Search Results (2,435)

Hepatic encephalopathy (HE) is a complex complication of liver failure involving oxidative stress, astroglial activation, mitochondrial dysfunction, and multiorgan disturbances along the gut–liver–brain axis. This study investigated the therapeutic effects of liraglutide (LIRA) in a thioacetamide (TAA)-induced rat model of HE. Thirty male Sprague–Dawley rats were assigned to control, TAA, and TAA+LIRA 100, 200, or 400 µg/kg groups. HE was induced with TAA (200 mg/kg, intraperitoneally) for three consecutive days, followed by subcutaneous LIRA treatment for 14 days. Serum biochemical parameters, tissue oxidative and inflammatory markers, histopathology, and Nrf2, MFN2, AKT1, mTOR, GFAP, and VEGFA immunoreactivity were evaluated. TAA caused marked hepatic and cerebral structural injury, increased serum and brain glutamine concentrations, disrupted redox homeostasis, elevated MPO activity, and increased cerebral GFAP and multiorgan VEGFA immunoreactivity. LIRA partially improved hepatic and cerebral histopathology, reduced glutamine disturbances, attenuated selected oxidative, nitrosative, and inflammatory alterations, and modulated Nrf2, MFN2, AKT1, mTOR, GFAP, and VEGFA immunoreactivity in a tissue- and dose-specific manner. The 200 µg/kg dose produced the most consistent overall improvement, whereas the 400 µg/kg dose was less favorable for several endpoints. LIRA may therefore alleviate multiorgan stress associated with experimental HE, although further studies are required to confirm functional and mechanistic relevance. Full article

Postmenopausal ovarian hormone deficiency (OHD) contributes to overactive bladder (OAB) through oxidative stress, mitochondrial dysfunction, and dysregulated estrogen receptor (ER) signaling. This study investigated whether estradiol (E2) alleviates dysfunction by modulating the ER/Smad/miRNA-200/KLF4/mTOR signaling pathway to restore mitochondrial quality control. Thirty female Sprague-Dawley rats were initially allocated to Sham, Ovariectomy (OVX) and OVX + E2 group; after attrition during the 12-month protocol, six surviving animals per group were included in the principal analyses. The OVX + E2 group received daily intramuscular E2 (IM, 30 μg/kg/day) for one month. Bladder function was assessed via micturition volume and frequency by metabolic cages, cystometrograms, and contractility assays. Mechanisms were analyzed using immunofluorescence, Western blotting, transmission electron microscopy (TEM), and miRNA sequencing. OVX rats exhibited significant overactivity and compromised contractility, accompanied by upregulated ERα and downregulated ERβ/GPER. Molecularly, OHD was associated with the upregulation of the miRNA-200 family (miRNA-200a-3p, miRNA-200b-3p and miRNA-200b-5p), which was accompanied by reduced levels of KLF4 and autophagy proteins (ATG7, ATG12 and Beclin-1), as well as elevated p-mTOR expression. TEM revealed the accumulation of damaged mitochondria with ultrastructural features associated with impaired mitophagy. However, E2 treatment ameliorated these abnormalities. These improvements were associated with the restoration of TGF-β/Smad signaling, downregulation of selected miRNA-200 family members, recovery of KLF4 level, and increased expression of autophagy-related markers, accompanied by improved mitochondrial ultrastructural integrity. This cellular restoration might be correlated with improved urodynamic parameters. E2 might exert therapeutic effects by improving mitochondrial quality, potentially via the ER/Smad/miRNA-200/KLF4 signaling pathway. These findings provided mechanistic insights into estrogen-mediated protection and highlight this proposed signaling pathway as a therapeutic target for postmenopausal OAB. Full article

