Resveratrol protects lens epithelial cells and delays cataract development via inhibiting TXNIP mediated oxidative stress and apoptosis.

ROS, identified as a driver for fibroblast activation, can be counteracted by glucocorticoid in LINC00605-dependent GMD machinery.

Bisphenol A (BPA) is an endocrine-disrupting chemical known to cause testicular toxicity through oxidative stress and apoptosis. Panax ginseng (PG) is a natural product with anti-inflammatory effects. This study aimed to evaluate the protective effect of PG against BPA-induced testicular damage in rats. Thirty-two Wistar Albino rats aged 10-12 weeks were divided into four groups: Control, PG, BPA, and BPA + PG. BPA (50 mg/kg/day) and PG (100 mg/kg/day) were orally administered for 6 weeks. BPA significantly increased serum total oxidant status and decreased antioxidant status (p < 0.001, p < 0.001). Also, the levels of superoxide dismutase (an antioxidant enzyme) (p = 0.0005) and androgen receptor-mRNA (an androgen signaling marker) decreased (p = 0.014). However, caspase 3 (an apoptosis marker) (p = 0.0067), 8-hydroxy-2'-deoxyguanosine (a marker of oxidative DNA damage) (p < 0.001), and tumor necrosis factor-α (a proinflammatory cytokine) (p < 0.001) levels increased in testicular tissues. Rats treated with PG showed improvements in all oxidative and inflammatory markers and significantly restored androgen receptor expression. Histopathological examination revealed degeneration in seminiferous tubules and reduced spermatozoa in the BPA group, while the BPA + PG group showed marked improvement. These findings suggest that PG may alleviate oxidative stress-related testicular damage at both molecular and histological levels and may offer insights for future clinical studies.

High temperature is a known abiotic stressor in broiler chickens, causing oxidative damage and altering gene expression. The present study was conducted to study the role of in ovo feeding of taurine against heat-induced damage in the broiler chickens. It was hypothesized that pre-hatch supplementation with taurine induces epigenetic changes such as DNA methylation and demethylation, which could help develop resistance to heat stress (HS) at later stages of life. For this, at 17.5 days of incubation, 360 fertile eggs from 37-week-old Arbor Acre breeder hens were divided into four groups: injected with distilled water (0TAU) × 2, and others injected with taurine at 1 %, 3 %, or 5 % concentrations (1TAU, 3TAU, 5TAU). For the in ovo feeding, a 23-gauge needle was used to deposit 0.6mL of solution into the amniotic sac. During rearing days 29 to 34, broiler chickens were exposed to a cyclic heat stress (HS, 31 ± 1 °C, 8 hours) or kept at a thermoneutral temperature (TN) zone (21 ± 1 °C). Hence, the treatment groups were: (i) 0TAU-TN, (ii) 0TAU-HS, (iii) 1TAU-HS, (iv) 3TAU-HS, and (v) 5TAU-HS. While the organ indices, average daily feed intake (ADFI) and feed conversion ratio (FCR) did not differ significantly, in ovo taurine linearly increased average daily gain (ADG) during the heat stress (HS) period (p = 0.032). The 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity% (DPPH-RSA%) in plasma showed a linear increase (p = 0.001) with taurine doses. Among the studied plasma metabolites, only alanine transaminase (ALT) was significantly affected, being lower in 1TAU-HS and 3TAU-HS compared to 5TAU-HS (p = 0.022). Individual gene expressions showed no significant variation across treatments. However, a planned contrast revealed upregulation of DNA methylation genes in the 5TAU-HS group compared to the 0TAU-TN group (p = 0.030). Strong positive correlations were observed among DNA methylation, demethylation, and NADPH oxidase (NOX) -related genes, suggesting coordinated regulation. Negative correlations between MDA and antioxidant enzymes indicated oxidative stress-related damage under HS. Hence, taurine linearly improved ADG under HS. While it did not significantly influence individual gene expression, 5TAU upregulated the overall DNA-methylation-related genes, suggesting a possible long-term adaptive response under HS.

