q NPs motivated significant up-regulation in the expression level of the P53 gene in hepatic CSCs. Conclusively, the obtained results shed light on the success of Q NPs and K NPs modified with CD133 antibody on their surfaces in targeting hepatic CSCs. This effect was evidenced by their ability to significantly induce apoptosis, inhibit metastasis, reverse drug resistance, and interfere with CSC-associated signaling pathways.

Psoriasis is a chronic skin disorder with significant individual and societal impacts. Current therapies often lack efficacy, are costly, or cause side effects, necessitating new treatments. This study explores regenerative therapies—exosomes, mesenchymal stem cells (MSCs), epigallocatechin-3-gallate nanoparticles (EGN), and EGN-loaded exosomes (EGN-Exo)—in regulating psoriasis-related markers (IL-6, IL-4, Bcl-2, Bax, NF-κB, CDC25B). An imiquimod-induced psoriasis model in Wistar rats was used, with six groups: negative control, positive control, and treatments (MSCs, exosomes, EGN, EGN-Exo). After seven days, ELISA revealed EGN-Exo most effectively reduced pro-inflammatory IL-6 and pro-apoptotic Bax while increasing anti-inflammatory IL-4 and anti-apoptotic Bcl-2. EGN-Exo also significantly lowered NF-κB and CDC25B, demonstrating superior anti-inflammatory effects. Apoptosis profiling showed EGN-Exo reduced late apoptotic cells, highlighting cytoprotective abilities. EGN had a moderate effect, while MSCs and exosomes showed modest improvements. Histopathological and immunohistochemical analyses confirmed EGN-Exo’s efficacy, notably reducing TGF-β expression. These findings suggest EGN-Exo combines EGCG’s antioxidant and anti-inflammatory properties with exosomes’ targeted delivery, offering a promising advanced therapy for psoriasis.

BackgroundThe volatile fraction of frankincense (Boswellia sacra) oleogum was extracted, formulated in nanoemulsion and tested against lung cancer A549 cell line. First, the gum was hydro-distilled to isolate the volatile fraction (essential oil), which was analyzed via gas chromatography to identify its major volatile constituents. Then, the oil was formulated in two water-based nanoemulsions which differ from one another in the presence of propylene glycol (PG), which is used in the formulation step as a co-surfactant. The pure essential oil as well as its major volatile compound (α-pinene), its two nanoemulsions and a reference drug (Doxorubicin) were evaluated against lung cancer A549 cell lines and WI-38 normal lung cells. The evaluation included cytotoxicity (MTT and IC50), apoptosis (flow cytometric analysis) in addition to genetic assessments for some intrinsic and extrinsic genes relevant to apoptosis and survival pathways.ResultsChromatographic analysis of frankincense essential oil revealed that α-pinene is the major volatile compound which constituent about 60% of that oil. Emulsification of the oil using the low energy technique gave nanoemulsions having major intense particles population (85–90%) with z-average diameter below 20.0 nm. Frankincense oil nanoemulsion fabricated with (PG) showed the best cytotoxic activity toward lung cancer A549 cell compared to PG-free nanoemulsion, α-pinene and the reference drug doxorubicin, along different incubation periods. Flow cytometric analysis also indicated that PG-containing nanoemulsion can induce cancer cells toward apoptosis better than the other formula and the pure oils. The same nanoemulsion was found to upregulate the pro-apoptotic genes [DR5, FAAD, Caspase 8 (Cas8), p53, and Bax] and downregulate the anti-apoptotic and reoccurrence genes (Bcl-2, NF-kB, and STAT-3). Most importantly, the PG-containing nanoemulsion had the least cytotoxic effect on the normal WI-38 lung cells.ConclusionsThese results point out to the potentials of frankincense essential oil (rich in α-pinene) and its PG-nanoemulsion as a promising adjuvant from plant-source to potentiate the activity of the systematic anti-lung cancer drugs.

Lipid oxidation significantly compromises the safety, nutritional quality, and shelf life of edible oils, while conventional analytical methods are costly, time-consuming, and unsuitable for real-time monitoring. This study presents a novel nanofiber-based colorimetric sensor for rapid visual detection of lipid oxidation in soybean oil (SBO) and extra virgin olive oil (EVOO) under accelerated storage conditions (70 °C for 35 days). Polyacrylonitrile (PAN) nanofiber mats containing Congo red dye (CR, 0.0025%, 0.005%, and 0.01%, w/w) were fabricated via solution-blowing spinning and characterized using scanning electron microscopy (SEM) and Fourier transform infrared spectroscopy (FTIR). Oxidative deterioration was evaluated through conjugated diene (CD) and triene (CT) values, para-anisidine value (p-AnV), total polar compounds (TPC), volatile oxidation compounds, Rancimat induction period (IP), FTIR analysis, and cytotoxicity assays. Among the developed sensors, Mat_III (0.01% CR) exhibited the highest sensitivity, showing distinct color responses with ΔE values of 12.83 ± 0.20 in SBO and 9.83 ± 0.15 in EVOO, and rapid response times of 2.94 s and 4.71 s, respectively. After 35 days, CD, CT, and TPC increased to 3.83%, 0.96%, and 12.17% in SBO and 2.49%, 0.62%, and 7.83% in EVOO, while IP values decreased markedly, particularly in SBO, from 7.89 h to 2.04 h. Overall, these sensors offer a low-cost, rapid, and user-friendly approach for real-time oil oxidation monitoring.