Peri-implantitis is characterized by progressive tissue destruction accompanied by dysregulated innate and adaptive immune responses. This study evaluated whether systemic treatment with 2-deoxy-D-glucose (2-DG) could attenuate experimental peri-implantitis and alter inflammatory markers associated with macrophage- and T-cell-mediated responses in a rat model. Experimental peri-implantitis was induced in Sprague–Dawley rats by Porphyromonas gingivalis-inoculated silk ligation around the implant neck. After disease induction, animals received intraperitoneal injections of 2-DG or normal saline for six weeks while ligature-associated challenge was maintained. Peri-implant tissues were assessed by micro-computed tomography (micro-CT), hematoxylin and eosin staining, immunohistochemistry (IHC), and reverse transcription-quantitative PCR (RT-qPCR). 2-DG treatment significantly reduced peri-implant bone resorption and was associated with less pronounced bone-resorptive morphology. RT-qPCR showed lower expression of M1-associated genes (CD86, iNOS, TNF-α, IL-6, and IL-18) and the Th17-associated genes IL-17 and RORγT, whereas IL-21, M2-associated genes, and the Treg-associated gene FOXP3 were not significantly changed. IHC showed qualitative trends toward lower iNOS- and IL-17-positive signals. These findings provide proof-of-concept evidence that 2-DG treatment reduces peri-implant bone loss and is associated with attenuated inflammatory changes and lower expression of M1- and Th17-associated inflammatory markers in experimental peri-implantitis. This study supports further investigation of 2-DG as a potential immunometabolic adjunct for peri-implantitis management. Full article

Blast-induced traumatic brain injury is a prevalent and underreported condition, particularly among military service members, for whom effective prophylactic interventions are lacking. Nano-pulsed laser therapy (NPLT) is a non-invasive neuromodulatory approach that delivers short pulses of near-infrared light to generate optoacoustic effects within cerebral tissue and has previously demonstrated therapeutic benefit following TBI. In this study, we evaluated whether a single pre-exposure application of NPLT could confer protection against neurological, cognitive, and cellular sequelae of mild blast injury. Adult male Sprague-Dawley rats were randomized to receive NPLT or Sham treatment 24 h prior to either Sham or mild blast exposure using the Advanced Blast Simulator. Neurological reflexes and vestibulomotor function were assessed on post-injury days (PIDs) 1–5, while cognitive performance was evaluated using the Morris Water Maze on PIDs 13–17. Histological analyses of microglia, astrocytes, and myelination were performed on PID 17. A single mild blast did not significantly alter gross neurological function but was associated with deficits in fine motor coordination and cognitive performance. Pre-exposure NPLT modestly attenuated blast-associated fine motor dysfunction, with a significant improvement compared with TBI on PID 4. In the Morris Water Maze, TBI animals exhibited significantly increased latency compared with Sham on PIDs 13 and 17, whereas NPLT + TBI animals did not significantly differ from Sham across the testing period, consistent with preservation of cognitive performance. Histological responses were regionally heterogeneous: NPLT alone produced distinct glial alterations, while NPLT + TBI animals exhibited a mixture of treatment- and injury-associated responses rather than uniform normalization to uninjured controls. NPLT did not prevent localized blast-associated reductions in corpus callosum myelin staining. In naive animals, NPLT significantly increased hippocampal brain-derived neurotrophic factor (BDNF) mRNA expression 24 h after treatment. A single pre-injury application of NPLT was associated with functional resilience following mild blast exposure despite persistent and regionally heterogeneous histopathological alterations. Increased hippocampal BDNF 24 h after NPLT, together with region-specific glial changes following NPLT in the absence of injury, demonstrates that a single treatment produces sustained molecular and cellular effects before blast exposure. These findings are consistent with the hypothesis that prophylactic NPLT establishes an altered pre-injury biological state that may modify the subsequent response to blast and support further investigation of NPLT as a prophylactic strategy and of the mechanisms underlying NPLT-associated preconditioning. Full article