Leaves of plants, especially soursop (Annona muricata), have been widely exploited for feed formulation, functional food, and medicinal purposes owing to their rich supply of phytochemicals and natural antioxidants. This study was aimed at investigating the phytochemical constituents and the antioxidant activity of soursop leaf extracts using Ferric Reducing Antioxidant Power (FRAP), 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical scavenging, and hydroxyl radical scavenging assays. In soursop leaves, a total of twelve phytochemicals were detected. The results revealed high amounts of anthocyanin (5.34±0.007%), phenol (3.80±0.077 mg/g), alkaloids (3.31±0.077%), cyanogenic glycosides (2.65±0.022%), cardiac glycosides (2.27±0.041%), saponin (1.78±0.021%), flavonoids (1.14±0.099%), tannins (1.06±0.020%), and steroid (1.03±011 mg/g), but low amounts of phytate (0.65±0.024%), oxalate (0.33±0.011%), and hemagglutinin (0.08±0.012 mg/g). Antioxidant assays proved concentration-dependent properties of the aqueous extract of soursop leaf. Strong Fe³⁺ ion reduction was demonstrated by the maximum FRAP activity (63.76±0.014%), which was recorded at 80 mg/ml. Also, the leaf extract was most effective at scavenging DPPH free radicals (87.541%) and hydroxyl radicals (64.045%) at 10 mg/ml and 20 mg/ml, respectively. High anthocyanin, phenolic, and flavonoid contents found in this study suggest that soursop leaf holds weighty antioxidant potential, with implications for protecting against oxidative stress-related damage and potential as a beneficial functional food.

Gelatin hydrolysate (GH), a bioactive compound derived from collagen, has demonstrated potential therapeutic benefits in various medical conditions. However, its effects on chronic cerebral hypoperfusion-induced vascular dementia remain underexplored. This study aimed to investigate the anti-oxidative stress effects of GH in alleviating brain damage and cognitive impairment in CCH-induced rats. Male Wistar rats underwent bilateral common carotid artery occlusion to induce CCH and were randomly divided into five groups: (1) sham, (2) 2-vessel occlusion (2VO), (3) 2VO + 250 mg/kg GH, (4) 2VO + 500 mg/kg GH, and (5) 2VO + piracetam. Treatments were administered for 35 days of post-operation. GH treatment significantly mitigated oxidative stress, as evidenced by reduced levels of reactive oxygen species (ROS), nitric oxide (NO), and the expression of 4-hydroxynonenal (4-HNE) and NADPH oxidase 4 (NOX4). Furthermore, GH exhibited antioxidant activity by upregulating superoxide dismutase (SOD) levels via nuclear factor E2-related factor 2 (Nrf-2) activation. This, in turn, reduced neuronal apoptosis by decreasing Bax and cleaved-caspase 3 levels and increasing Bcl-2 expression. Additionally, GH treatment ameliorated Tau protein hyperphosphorylation and improved synaptic function. Overall, GH exerted neuroprotective effects against oxidative stress-related neuronal damage and enhanced neuroplasticity, learning, and memory in rats with CCH-induced cognitive impairment.

Anti-Müllerian hormone (AMH) is widely used in veterinary medicine to assess reproductive health. Cyclophosphamide (CP) is a chemotherapeutic and immunosuppressive drug that has been reported to reduce AMH levels and cause damage to ovarian reserves, although findings vary depending on study design. Coenzyme Q10 (CoQ10), known for its antioxidant properties, has been suggested to have a protective role against oxidative stress-related ovarian damage. This study was conducted to examine how CP affects serum AMH levels in rats and whether CoQ10 supplementation could help reduce any negative impact. A total of 35 Wistar Albino rats were used in the study. They were divided into five groups: control, sham, CP, CoQ10, and CP+CoQ10. All substances were administered by oral gavage. CP was dissolved in distilled water and administered at a dose of 6 mg/kg/day, while CoQ10 was dissolved in olive oil and given at a dose of 2.8 mg/kg/day. The treatments lasted for four weeks. Results showed that CP alone did not significantly change AMH levels (p&amp;gt;0.05). In contrast, CoQ10 alone led to a significant increase in serum AMH levels (p&amp;lt;0.05). However, when CP and CoQ10 were given together, no significant difference in AMH levels was observed. This may suggest that CP interferes with or masks the effect of CoQ10 on the ovaries. These findings may contribute to a better understanding of the interaction between CP and CoQ10, especially in terms of dosage, duration and timing of treatment, in future studies.

