Nanocoatings for the biomineralization membrane were developed on a gelatin (Gel) and carbonated hydroxyapatite (CHA) composite, namely, Gel/CHA membrane. The membrane, which contains bioactive polymer and a mineral phase, was further modified using plasma to deposit thin functional polymeric films. These surface-tailored nanocoatings improved the membrane's performance by increasing its swelling capacity to better mimic a tissue-like environment, strengthening its mechanical stability during application, and modulating interactions with biological components such as proteins to support tissue engineering and regeneration. Four types of thin films were explored, namely, 2-methyl-2-oxazoline (OX), 1,7-octadiene, acrylic acid (AC), and allylamine (AA). The physicochemical, mechanical, and biological properties of these plasma-functionalized membranes were systematically investigated. Fourier-transform infrared spectroscopy, energy-dispersive X-ray spectroscopy (EDX), and X-ray photoelectron spectroscopy (XPS) confirmed the successful deposition of functional coatings, while scanning electron microscopy (SEM) and atomic force microscopy demonstrated variations in the surface morphology and roughness. Water contact angle and swelling ratio measurements revealed tunable hydrophilicity and water uptake properties, with AC- and OX-coated membranes exhibiting enhanced hydration. Mechanical testing in dry state indicated that the OX-coated membranes achieved an optimal balance between tensile strength and elongation, thereby enhancing their mechanical resilience. Protein adsorption studies highlighted increased biomolecular interactions with hydrophobic surfaces demonstrating higher protein affinity. Cytocompatibility assessments, following ISO 10993-5:2009 standards, confirmed that all plasma-coated membranes were noncytotoxic to osteoblast MC-3T3-E1 cell lines, with cell viability exceeding 80%. The in vitro evaluation of MC-3T3-E1 cell adhesion was confirmed using DAPI staining and SEM observation and revealed that the MC3T3-E1 cells attached on control, AC, and AA membranes with a flatter shape. Additionally, the mineralization potential was assessed via simulated body fluid immersion for up to 360 min. EDX analysis showed time-dependent deposition of calcium and phosphate, with AA-coated membranes exhibiting the highest mineral accumulation. These findings demonstrate that plasma-assisted functionalization can significantly improve the membrane properties, making it a promising candidate for advanced bone tissue engineering applications.

BackgroundJC Polyomavirus (JCPyV) infects 40-90% of the adult population in a benign kidney infection. However, in a subset of immunocompromised individuals it causes a rapid and often fatal infection known as Progressive Multifocal Leukoencephalopathy (PML). Currently there are no treatments for PML and those that survive the initial infection are left with severe lifelong complications. Much of the process the virus must undergo to travel to the brain and establish infection is currently unknown. The non-coding control region (NCCR) of the viral genome is thought to have an important role in establishing infection in the central nervous system (CNS) as it contains many transcription factor binding sites. In neurotropic strains of the virus there are many insertions, duplications, and deletions in this region that may contribute to cell tropism and increased replication in the CNS. However, two published cases have reported JCPyV in the CNS without NCCR rearrangement suggesting the role of the region may be more complex than previously hypothesized. Studies in this area have been limited previously due to a lack of realistic models for infection and there is confusion over which cells in the CNS are being infected and what changes in the virus permit infection.JC virus infection of primary astrocytesRNAscope detection of the human polyomavirus JC virus transcripts in iPSC-derived human astrocytes. Shown is DAPI staining of nuclei (top left and merged images) and detection of viral RNA (bottom left and merged image). Scale bar = 50umJC virus infection of human brain organoid.JC virus capsid protein VP1 was colocalized with the oligodendrocytes marker MBP, near astrocytes (GFAP). Merged staining on the right include DAPI.MethodsWe have developed several novel primary cell infection models, including a brain organoid model, to test infection by wildtype virus with and without NCCR rearrangements. Additionally, we are using advanced molecular techniques including single cell RNA sequencing to identify the interactions between JCPyV and host cells.ResultsPrimary oligodendrocytes and tubule epithelial cells can be infected by wildtype archetype and neurotropic JCPyV. Rearranged JCPyV infects both cell types at a significantly higher level than archetype. Virus with non-rearranged NCCR is capable of infecting oligodendrocytes, but is less efficient than rearranged virus. Brain organoids appear to be infectable with JCPyV neurotropic virus (MAD-1).ConclusionThe knowledge gained from these studies will aid in understanding how JCPyV changes from a benign kidney disease to a deadly neuro pathogen and potentially lead to innovative therapeutics and preventatives for patients.DisclosuresAll Authors: No reported disclosures