Background: High-altitude hypobaric hypoxia (HH) is a major environmental stressor that impairs cognitive function, yet effective and widely available therapeutics remain limited. Although Rhodiola rosea has shown neuroprotective effects, its resource scarcity restricts large-scale application. Cistanche tubulosa (Schrenk) Wight, a traditional Chinese functional food, has been increasingly used in health supplements due to its anti-fatigue, anti-dementia, and memory-enhancing properties, suggesting potential benefits against hypoxia-induced cognitive impairment. Objective: This study aimed to investigate the effects of C. tubulosa ethanol extract (CTE) on hippocampal tissue and gut microbiota upon chronic HH exposure using SPF male Sprague–Dawley (SD) rats. Methods: A total of 60 male SD rats were randomly assigned to six experimental groups (n = 10 per group): normoxic control, untreated HH model, positive control (R. rosea), and low-, medium-, high-dose CTE treatment groups. Behavioral tests (Morris water maze), hippocampal histopathology, serum and hippocampal oxidative stress markers (SOD, GSH-Px, MDA), expression of PI3K/Akt/mTOR-HIF-1α signaling pathway proteins (by immunohistochemistry), and gut microbiota composition (by 16S rRNA sequencing) were evaluated. Results: The results demonstrated that CTE significantly improved cognitive function, enhanced SOD and GSH activities, and reduced MDA levels in both hippocampus and serum. CTE also modulated the expression of PI3K/Akt/mTOR-HIF-1α pathway proteins in the hippocampus. Furthermore, CTE altered gut microbial diversity and abundance, increasing the proportion of beneficial bacteria, which may further influence hippocampal function via the gut–brain axis. Conclusion: These findings provide scientific evidence for the application of C. tubulosa as a potential health supplement for high-altitude adaptation and lay a foundation for subsequent research. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease, characterized by hepatic steatosis, mitochondrial dysfunction, and oxidative stress. Food-derived polyphenols are promising ingredients that modulate cellular metabolism and redox balance. Açaí (Euterpe oleracea Mart.) seed, a polyphenol-rich agro-industrial by-product, has shown hepatoprotective potential; however, no previous study has comprehensively evaluated its effects on key mitochondrial functions in experimental MASLD. Therefore, this study investigated whether açaí seed extract (ASE), administered alone or in combination with physical training, could improve hepatic mitochondrial respiration, biogenesis, ultrastructural integrity, and redox homeostasis in HF diet-fed Sprague–Dawley rats. Male rats were fed a control or HF diet for 16 weeks and treated with ASE (200 mg/kg/day), aerobic training, or both during the final six weeks. ASE reduced hepatic steatosis by approximately 52% compared with the HF group, improved mitochondrial ultrastructure, increased the expression of the mitochondrial biogenesis regulators PGC-1α and NRF-1, with a 3-fold increase in PGC-1α mRNA expression, increased TFAM immunoreactivity, increased PPARα expression, reduced oxidative stress, and restored lipid-driven mitochondrial respiration. Physical training improved glycemic control and mitochondrial structure, with limited effects on mitochondrial function and redox balance. Combined treatment reduced plasma triglycerides by 41%, increased CPT1α expression, and enhanced carbohydrate-supported mitochondrial respiration. These findings provide mechanistic support for further investigation of açaí seed-derived polyphenols as candidates for nutritional strategies targeting MASLD. Full article

Background: Norepinephrine is commonly used during acute burn resuscitation to maintain adequate perfusion pressure. However, its effects, together with the burn-induced catecholamine surge, on arterial α₁-adrenergic receptors (α₁-AR) remain unclear. This study examined whether burn injury and continuous norepinephrine infusion alter arterial α₁-AR subtype expression at the transcriptional and protein levels. Methods: Sprague–Dawley rats were randomized to full-thickness scald burn involving 25% total body surface area with continuous intravenous norepinephrine or sodium chloride (NaCl) infusion, sham injury with norepinephrine infusion, or untreated controls. Mean arterial pressure (MAP) was measured at baseline and before euthanasia (six or 24 h). Aorta, carotid, and renal arteries were collected for analysis of α₁-AR subtypes (Adra1a, Adra1b, and Adra1d) using quantitative PCR (qPCR) and immunohistochemistry (IHC). Results: Norepinephrine efficiently increased MAP in sham animals. In burned animals with norepinephrine, MAP increased at six hours (+10.6 mmHg) but fell below baseline at 24 h (−6.4 mmHg). Burned animals given NaCl had persistently lower MAP than those given norepinephrine, at six hours (−19.1 mmHg) and 24 h (−21.1 mmHg). qPCR demonstrated significant downregulation of Adra1b in the renal artery across all groups compared to control (7.8–16.4-fold, p < 0.001). Overall, changes in protein expression across different vascular beds and receptor subtypes were inconsistent. Conclusions: Norepinephrine increased MAP in both sham and burned animals, confirming the drug’s efficacy. Burn injury and sustained norepinephrine exposure were associated with early, vessel-specific alterations in α₁-AR mRNA expression. The absence of consistent protein-level changes within 24 h suggests a delay in receptor expression on protein level. Full article