Traditionally, wild jujube (Ziziphus jujuba Mill. var. spinosa (Bunge) Hu ex H. F. Chou) has been used to nourish the heart, calm the spirit, and arrest spontaneous sweating. Modern research confirms its broad pharmacological activities, including antioxidant, anti-inflammatory, neuroprotective, and cognitive-enhancing effects. This study aims to isolate and characterize the structure of jujube polysaccharides and evaluate their protective effects against oxidative stress damage in neural stem cells (NSCs). We successfully isolated and purified a novel pectin polysaccharide (ZJP-2) from wild jujube. Its structure was characterized in detail using high-performance liquid chromatography coupled with multi-angle laser light scattering and refractive index detection (HPLC-MALS-RI), high-performance anion exchange chromatography (HPAEC), gas chromatography-mass spectrometry (GC-MS), and nuclear magnetic resonance (NMR) spectroscopy. Structural analysis revealed that ZJP-2 is a pectin heteropolysaccharide with a molecular weight of approximately 67.93 kDa. Its monosaccharide composition primarily includes galac-turonic acid (GalA), arabinose (Ara), rhamnose (Rha), galactose (Gal), and glucose (Glc). The backbone consists of α-GalA and rhamnose-galacturonic acid-I (RG-I) domains linked by (1→4)-glycosidic bonds. NMR spectroscopy further confirmed its glycosidic bond types. In activity assessment, our study demonstrated that ZJP-2 significantly alleviated DMNQ-induced oxidative stress damage in C17.2 neural stem cells. Its protective effect was achieved by reducing intracellular reactive oxygen species (ROS) levels and upregulating the mRNA expression of antioxidant genes associated with the signaling axis (p < 0.05). Moreover, ZJP-2 suppressed DMNQ-induced overexpression of Nestin and NeuN (p < 0.05), contributing to the maintenance of NSCs' undifferentiated state and functional homeostasis. In conclusion, ZJP-2 possesses distinct structural characteristics and significant neuroprotective potential, supporting its development as a natural functional food or dietary supplement for preventing oxidative stress-related neural damage.

Growing evidence suggests an association between SARS-CoV-2 infection and oxidative stress-related genomic damage, primarily from cross-sectional studies. However, longitudinal evaluations remain limited. Here, we assessed DNA damage in peripheral blood mononuclear cells (PBMCs) from hospitalized COVID-19 patients during the first days of hospitalization, using the alkaline comet assay. A longitudinal descriptive study was conducted at a modular COVID-19 hospital in Lima, Peru, throughout October 2020. Blood samples were collected at admission (day 0), day 3, and day 6. DNA damage was assessed by measuring tail length, tail moment, and tail intensity, which were modeled using mixed-effects linear models. Concurrent hematological parameters and acute-phase proteins were also analyzed to characterize their time-course patterns in conjunction with DNA damage. Results from the adjusted mixed-effects model showed a significant temporal increase in DNA damage parameters, particularly tail intensity (β = 0.25 per day, p = 0.003), relative to baseline measurements, with a peak observed on day 3 of hospitalization. These changes aligned with variations in platelet counts and transferrin levels, while lymphocyte and monocyte counts, along with C-reactive protein, showed an inverse trend, reflecting the dynamic interplay of the inflammatory response and DNA damage. No significant differences in comet assay parameters were observed between survivors and non-survivors, likely due to the limited and unbalanced sample. The findings indicate the presence of a measurable DNA damage burden in PBMCs of hospitalized COVID-19 patients, highlighting the need to further studies to clarify the mechanisms underlying DNA damage and its potential long-term biological implications.

Adding lycopene to the freezing media enhances the quality, antioxidant capacity, and fertilization ability of frozen-thawed Oure-type Tibetan sheep (Ovis aries) sperm.