Heat-induced antigen retrieval by using Tris-EDTA solution destroys nuclear structure in certain tissues

Nasopharyngeal carcinoma (NPC) occurs frequently, and NPC poses a significant risk to public health in areas where it is endemic. Better care is needed because NPC is associated with considerable morbidity and mortality. A natural anticancer substance called scutellarin fights cancer by acting on a variety of signalling pathways. Nevertheless, little is known about the underlying apoptotic and anti-proliferative actions of scutellarin. The current study aimed to determine the molecular effects of in vitro scutellarin on CNE1 human NPC cells through mechanisms such as cell proliferation, anti-inflammatory, and anti-apoptotic effects. NPC cells were exposed to scutellarin (20 and 30 μM/ml), and their proliferation and apoptosis were evaluated using the MTT assay, AO/EB, Rh-123, DCFH-DA, DAPI, and PI staining, cell adhesion, cell migration, and western blot analysis. We evaluated putative molecular pathways, MAPKs/NF-κB signaling, MMP, and intracellular ROS, cell proliferation regulatory proteins. By generating intracellular ROS, causing MMP loss and inducing apoptosis via the signalling pathways of TNF-α, COX-2, iNOS, and IL-6, pRB, cyclin-D1, CDK4/CDK6, and MAPKs/NF-κB, it has been found that scutellarin may reduce the proliferative, inflammatory, migratory, and invasive capacity of NPC cells. Our research supports the MAPKs/NF-κB pathway as a therapeutic target and suggests that it may play a key role in mediating the scutellarin actions against nasopharyngeal cancer malignancy. In summary, scutellarin may be an effective conventional therapeutic drug in preventing the progression of NPC.

Elucidating the antibacterial effect of terpinen-4-ol against Listeria monocytogenes and evaluating its efficacy in lettuce preservation via fumigation.

Poly(A) probe HCR RNA-FISH specifically marks pyriform nurse cells in the brown anole lizard ovary.

Hernia development is a common abdominal wall condition observed in calves, frequently manifesting in the umbilical region. This innovative biological dermoid scaffold is considered superior because of their inherent ability to combat infections through the release of antimicrobial peptides and non-complement fixing antibodies. The Division of Surgery at ICAR-IVRI, Izatnagar, has pioneered the development of bioinspired-bioactive dermoid scaffolds, as an initiative aimed at addressing hernias in large animals. The in vitro evaluation of the scaffold included crucial parameters such as H and E staining, SEM evaluation, and scaffold-cell interaction. Histocompatibility, cyto-toxicity, cell attachment, and proliferation of the seeded scaffolds were assessed using DAPI staining, along with an examination of porosity and density. All cases share a common history of a large swelling in the abdominal region. Physical examination, palpable hernial ring was identified followed by USG examination leading to the diagnosis of a large ventral hernia. Hematobiochemical analysis indicated a slight metabolic alkalosis, along with mild anaemia and azotaemia. Subsequent exploratory laparotomy was performed, to address the large abdominal defect, we decided to repair it using an allogenic dermoid graft in an overlaid fashion. Postoperative care included a 7-day course of antibiotics, analgesics, and antihistamines. All buffaloes in the study exhibited uneventful recovery, with no recurrence observed during the 5-month follow-up period. No reports on treatment of large abdominal wall defects with dermoid graft reported, which prevent reoccurrence of hernia. This study marks for the first time, where we outline the successful closure of a hernia in clinical cases.