Background/Objectives: Skin aging involves interconnected inflammatory, oxidative, hormonal, extracellular matrix (ECM), and cellular senescence-related mechanisms, supporting the need for multitarget approaches. This study aimed to evaluate the effects of a multicomponent natural product-based injectable formulation developed in Korean medicine practice, Dong-An Pharmacopuncture (DAP), on skin aging-related pathways. Methods: A network pharmacology approach was used to identify the active compounds, predicted molecular targets, and signaling pathways associated with DAP. Sixty-two active compounds from 11 constituent materials were screened, and 70 final targets were identified using STITCH-based prediction, intersection with GeneCards-derived skin aging-related targets, and quality filtering. Results: Herb-compound-target network analysis yielded 225 compound–target interactions across 292 edges. Protein-protein interaction analysis identified a highly connected network with 1,334 edges, and hub analysis converged on 10 core targets: TNF, IL6, ESR1, TP53, AKT1, PPARG, EGFR, PTGS2, CASP3, and PPARA. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses identified four major mechanistic axes: inflammatory and oxidative stress regulation, hormonal skin homeostasis, tissue repair and ECM remodeling, and cellular senescence-related regulation. Because DAP is administered by injection, a Good Laboratory Practice-compliant single-dose subcutaneous toxicity study was additionally conducted in Sprague–Dawley rats, which showed no mortality, abnormal clinical signs, or histopathological findings attributable to DAP at 1.0 mL/head. Conclusions: The findings in this study provide a systems-level framework for the predicted multitarget mechanisms of DAP in skin aging-related pathways and support the need for further experimental validation of its predicted mechanisms and repeated-dose safety. Full article

Testicular torsion is a urological emergency that causes ischemia–reperfusion (I/R) injury and may result in irreversible germ cell loss and impaired fertility. Oxidative stress, inflammation, and apoptotic pathways play central roles in its pathogenesis. Transient Receptor Potential Melastatin-7 (TRPM7), a bifunctional ion channel/kinase, has recently been implicated in I/R-related cellular injury. Iloprost, a prostacyclin analogue with vasodilatory and antioxidant properties, may offer protective effects; however, its impact on TRPM7-mediated pathways in testicular I/R injury remains unclear. This study aimed to investigate the effects of iloprost on oxidative stress, apoptosis, and TRPM7 expression in an experimental testicular torsion–detorsion model. Thirty-five male Sprague Dawley rats were randomized into five groups: control, sham, iloprost, torsion–detorsion (T/D), and T/D + iloprost. After 60 min of torsion and subsequent detorsion, iloprost (2 µg/kg, intraperitoneal) was administered in the treatment group. Testicular tissues and serum samples were analyzed after 48 h. Histopathology (H&E), apoptosis (TUNEL assay), TRPM7 immunohistochemistry and mRNA expression (RT-qPCR), and serum total antioxidant status (TAS) and total oxidant status (TOS) were evaluated. Torsion–detorsion significantly increased TOS levels, apoptotic cell ratio (ACR), TRPM7 expression, and Bax mRNA expression, while reducing TAS levels (p < 0.05). Iloprost administration significantly improved oxidative stress parameters, restoring TAS and reducing TOS compared with the untreated T/D group. However, it did not significantly reduce histopathological damage, ACR, TRPM7 expression, or Bax mRNA expression. Bcl-2 expression remained largely unchanged across groups. Iloprost improved systemic oxidative status in testicular I/R injury but did not significantly attenuate TRPM7 expression, apoptotic changes, or structural damage under the experimental conditions used. The concurrent increase in TRPM7 expression and apoptotic indices following torsion–detorsion suggests an association between these alterations; however, the present study does not establish a causal relationship between TRPM7 and apoptosis. As TRPM7 activity was not directly assessed or experimentally manipulated, further studies involving TRPM7 inhibition or genetic silencing are required to determine its mechanistic role in testicular I/R-induced apoptosis. Full article

Background: Facial nerve regeneration across segmental defects remains challenging despite advances in nerve guidance conduits. Tissue engineering strategies that combine biomaterial scaffolds with bioactive and cellular components may enhance functional and structural nerve repair. This study investigated the regenerative efficacy of a cellulose-based nerve conduit augmented with Matrigel, mesenchymal stem cells (MSCs), and placental extract (PE) in a rat facial nerve gap model. Methods: A 2 mm defect was created at the main trunk of the facial nerve in adult Sprague–Dawley rats. Animals were divided into three groups: control group (Cellulose/Matrigel), group I (Cellulose/Matrigel/MSC), and group II (Cellulose/Matrigel/MSC/PE). Functional recovery was assessed at 2, 4, 6, and 8 weeks postoperatively using slow-motion vibrissa movement analysis, electrically stimulated facial nerve action potential measurements, and facial nerve blood flow by laser Doppler blood flow analysis. Morphological regeneration was evaluated using light microscopy and transmission electron microscopy. Western blotting using facial muscle was performed. Results: All groups exhibited time-dependent facial nerve regeneration. However, group II demonstrated significantly enhanced functional recovery, greater electrophysiological responses, increased nerve blood flow, and superior histological and ultrastructural regeneration compared with the other groups. These improvements were particularly prominent at 6 and 8 weeks postoperatively. Conclusions: The combination of mesenchymal stem cells and PE within a cellulose-based nerve conduit synergistically enhanced facial nerve regeneration. This tissue-engineered strategy may represent an effective approach for improving peripheral nerve repair. Full article