Glioblastomas are highly invasive brain tumors associated with oxidative stress (OS) and chronic inflammation. Curcumin (CUR), the principal bioactive compound of Curcuma longa, as well as its natural analogues demethoxycurcumin (DMC) and bisdemethoxycurcumin (BDMC), exhibit promising therapeutic properties. The aim of this study was to evaluate the antioxidant effects of CUR, DMC, and BDMC in an in vitro model using the LN229 glioma cell line. LN229 glioblastoma cells and MO3.13 cells as a non-tumor control were cultured in Dulbecco’s Modified Eagle Medium (DMEM) under standard conditions. Cells were treated with CUR, DMC, and BDMC for 24 h and 48 h at concentrations selected based on MTT assay results. Antioxidant capacity was assessed using the ferric reducing antioxidant power (FRAP) assay, while lipid peroxidation and protein oxidation were evaluated by measuring malondialdehyde (MDA) and protein carbonyl group levels, respectively, in cell lysates. Curcumin, demethoxycurcumin, and bisdemethoxycurcumin reduced LN229 cell viability in a time- and dose-dependent manner. Curcumin exhibited the strongest antioxidant activity, significantly decreasing MDA levels and protein carbonyl content (p &lt; 0.001). Demethoxycurcumin was the most effective compound in reducing protein oxidation after 48 h, whereas bisdemethoxycurcumin increased MDA levels, suggesting a potential pro-oxidative effect. The FRAP assay confirmed a sustained antioxidant capacity of all compounds, particularly at higher concentrations. In conclusion, curcumin and its derivatives demonstrated both antioxidant and cytotoxic activities in a time- and dose-dependent manner. Among the tested compounds, curcumin showed the most stable and long-lasting antioxidant and cytotoxic effects, indicating its potential therapeutic value in mitigating oxidative stress–related damage in glioma cells.

Background: Seizures and associated oxidative stress are hallmark features of epilepsy and other neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and traumatic brain injury. These conditions share common pathophysiological mechanisms including excitotoxicity, mitochondrial dysfunction, and redox imbalance that contribute to neuronal damage and disease progression. Targeting oxidative stress pathways has emerged as a promising translational strategy for neuroprotection and seizure control. This study aims to evaluate the effects of wogonin, a flavonoid compound, on seizure latency and oxidative brain damage induced by pentylenetetrazol (PTZ) in a mouse model. Methods: Adult male mice (25–30 g) were randomly assigned to control and experimental groups (n=10 per group). Seizures were induced via intraperitoneal injection of PTZ (100 mg/kg). Experimental groups received wogonin (1, 5, or 10 mg/kg, i.p.) 30 minutes prior to PTZ administration. Seizure latency was recorded. Post-seizure, mice were euthanized, and hippocampal and cortical tissues were harvested for biochemical analysis of oxidative stress markers, including nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and total thiol content. Results: PTZ administration significantly decreased the latency to both minimal clonic seizures (MCS) and generalized tonic-clonic seizures (GTCS). Wogonin pretreatment significantly increased MCS and GTCS latencies in a dose-dependent manner. Oxidative stress markers NO and MDA were significantly elevated following PTZ administration, and wogonin pretreatment at doses of 5 and 10 mg/kg significantly reduced their levels. SOD and CAT activities were significantly restored in groups treated with 5 and 10 mg/kg of wogonin, while total thiol content was notably increased at the highest dose. Conclusion: These findings suggest that wogonin may serve as a potential therapeutic agent for managing seizure disorders and oxidative stress-related neurological damage, although further studies including pharmacokinetic profiling and validation in human models are needed to confirm its clinical relevance.

A dual-responsive fluorescent probe for simultaneous detection of H2S and SO2 and its application in an oxidative stress model of neuronal cells.

ObjectiveThis study aimed to investigate the anti-inflammatory and antioxidant effects of ozone on liver and kidney tissues as an adjuvant therapy in the treatment of sepsis in individuals with diabetes.Materials and Methods46 Swiss Albino mice were divided into six groups: control (C), diabetes (D), diabetes + ozone (DO), diabetes + cecal perforation (DCP), diabetes + cecal perforation + ozone (DCPO), and diabetes + ozone + cecal perforation (DOCP). The diabetes groups received 125 mg/kg intraperitoneal (i.p). Streptozotocin (STZ). The DCPO and DOCP groups received 1 mL (20 µg mL−1 i.p.) ozone. Liver and kidney tissues were collected 24 hours later. Tissue samples were stored under appropriate conditions for histopathological and biochemical analyses.ResultsHistopathological analysis of liver and kidney tissue revealed that all acute inflammatory markers were more pronounced in the DCP group compared to the C, D, and DO groups. Acute inflammatory markers were lower in the ozone-treated groups compared to the DCP group. In the diabetes and sepsis groups, malondialdehyde (MDA) levels increased in both liver and kidney tissues, while catalase (CAT) activity decreased. MDA levels were lower in the ozone-treated groups, and CAT activity was higher than in the no-ozonized groups. Blood urea nitrogen (BUN), creatinine, AST, and ALT levels were significantly higher in the DCP group compared to the C, D, and DO groups. Conversely, these values were lower in the DCPO and DOCP groups compared to the DCP group.ConclusionOur findings suggest that ozone therapy may alleviate inflammatory and oxidative stress-related damage to the liver and kidneys caused by diabetes and sepsis. Additionally, ozone therapy appears to reduce serum markers of liver and kidney function such as AST, ALT, BUN, and creatinine.