The sclera, a dense tissue that provides structural support to the eye, can be damaged by various factors, necessitating surgical repair. Decellularization techniques, which preserve the essential extracellular matrix (ECM) while removing cells, offer a promising solution. This study aimed to develop an optimized decellularization protocol for human sclera and evaluate its effectiveness using a rabbit model for scleral defects. Twelve New Zealand white rabbits underwent lamellar sclerectomy. The right eye was grafted with human native sclera (HNS), while the left eye received human acellular sclera (HAS) patches prepared by methods A, B, and C. Method A used sodium dodecyl sulfate (SDS); Method B combined SDS with Triton X-100; and Method C used a mix of SDS, EDTA, Triton X-100, and trypsin. Outcomes were assessed through cell nucleus visualization, cytotoxicity tests, SDS residue checks, structural assessments, slit lamp evaluations, AS-OCT scans, and histopathological reviews. All protocols successfully decellularized tissues, confirmed by DAPI staining. With 80% cell viability, cytotoxicity was minimal and SDS residues were safely reduced. Method C best preserved collagen structures and ECM integrity. Slit lamp tests showed distinctions between HNS and HAS patches for Methods A and B, while Method C had superior biodegradability. All rabbits displayed conjunctival congestion, more so with HNS patches. AS-OCT showed the thinnest grafts with Method C. By the study's end, all patches had effectively healed the defects. Despite evident inflammation, especially in HNS patches, inflammation levels across HAS patches remained consistent. The decellularized human sclera emerges as an ideal material for reconstructing the sclera. The proposed decellularization processes efficiently retained ECM while eliminating cells, making them robust and safe choices for mending damaged scleral tissue. This optimized biomaterial holds the potential to improve surgical outcomes in scleral reconstruction procedures.

Recently, combination therapy has gotten more attention for some progressive therapeutic cancers. In in vivo studies, combination therapy requires better delivery, even though, in vitro studies, effective inhibition of various tumor cells has been identified due to uncontrolled ratiometric delivery. To target tumors with lipodisk nanoparticle formulations, this study established ratiometric loading and transport of cancer drugs such as paclitaxel (PTX) and salinomycin (SAL) on a single platform. Furthermore, including slightly pH-responsive peptides (PRPs) to lipodisks significantly improved cell and tumor-specific integration. The resulting lipodisks had a pH-sensitive characteristic of approximately 40 nm and were co-loaded. The ratiometric administration of two drugs through lipodisks was established in vitro in A549 and H1299 cells. Co-loaded lipodisks’ synergistic drug ratio enhanced their cytotoxicity to tumor cells. Apoptosis in lung cancer A549 and H1299 cells is embedded in nanoparticles in biochemical models like nuclear DAPI staining and acridine orange/ethidium bromide (AO/EB). Cytotoxicity data on coloaded lipodisks in vitro can be used to predict their inhibitory activity and improve the clinical outcome of the synergistic treatment. Moreover, co-loaded lipodisks exhibit a high tumor inhibition after intravenous administration, which results in significant anticancer effects in H1299tumor-bearing mice with minimum damage to normal organs. Finally, this work presents a simple pH-responsive lipodisk nanoparticle platform for co-loaded drug delivery to improve therapeutic potential against lung cancer cells.Graphical

Accurate cellular dosimetry is essential to investigate fundamental mechanisms of targeted radionuclide therapy. The aim of this study was to assess how morphological cellular geometry models influence cellular dosimetry estimates, in comparison to simplified spherical models that do not properly represent an adherent cell geometry. Virtual cell models of the CA20948 cell line were generated by confocal microscopy of SSTR2 and DAPI staining and served as input to derive morphological S-values for 177Lu and 161Tb. Absorbed dose-response relationships were established for [177Lu]Lu-DOTA-TATE, [161Tb]Tb-DOTA-TATE, [177Lu]Lu-DOTA-LM3 and [161Tb]Tb-DOTA-LM3 using S-values from both morphological and spherical cell geometries. Thirty-four cell geometries were modeled and a spherical model with equivalent volume was generated with a radius for the cell and nucleus of 8.6(7) µm and 5.5(6) µm, respectively. Compared to spherical cell models, morphological cell models significantly changed the S-value with an increase of 13% (177Lu) and 22% (161Tb) with the cell membrane as source region and a decrease of 11% (177Lu) and 12% (161Tb) with the cytoplasm as source region. Absorbed dose-response relationships based on morphological cell geometries showed a linear dose-response model for [177Lu]Lu-DOTA-TATE and [161Tb]Tb-DOTA-TATE with α = 0.22[0.18,0.26] Gy-1, and a linear-quadratic dose-response model for [177Lu]Lu-DOTA-LM3 and [161Tb]Tb-DOTA-LM3 with α = 0.000[0.000,0.022] Gy-1 and β = 0.064[0.055,0.072] Gy-2. The assumption of a spherical cell model did not significantly affect the dose-response models, while underestimating the cell dimensions did induce a rescaling of the dose-response models. These findings validate the use of simplified spherical models for CA20948 cells but highlight the importance of a correct estimation of the cell dimensions.