An evaluation of the safety profile of palatinose/fructooligosaccharide (P/FOS) and palatinose/invert sugar (P/IS), as novel low-glycemic and functional sweetener combinations, is essential for their application. This study aimed to evaluate the safety of 1000 mg/kg/day of P/FOS and 1000 mg/kg/day of P/IS through a 14-day repeated-dose oral toxicity study using male and female Sprague–Dawley (SD) rats. Clinical signs, such as body weight and organ weights, food/water consumption, hematology results, blood biochemical analysis results, urinalysis results, and histological changes in the liver and kidneys, were recorded in all SD rats. Barely any significant changes in food/water consumption, body weight, and organ weight were observed during the experimental period. Although there were some alterations in the results of hematological analysis, serum biochemical analysis, and urinalysis, these changes were not considered toxicologically significant within the normal ranges in both male and female SD rats administered with P/FOS and P/IS at 1000 mg/kg/day. Additionally, a histopathological analysis of the liver and kidneys showed no toxicological changes in P/FOS- and P/IS-treated SD rats of both sexes at the tested dose. Collectively, the above results confirmed that no overt treatment-related adverse effects of P/FOS and P/IS were observed under the tested conditions. Full article

Background/Objectives: Ocular surface inflammation has been identified as a key causative factor for dry eye. The current study investigates the feasibility, safety, and efficacy of fenofibric acid (FFA) as a topical eye drops in controlling ocular surface inflammation. Methods: FFA was tested for its dissolution profile and its cytotoxicity in vitro, and its permeability through ocular surface tissues was tested ex vivo. A safe dose was tested on the Sprague–Dawley (SD) rat eye as an eyedrop for ocular safety and ocular pharmacokinetics. The efficacy was tested on a benzalkonium chloride (BAC)-induced dry eye model in the SD rats. The outcome measurements were analyzed against the untouched contralateral eyes of the animals. Results: The study found that FFA had a similar dissolution profile in PBS (phosphate-buffered saline) as is in saline; however, the saturated concentration in PBS was 81 times higher. FFA had an IC50 (half maximal inhibitory concentration) of 282.4 µM on HCECs (human corneal epithelium cells). The FFA permeation rate for the cornea was 1.77 × 10⁻⁶ µg/cm²/min, 4.95 × 10⁻⁶ µg/cm²/min for the conjunctiva, and 11.32 × 10⁻⁶ µg/cm²/min for the complex of the sclera/choroid. A regimen of twice-a-day eyedrops (500 µg/mL) demonstrated good ocular safety and therapeutic efficacy on the BAC-induced dry eye model in SD rats, with significant effects on the reduction in corneal edema and on preventing the loss of goblet cells from dry eye pathology. Conclusions: These findings strongly suggest that FFA eye drops at a concentration of 500 µg/mL may effectively control ocular surface inflammation and relieve dry-eye discomfort. Full article

The effect of Corosolic acid (CA) on vascular tone and the possible mecha-nisms involved remain unclear. The SPF-grade male Sprague-Dawley rats (Animal Ethics Approval ID: USM/IACUC/2025/(155)(1406)) were used. The vasorelaxant effects of CA were evaluated in endothelium-intact and endothelium-denuded rings precontracted with phenylephrine (PE), and in endothelium-intact rings precontracted with KCl. Possible mechanisms were examined using L-NAME, ODQ, methylene blue, indomethacin, atropine, propranolol, and potassium channel blockers (glibenclamide, TEA, BaCl₂, and 4-AP). The effects of CA on voltage-operated calcium channels (VOCCs) and IP₃ receptor (IP₃R)-mediated sarcoplasmic reticulum calcium release were also assessed. CA concentration-dependently relaxed endothelium-intact aortic rings precontracted with PE (RMAX = 90.08 ± 7.33%; pD₂ = 4.21 ± 0.08). The relaxation response was markedly reduced after endothelial removal and in KCl-precontracted rings. EDRF pathway inhibitors (L-NAME, ODQ, methylene blue, and indomethacin) and GPCR-related antagonists (atropine and propranolol) attenuated CA-induced relaxation. Among potassium channel blockers, glibenclamide and TEA showed stronger inhibitory effects. CA did not significantly inhibit VOCC-mediated CaCl₂-induced contraction but partially reduced PE-induced contraction under calcium-free conditions. The mechanisms for CA treating hypertension may involve NO/cGMP signalling, COX-related prostanoid pathways, GPCR-related mechanisms, potassium channel modulation, and partial inhibition of IP₃R-mediated calcium release. Full article