Background. Systemic sclerosis (SSc) is characterised by immune dysregulation, microvascular injury, and progressive fibrosis. Macrophages are increasingly recognised as key drivers of fibro‐inflammation, yet their ultrastructural responses in SSc-like conditions and the potential for micronutrient/antioxidant correction remain underexplored. Objectives. To examine the electron-microscopic changes in macrophages in an experimentally induced SSc model and to evaluate whether vitamin D3 (VD3) plus α-tocopherol acetate (VE) mitigates macrophage injury. Methods. Eighty-five adult Wistar rats were randomised to: intact (IG, n=15), vehicle control (CG, n=20), SSc-like induction (EG1, n=25), and induction plus corrective treatment (EG2, n=25). SSc-like changes were induced with subcutaneous 5% sodium hypochlorite (0.5 mL, three times weekly for six weeks). EG2 additionally received VD3 (1,000 IU/100 g, i.m.) and VE (10 mg/100 g, i.m.) during weeks 4-6. Electron microscopy processing, imaging, and analysis were performed in a blinded manner. At week 8, lungs were sampled under thiopental anaesthesia. Ultrastructure of alveolar macrophages was assessed by electron microscopy using standardised fixation, embedding, sectioning, and imaging protocols. The IFNMU Bioethics Committee approved all procedures. Results. CG macrophages displayed preserved ultrastructure. EG1 showed marked injury, characterised by swollen, low-electron-density cytoplasm; severely deformed mitochondria with loss of cristae; dilated, granular endoplasmic reticulum with sparse ribosomes; and abundant lysosomes/phagosomes, consistent with oxidative and proteostatic stress. In EG2, ultrastructure improved relative to EG1. Visible nucleoli and shallow envelope indentations characterised the nuclei. Mitochondria were enlarged but structurally more coherent, and mildly dilated endoplasmic reticulum tubules were present. There were fewer lysosomes/phagosomes, indicating partial restoration of cellular organisation and a trend toward homeostatic recovery. Conclusions. In an SSc model, alveolar macrophages undergo profound ultrastructural injury that is partially reversed by combined VD3 and VE. These data support macrophages as actionable targets and suggest that micronutrient/antioxidant modulation can attenuate immune-metabolic and oxidative stress–related damage, warranting translational studies on adjunctive strategies for systemic sclerosis (SSc).

BackgroundAcute kidney injury (AKI) is a common and serious complication of cisplatin chemotherapy in cancer patients, with no effective treatment currently available. Oxidative stress and renal tubular damage are key contributors to its pathogenesis. This study aimed to investigate the antioxidant and renoprotective effects of black garlic water extract in a cisplatin-induced AKI mouse model.MethodsMice were randomly divided into six groups: Control, Cisplatin only (20 mg/kg), black garlic extract pretreatment at 50 or 100 mg/kg followed by cisplatin (Cis + B50, Cis + B100), amifostine pretreatment (200 mg/kg) as positive control (Cis + A200), and black garlic extract only (100 mg/kg). Black garlic extract was characterized for its sulfur compound content and antioxidant potential.ResultsBlack garlic contained significantly higher levels of S-allyl-L-cysteine (191.2 ± 32.87 µg/g) than raw garlic (20.7 ± 0.8 µg/g) and effectively delayed low-density lipoprotein oxidation. Pretreatment with black garlic extract reduced cisplatin-induced weight loss, renal index elevation, and tubular damage. Antioxidant enzyme activities, including superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, were significantly increased in the Cis + B100 and Cis + B50 groups.ConclusionsBlack garlic extract confers protection against cisplatin-induced AKI by enhancing renal antioxidant defenses and mitigating oxidative stress-related damage. These findings support its potential as a complementary approach for preventing nephrotoxicity during cisplatin therapy.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12906-025-05178-1.