This study aimed to characterize the phytochemicals in Ficus hispida fruits and evaluate the anticancer potential of gallic acid against breast cancer using in-silico and in-vitro approaches. The objectives were to identify bioactive compounds using LC-MS, assess gallic acid's binding affinity with breast cancer-related targets via molecular docking and dynamics, and validate its cytotoxicity and apoptotic effects in breast cancer (MDA-MB-231) cells. Ethyl acetate extract of Ficus hispida fruits was prepared via Soxhlet extraction and analyzed using LC-MS/MS. Molecular docking studies were performed to evaluate gallic acid's interactions with breast cancer proteins (2VCJ-Heat shock protein HSP90-alpha, 1P7K-Anti-ssDNA antibody Fab fragment, 5OTE-Serine/threonine-protein kinase MRCK beta), followed by molecular dynamics (MD) simulations for stability analysis. In-vitro cytotoxicity (MTT assay) and apoptosis detection (AO/EB staining, DAPI staining) were conducted on MDA-MB-231 cells. LC-MS analysis identified key phytochemicals, including gallic acid (m/z 169.14), quercetin (m/z 302.33), and β-sitosterol (m/z 414.58). Molecular docking revealed strong binding of gallic acid to Heat shock protein HSP90-alpha (-6.2kcal/mol), stabilized by hydrogen bonds and hydrophobic interactions. MD simulations confirmed stable protein-ligand complexes with an RMSD of 2.1 Å for the protein and 3.2 Å for the ligand. In vitro studies showed the dose-dependent cytotoxicity of gallic acid against MDA-MB-231 cells, with an IC₅₀ of 15-20µg/mL and 34.80% viability at 20µg/mL. Apoptosis was confirmed through nuclear fragmentation and chromatin condensation. Ficus hispida fruits are rich in bioactive compounds, particularly gallic acid, demonstratinga strong binding affinity to breast cancer targets and potent cytotoxic effects against MDA-MB-231 cells. These findings highlight its potential as a therapeutic candidate for breast cancer treatment, warranting further clinical exploration.

Cannabidiol (CBD), a phytocannabinoid derived from Cannabis sativa, has demonstrated therapeutic potential across various diseases, including cancer. This study evaluates the cytotoxic effects of CBD on three human cancer cell lines (HeLa, MDA-MB-231, and CaCo-2) and two non-cancerous cell lines (HaCaT and HUVEC) used as a control. Cells were treated with CBD at concentrations of 5, 10, and 20 µM for 24, 48, 72, and 96 h. Cytotoxicity was assessed using MTT assays, nuclear morphology was evaluated via DAPI staining, and cell death mechanisms were analyzed through flow cytometry with apoptosis/necrosis markers. The LC50 values at 24 h were determined as follows: HeLa (9.4 µM), MDA-MB-231 (10.3 µM), and CaCo-2 (4.3 µM). CBD treatment induced morphological changes characteristic of cell stress and death in cancer cells, observed by optical microscopy after 24, 48, 72, and 96 h of exposure. These findings highlight the potential of CBD as an adjunctive therapeutic agent for cancer treatment versus non-malignant cells.

Synthesis and biological evaluation of Cu(II) Aroyl-Hydrazone Schiff Base complexes with anticancer activity against breast cancer cells.