BackgroundPhytochemicals and plant extracts are showing promising anticancer potentials. In the current study, the volatile faction (essential oil) of Nigella sativa seeds was evaluated against some hepatocellular carcinoma (HCC). The essential oil was extracted and characterized by chromatographic techniques to reveal its chemical composition, especially thymoquinone. Then, the oil was fabricated in two nanoemulsion formulations (F1 and F2), which differ in their composition of surfactants. The cytotoxicity and apoptotic activities of the essential oil and its nanoemulsions were evaluated in vitro against HepG2 and Huh-7 cell lines. Normal WI-38 cell line was also included in that evaluation to study the selectivity and safety of the different formulations on normal cells.ResultsGas chromatographic analysis indicated that the essential oil is composed mainly of p-cymene (40.0%), thymoquinone (31.2%) and trans-α-thujene (12.8%). Particle size of the nanoemulsions ranged between 9.4 and 119.7 nm depending on the type of surfactant used in the formulation process. The pure essential oil and its two nanoemulsions (F1 and F2) showed dose-dependent antiproliferative activity against both HCC cells. This activity reached its highest cell inhibition in the case of nanoemulsion (F2) where the proliferation percentage was only 21.9% and 9.2% against HepG2 and Huh-7 cells, respectively. The same nanoemulsion (F2) also showed the lowest IC50 values (55.7 and 35.5 µg/ml) against both HepG2 and Huh-7 cells, respectively, compared to 100 µg/ml for the reference drug Doxorubicin. Flow cytometric analysis also confirmed that nanoemulsion (F2) has the highest apoptotic activity compared to nanoemulsion (F1) and the pure unformulated essential oil. Genetic expressions of pro-apoptotic (Bax) and the anti-apoptotic (Bcl-2) gene markers evaluation revealed that nanoemulsion (F2) has better activity in upregulating (Bax) and down-regulate (Bcl-2) with the highest Bax/Bcl-2 ratio (69) was found against Huh-7 cells. All N. sativa nanoemulsions showed minimal cytotoxicity on the normal WI-38 cell, indicating wide safety margins due to selective properties.ConclusionOverall, the study revealed the potentials of N. sativa essential oil, after formulation in specially tailored nanoemulsion for application as potential adjuvant liver anticancer agent.

Background Colorectal malignant cells (CRC) are one of the world’s main causes of cancer mortality and morbidity. Notwithstanding the plenty of anti-CRC therapeutics, its prognosis remains not selective owing to cancer resistance to these therapeutics. Raloxifene (RX), a medication firstly used to treat osteoporosis, was recently licenced for the prevention of CRC. Unfortunately, due to medication resistance, many RX-based therapies are likely to become ineffective. Recently, we identified a novel method of administration to lengthen the half-life of RX by mixing it with chitosan (CS) and hyaluronic acid (HA). Thus, the rationale of the current study was to investigate how colon cancer cells were affected by RX-HA-CS nanoparticles (RX NPs) in terms of targetability, cytotoxicity, and epigenetic cascade alteration. Results RX NP had an entrapment efficiency (EE%) of 90.0 ± 8.12%. Compared to HCT 116 cells, Caco-2 cells were more susceptible to the cytotoxic effects of RX and its NP as well as they had a higher binding affinity to CD44 receptors compared to normal WI-38 cells. In comparison to the free RX, the RX NP’s cytotoxic fold changes in HCT 116 and Caco-2 cells were 2.16 and 2.52, respectively. Furthermore, the epigenetic cascade of some noncoding RNAs was examined. Moreover, particular protein concentrations were investigated in all tested cells after application of the proposed therapies. Our results showed that the RX NP recorded higher remarkable cytotoxic impact on CRC cells compared to the free RX. Intriguingly, it was hypothesized that RX nanoparticles attacked colon cancerous cells by up-regulating miR-944 and E-cadherin (ECN) expressions, while down-regulating the expressions of PPARγ, YKL-40, VEGF, H-19, LINC00641, HULC, HOTTIP, miR-92a, miR-200, and miR-21. Conclusions We may conclude that the RX NP effectively targets CRC cells in vitro via altering lncRNAs and miRNAs epigenetic cascade as well as cellular uptake through CD44-expressed CRC cells.

Background Graviola emerged as a promising anticancer agent, with nanotechnology enhancing drugs’ therapeutic potential. The purpose of this work was to explore graviola extract and its nano-platform’s effects on tongue carcinoma (SCC154 cells) in vitro model. Methods Graviola leaves extract (GLE) was isolated, and its phenolic content was identified. Three nano-formulations (F1-F3) were optimized for GLE delivery, with F1 chosen for its optimal size and stability to synthesize graviola nanoparticles (GNPs). SCC154 cells were split into three groups: group Ι (untreated SCC154 cells), group ΙΙ: SCC154 cells + ethanolic GLE, and group ΙΙΙ: SCC154 cells + GLE encapsulated in a nano-void delivery system (GNPs). In vitro tests assessed cell viability via MTT assay, cell cycle, and apoptosis by flow cytometry, DNA damage using comet assay, and gene expression of the key molecular markers (PI3K, AKT, mTOR, and GSK-3β) by quantitative real-time polymerase chain reaction. Transmission electron microscopic examination of cells was also performed. Results GLE and GNPs reduced SCC154 cells’ proliferation compared to untreated cells, with GNPs showing significantly higher cytotoxicity. Both treatments also induced apoptosis, arrested the cell cycle, and caused DNA damage with a significant pronounced effect in the GNPs-treated group. Gene expression analysis revealed a substantial decline in PI3K, AKT, mTOR, and GSK-3β in both treated groups relative to the control group, with a significant downregulation in the GNPs-treated group. Ultrastructural examination revealed severe destruction in tongue carcinoma cells of both treated groups, with substantial damage in the GNPs-treated group. Conclusion GNPs showed a better impact than GLE in tongue carcinoma therapy, causing cytotoxicity and apoptosis, potentially through the PI3K/AKT/mTOR pathway.