Background: Oxidative stress arises from an imbalance between excessive oxidant production and impaired antioxidant defense systems. This imbalance leads to biomolecular damage, contributing to aging and age-related diseases such as chronic kidney disease (CKD). Oxidative stress is a well-established risk factor for CKD and has been reported to accelerate disease progression. Hesperidin, a flavanone glycoside abundant in citrus fruits, exhibits antioxidant, anti-hypertensive, and anti-inflammatory properties and has been suggested to attenuate CKD progression. However, its potential role in reversing oxidative damage in kidney cells remains unclear. Methods: This study aimed to investigate whether hesperidin can reverse oxidative damage in human kidney proximal tubular epithelial (HK-2) cells. Oxidative stress was induced by exposing HK-2 cells to 500 μM hydrogen peroxide (H2O2) for 6 h, followed by treatment with 100 μM hesperidin for 24 h. Results: Our results showed that hesperidin significantly ameliorated H2O2-induced cytotoxicity. In the hesperidin post-treatment group (H2O2 + hesperidin), the expression of the antioxidant gene manganese superoxide dismutase (MnSOD) and the longevity-associated gene sirtuin 1 (SIRT1) was upregulated, while the expression of the senescence-associated gene β-galactosidase was downregulated compared to the H2O2-only treatment. Conclusions: These findings suggest that hesperidin promotes recovery from oxidative injury in kidney cells by enhancing antioxidant and longevity pathways and reducing cellular senescence. This may contribute to improved renal health and potentially slow CKD progression in patients suffering from oxidative stress-related kidney damage.

Premature greying of hair (canities) in children is an increasingly recognized concern among parents and pediatricians. Although often benign, early hair depigmentation may be a clinical marker of nutritional deficiencies, autoimmune disorders, genetic predisposition, endocrine abnormalities, or oxidative stress related damage. The absence of standardized pediatrics guidelines leads to misdiagnosis, unnecessary anxiety, and missed opportunities for early intervention. This review synthesizes current evidence on epidemiology, pathophysiology, risk factors, diagnostic approach, and management of premature greying in children. A structured evaluation and targeted treatment of reversible causes especially vitamin B12, iron, vitamin D, zinc deficiency, and hypothyroidism can halt or partially reverse greying in many children. This article provides an evidence-based, clinically practical approach suitable for pediatricians, dermatologists, and general practitioners.