Current cancer treatments, including surgery, radiotherapy, and chemotherapy, frequently have significant adverse effects, which restrict treatment options due to their toxicity. It is crucial to identify supplementary therapies using natural compounds that can inhibit tumor growth without causing severe side effects. This study explored the anti-cancer potential of earthworm coelomic fluid (ECF) protein (CF-P), non-protein (CF-NP), and crude (CF-C) from Eudrilus eugeniae against various human cancer cell lines (A549, MCF-7, MDA-MB-231, ME180, HEPG2, and HT-29). In vitro assays, such as MTT, cell cycle analysis, ROS analysis, apoptosis assays, and DAPI staining, revealed strong and variable cytotoxic effects of ECF fractions across different cell lines, with CF-P demonstrating the most substantial anti-cancer activity by inducing early G2/M cell cycle arrest and apoptosis more effectively than CF-C and CF-NP. In vivo studies using a DEN-induced hepatocellular carcinoma (HCC) mouse model indicated that CF treatments significantly enhanced body weight, alleviating cancer-induced cachexia, and reduced liver weight, with CF-P exhibiting the most notable therapeutic effects. Haematological and biochemical analyses showed improved RBC counts, decreased leukocytosis, and normalized liver and renal function markers. Histopathological assessments of liver and lung tissues revealed fewer neoplastic nodules, reduced necrosis, and improved tissue structure, underscoring the protective effects of CF fractions. These findings suggest that CF fractions, particularly CF-P, have potential as cytoprotective and anti-tumor agents in cancer therapy. This study provides novel insights into the in-vitro and in-vivo anti-cancer activity of non-protein, protein, and crude Eudrilus eugeniae coelomic fluid across various cancer cells in vitro, shedding light on their potential mechanisms of action.

Healthy mitochondria and mitochondrial quality control are essential for vital cell activities. Cell health is fundamentally maintained by the coordinated regulation of processes such as mitochondrial fusion, fission, and mitophagy. Their disruption plays a role in cancer pathogenesis, as well as in many diseases. This study investigated the effects of thymoquinone (TQ), a bioactive compound from Nigella sativa, on mitochondrial dynamics and quality control in Hepatocellular Carcinoma Cells (HepG2) and Human Dermal Fibroblasts (HDF). Results from molecular techniques such as the MTT assay, colony formation assay, wound healing assay, DAPI staining, and JC-1 staining, as well as Real-Time Polymerase Chain Reaction (RT-PCR) and Western blot analysis, were evaluated. TQ treatment caused dose-dependent decreases in cell viability and migration in both cell types, according to the MTT and wound healing assay results. While nuclear morphology assessments with DAPI staining served as a parameter for apoptotic changes, JC-1 analysis revealed a significant loss of mitochondrial membrane potential (ΔΨm) in HepG2 cells, while a relatively milder decrease was observed in HDF cells. At the molecular level, TQ exposure increased Cytochrome c (Cyt c) and Transcription Factor EB (TFEB) levels in both cell lines, but Dynamin-Related Protein 1 (DRP1) upregulation was more pronounced in HDF cells. Specifically, Western blot results showed an increase in PTEN-Induced Kinase 1 (PINK1) protein in HepG2 cells, but not in HDF cells. These findings suggest that TQ can trigger the mitochondrial stress response in HepG2 cells through DRP1-dependent fission, TFEB-associated lysosomal activation, and PINK1-associated mitophagy signaling. The stronger suppression of ΔΨm and PINK1 induction in HepG2 suggests an increased likelihood of activation of the intrinsic apoptotic pathway, while the partial preservation of mitochondrial integrity in HDF cells suggests a mild adaptation to stress. Further studies on mitophagy flux, Cyt c intracellular distribution, and TFEB nuclear translocation will be needed to define the mechanisms underlying these cell-type-specific responses.

Laryngeal squamous cell carcinoma (LSCC) remains a significant global health challenge, showing minimal improvement in survival rates even with advancements in standard treatments. The growing interest in phytochemicals as potential anticancer agents has highlighted Alpha-tomatine (AT) a steroidal glycoalkaloid derived from tomato plants, because of its strong cytotoxic properties. However, the effects of AT on laryngeal cancer have not been explored previously. This study aims to evaluate the anticancer efficacy of AT in HEp-2 human laryngeal carcinoma cells and to clarify the molecular pathways involved. AT significantly inhibited cell growth in a dose-dependent manner, with an IC₅₀ of 29.6 μM. The DCFH-DA staining results showed a marked increase in intracellular reactive oxygen species (ROS), underscoring oxidative stress as a crucial factor in cytotoxicity. Cells treated with AT exhibited significant mitochondrial membrane depolarization (loss of Δψm) and displayed notable apoptotic morphological changes, as evidenced by AO/EtBr and DAPI staining. Results from Annexin V/PI flow cytometry indicated a concentration-dependent increase in both early and late apoptotic cell populations. The comet assay revealed substantial DNA fragmentation, highlighting the genotoxic effects mediated by reactive oxygen species. The findings indicate that AT induces intrinsic apoptosis in HEp-2 cells through mechanisms related to oxidative stress, mitochondrial dysfunction, and DNA damage. These results suggest that AT may be a valuable phytochemical candidate for further investigation as a treatment for laryngeal cancer.