Background: Cisplatin is a widely used chemotherapeutic agent whose gonadotoxic effects, largely driven by oxidative stress and inflammation, pose a major threat to male reproductive health. This study evaluated whether hesperetin (HES) and hesperetin-loaded poly (lactic-co-glycolic acid) nanoparticles (HES-PLGA-NPs) can protect against cisplatin-induced testicular dysfunction in adult male Sprague Dawley rats. Methods: Sixty rats were randomly assigned to six groups: control, HES, HES-PLGA-NPs, cisplatin (CIS), CIS + HES, and CIS + HES-PLGA-NPs. CIS (7.5 mg/kg/week, i.p.) was given intraperitoneally for four weeks, while HES and nano-HES (50 mg/kg/day, p.o.) were orally administered concurrently. Reproductive hormones, testicular weight, sperm parameters, oxidative stress and antioxidant markers, NRF2/HO-1 and NF-κB signaling, apoptotic indices, ferroptosis-related markers, histopathology, and GPX4/ACSL4 immunoexpression were assessed. Results: CIS caused marked reproductive dysfunction, including reduced testosterone, FSH, and LH, decreased testicular weight, and impaired sperm quality. These changes were associated with severe oxidative and nitrosative stress (↑ MDA, NO, 8-OHdG), depletion of antioxidant defenses (↓ SOD, CAT, GSH), reduced NRF2/HO-1, elevated NF-κB activity and pro-inflammatory cytokines, apoptosis-related changes (↑ Bax, caspase-3; ↓ Bcl-2), and ferroptosis-associated alterations (↑ Fe²⁺, TFR1, lipid ROS, ACSL4, 4-HNE; ↓ GPX4, SLC7A11). Both HES and HES-PLGA-NPs were associated with significant amelioration of these alterations, but the nanoformulation showed more pronounced protection, normalizing several oxidative and ferroptosis-associated markers toward control levels and more effectively preserving seminiferous tubule architecture and spermatogenesis. Conclusions: HES-PLGA-NPs were associated with multi-mechanistic protection against cisplatin-induced oxidative, inflammatory, apoptotic, and ferroptosis-associated damage in the testes, and may represent a promising nanoantioxidant candidate warranting further investigation for preserving male reproductive function during chemotherapy. Full article

This exploratory in vivo study investigated the therapeutic potential of intradiscal platelet-rich plasma (PRP) in a rat model of degenerative disc disease (DDD) using quantitative 4.7-T MRI and histologic correlation. Eight female Sprague-Dawley rats underwent induction of disc–vertebral complex degeneration through combined mechanical injury and type I collagenase injection. Immediately thereafter, a single intradiscal injection of leukocyte-poor PRP was administered. Longitudinal MRI evaluation included 3D ultrashort echo time (UTE) imaging, T1 mapping, and T2 mapping at baseline and during follow-up. In untreated discs, degeneration was associated with progressive decreases in nucleus pulposus T1 and T2 values and increased annulus fibrosus T2 values, reflecting dehydration and structural disorganization. In contrast, PRP-treated discs showed relative preservation of nucleus pulposus T1 and T2 relaxation times, while annulus fibrosus T2 values remained more stable, suggesting attenuation of degenerative changes. UTE-derived signal changes were less discriminatory between treated and untreated groups. Histologic analysis confirmed severe nucleus pulposus and annulus fibrosus disorganization in untreated discs, whereas PRP-treated discs demonstrated milder alterations with preserved vertebral endplate architecture. Overall, these preliminary findings suggest that the longitudinal effect of a treatment through intradiscal PRP is feasible and this injection may modulate early degenerative changes in the current animal model. However, the results should be interpreted with caution because of the exploratory design, the aggressive animal degeneration model, the absence of a sham-injection comparator group, and the small number of animals studied. Full article