Introduction: Inflammation is mainly caused by cellular and vascular factors. Lymphocytes and macrophages are among the circulating cellular constituents. It is indisputable that macrophages play a part in inflammation. Harpullia cupanioides (Sapindaceae) methanol extract was investigated in vitro against the RAW 264.7 murine macrophage cell line to discover its cytotoxic and anti-inflammatory activities. An in vivo study was conducted to investigate the anti-inflammatory and anti-fibrotic effects of Harpullia cupanioides (HC) in Thioacetamide–induced rats (TAA), through the determination of oxidative stress markers Glutathione (GSH), lipid peroxide (MDA), and Total Antioxidant Capacity (TAC). Additionally, lipid profile, liver function enzyme activities, Gamma-Glutamyl Transferase (GGT), total bilirubin, Tumor Necrosis Factor-α (TNF-α), Interleukin-6 (IL-6), collagen type I, Tumor Growth Factor-β (TGF-β), and Metalloproteinase-9 (MMP-9) were assessed. Material and Methods: This research aimed to investigate the beneficial impact of HC extract in vitro and in vivo in rats induced by TAA, as determined by the measurement of several biomarkers. Fibrosis was triggered through the administration of TAA (200 mg/kg, intraperitoneally) twice a week for a duration of six weeks. The activities of serum transaminases (AST, ALT), inflammatory cytokines, including TNF-α, IL-6, TGF-β, and fibrotic biomarkers (collagen 1V and MMP-9), as well as liver histopathological alterations, were evaluated. results: TAA induced marked histopathological changes in liver tissues coupled with elevations in serum transaminases activities. Furthermore, hepatic content of lipid peroxidation (MDA) and tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), collagen 1V and TGF β were elevated, together with a reduction of metalloproteinase -9 (MMP-9) in the liver. Treatment with Harpullia cupanoide ameliorated liver tissue against TAA-induced liver fibrosis, as proved by the alleviation of inflammatory and fibrotic biomarkers. Results: TAA caused marked histopathological alterations in liver tissues, accompanied by an elevation in hepatic lipid peroxide (MDA, 71.66%), while there was a significant reduction in TAC and GSH levels (64.86% and 56.73%, respectively) in fibrotic rats. Treatment of liver fibrosis with HC showed remarkable improvement, as evidenced by 17.11%, 17.78%, and 71.66% reductions in TAC, GSH, and MDA, respectively, compared with the silymarin reference drug (26.13%, 26.18%, 95%, and 95.00%, respectively). Marked elevation in liver function enzyme activities in serum of fibrotic rats reached 184.15%, 436.13% and 470.57%, respectively, for ALP, ALT, and AST. Upon treatment of fibrotic rats with HC, more or less normalization in the liver enzymes with improvement percentages of 96.79%, 190.29%, and 170.00%, respectively, for ALP, ALT, and AST, compared to the standard drug (105.96%, 291.67%, and 225.61%). The present results showed a significant increase in TGF-β and type IV collagen, while a significant reduction in metalloproteinase-9 (MMP-9) was observed in TAA-induced liver fibrosis with percentages of 368.96%, 104.23% and 35.34%, respectively. A noticeable improvement in the fibrotic markers post-treatment of HC extract reached 160.83%, 73.24%, and 14.81% for TGF-β, type IV collagen, and MMP-9, respectively, compared to the Silymarin reference drug. Discussion: The creation of fibrosis and cirrhosis models in rats is a well-established technique that involves the delivery of TAA both orally and intraperitoneally. TAA is a necrogenic sulfur-containing molecule and a carcinogen. It is frequently employed to cause fulminant hepatic failure and liver cirrhosis in animal models. During the biotransformation of TAA, the enzymes flavin-containing monooxygenase (FMO) and cytochrome P450 facilitate the conversion of dioxygen into superoxide anion, leading to the production of hydrogen peroxide (H2O2). As a result, oxidative stress-related liver damage occurs, and the release of liver enzymes into the circulation is associated with an elevation in inflammatory markers and collagen deposition. The administration of crude extract from Harpullia cupanioides effectively decreased the oxidative damage and inflammation in the liver caused by TAA administration. In particular, the treatment of crude extract made MDA, TAC, IL-6, and TNF-α levels roughly normal, reversing the effects of TAA-induced hepatic fibrosis in rats, this may be due to Harpullia cupanioide's potent antioxidant activity it possesses anti-inflammatory properties that modulate the immunological response of macrophages, restrict the secretion of proinflammatory cytokines (TNF-α and IL-6) and reverse the course of fibrosis, steatosis, and inflammation by repressing macrophage activation. Conclusion: The effects of HC were found to be similar to those of Silymarin, a natural antioxidant, suggesting that the extract may possess anti-inflammatory and anti-fibrotic properties. The findings of this study further demonstrated the anti-inflammatory effects of this plant. However, further research is recommended to investigate its therapeutic potential in treating inflammatory disorders.

Peri-implantitis (PI) is a prevalent complication of denture implantation, and the consequences of PI on dental implantation are irreversible. This research examined the levels and clinical significance of miR-486-5p in PI patients, while also investigating its biological role in the PI progression using a cellular model. Quantitative polymerase chain reaction (qPCR) was employed to assess the miR-486-5p levels. The diagnostic significance of miR-486-5p, along with its relationship to periodontal indicators and prognosis, was evaluated through ROC and Pearson correlation analysis. Additionally, the LPS cell injury model was established to investigate the effects of both the miR-486-5p overexpression and inhibition on the proliferation and apoptosis of hPDLFs utilizing CCK-8 and flow cytometry. Furthermore, the miR-486-5p regulation on inflammatory factors and oxidative stress levels was assessed through ELISA. The miR-486-5p levels in PI patients were elevated, demonstrating considerable diagnostic potential for this condition. miR-486-5p might serve as an important indicator for assessing the periodontal status and prognosis of PI patients. In cell models, miR-486-5p overexpression could inhibit proliferation and promote apoptosis of hPDLFs, as well as enhance the inflammatory mediators release and oxidative stress-related damage. Conversely, the inhibition of miR-486-5p expression could counteract the promoting effect of LPS on inflammatory response. miR-486-5p is a potential diagnostic biomarker of PI. The up-regulated miR-486-5p might intensify inflammatory responses and impair cellular functionality, consequently facilitating the progression of PI.