1,2,3-Triazole-modified sorafenib derivatives induce DNA damage, apoptosis, and PI3K/AKT pathway suppression in hepatocellular carcinoma: Design, synthesis, and evaluation.

Deciphering the role of zingiber officinale phytochemicals for the treatment of prostate cancer: Interactions of phytochemicals with androgen receptor prostate cancer mutant H874Y ligand binding domain.

Drug-induced nephrotoxicity is a significant clinical complication associated with several chemotherapeutic agents, including 5-fluorouracil (5-FU). This study was aimed to investigate the nephroprotective potential of boldine, an aporphine alkaloid, against 5-FU-induced renal toxicity using in vitro (HEK293 cells) and in vivo (Wistar rats) models. In vitro cytotoxicity was evaluated using the MTT assay, AO/EB and DAPI staining was performed to identify apoptotic alterations. The expression of apoptotic and antioxidant genes was analyzed by quantitative and semi-quantitative PCR. For the in vivo study, rats were divided into five groups. One group received a single intraperitoneal dose of 5-FU (150 mg/kg) to induce nephrotoxicity. In the remaining groups, 5-FU was administered followed by oral treatment with boldine (10 or 20 mg/kg) or silymarin (100 mg/kg) for 7 days. Biochemical markers including creatinine, urea, blood urea nitrogen, uric acid in serum and oxidative stress indicators in kidney tissue were analyzed. MAPK pathway-related gene expression and histopathological changes were assessed. Treatment of HEK cells with 5-FU markedly reduced cell viability and induced apoptosis, while co-treatment with boldine restored viability and normal cell morphology. Boldine modulated the 5-FU-induced downregulation of SOD, CAT, GPx, and Bcl-2 and upregulation of Bax and caspase-3. In vivo, boldine treatment normalized elevated nephrotoxic markers in serum, enhanced antioxidant enzyme activities, and inhibited activation of ASK1, ERK1, c-Jun, and NF-κB1. Histopathological findings further confirmed that boldine preserved renal tissue integrity and prevented tubular and glomerular damage. Overall, boldine significantly protected against 5-FU-induced renal injury via anti-apoptotic, antioxidant, and anti-inflammatory mechanisms.

Liver fibrosis, which is promoted through the activation of hepatic stellate cells (HSCs) and aggravated through oxidative and nitrosative stress induced by cisplatin, may be alleviated by L-carnitine. This study evaluates its antifibrotic efficacy in LX-1 cells through an assessment of inflammation regulation, oxidative/nitrosative stress (indicated by iNOS expression and nitric oxide production), DNA damage, and extracellular matrix (ECM) remodeling. Nitrosative stress was evaluated by measuring the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) generation, both of which signify reactive nitrogen species (RNS) activity. Human hepatic stellate (LX-1) cells were treated with cisplatin (10 μM for 6 h) to induce fibrogenic stress, followed by L-carnitine (0-15 μM) exposure. Cell viability was assessed by the MTT test. To calculate the number of inflammatory cytokines, the ELISA assay was utilized. Antioxidant activity was measured using the superoxide dismutase (SOD) assay. Apoptosis was identified using DAPI staining and DNA damage was measured. Statistical analysis was conducted utilizing one-way ANOVA and Tukey's post hoc analysis (p < 0.05). L-carnitine showed a limit of concentration-dependent protection from the effects of fibrosis initiated by cisplatin. Cell viability decreased from ~85% at 2 μM to ~40% at 14 μM (p < 0.001). At 15 μM, the pro-inflammatory cytokines examined (IL-1α, IL-1β, IFN-γ, IL-6, IL-10, TGF-β1) decreased by 60%-70% (p < 0.001) with a concurrent 80% increase in the activity of SOD. A 70% decrease in the amount of DNA damage and a dose-dependent increase in apoptosis were also observed. Meanwhile, iNOS and pERK1/2 decreased ~70% and the activity of MMP-2 and MMP-9 was significantly inhibited. L-carnitine protects LX-1 hepatic stellate cells against cisplatin-induced activation by attenuating inflammation, nitrosative stress, DNA damage, and ECM remodeling. These findings suggest its therapeutic potential for preventing chemotherapy-induced hepatic fibrosis.