Inflammopharmacology最新文献

{"title":"Acitretin shows promising potential in Alzheimer's disease: retinoid-driven modulation of amyloid processing, neuroinflammation, and translational prospects.","authors":"Varun Sharma, Kanika Vashisht, Garima Choudhary, Vaishali Choudhay, Vandana Bhatia, Mahendra Singh Ashawat, Ashish Baldi, Shiv Kumar Kushawaha","doi":"10.1007/s10787-026-02392-2","DOIUrl":"10.1007/s10787-026-02392-2","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder driven by the convergence of amyloid-β (Aβ) accumulation, tau hyperphosphorylation, synaptic failure, and chronic neuroinflammation, for which effective disease-modifying therapies remain elusive. Increasing evidence identifies dysregulated retinoid signaling as a critical yet underexplored contributor to AD pathogenesis. Retinoic acid, acting through retinoic acid receptors (RARs) and retinoid X receptors (RXRs), is essential for maintaining neuronal homeostasis, synaptic plasticity, and neuroimmune equilibrium in the adult central nervous system. In AD, impairment of RAR/RXR signaling shifts amyloid precursor protein (APP) processing toward amyloidogenic pathways, sustains NF-κB-driven inflammatory cascades, and promotes microglial dysfunction, thereby accelerating the progression of neurodegenerative processes. This review integrates mechanistic, preclinical, and translational evidence supporting acitretin, a second-generation synthetic retinoid, as a multi-target therapeutic candidate for AD. Acitretin enhances ADAM10-mediated non-amyloidogenic APP cleavage, increases soluble APP-α production, and reduces Aβ generation in transgenic AD models, while concurrently modulating microglial activation to attenuate pro-inflammatory cytokine signaling, including IL-6 and TNF-α, and preserve synaptic integrity. Importantly, biomarker-based clinical studies demonstrate increased cerebrospinal fluid APP-α following acitretin administration, confirming central target engagement in humans. Although definitive clinical efficacy remains to be established, acitretin's pleiotropic mechanism, established pharmacological profile, and biomarker responsiveness position it as a promising repurposed candidate within biomarker-guided and combination-based therapeutic strategies for AD.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6549-6560"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of p38 MAPK signaling in spinal cord injury by curcumin: targeting inflammation, oxidative stress, and apoptosis.","authors":"Shokoufeh Rahmani, Arman Gholami Abroumand, Salim Davlatov, Fatemeh Mortazavi Moghadam, Natalia V Kolaeva, Fatemeh Tahmasebi, Hamideh Babaloo, Madjidova Yakutkhon, Kosim Rakhmanov","doi":"10.1007/s10787-026-02405-0","DOIUrl":"10.1007/s10787-026-02405-0","url":null,"abstract":"<p><p>Spinal cord injury (SCI) triggers a complex secondary injury cascade characterized by neuroinflammation, oxidative stress, and programmed cell death, in which p38 mitogen-activated protein kinase (MAPK) signaling has emerged as an important regulatory node. Curcumin, a pleiotropic polyphenol derived from Curcuma longa, has attracted considerable interest as a potential neuroprotective agent because of its anti-inflammatory, antioxidant, and anti-apoptotic properties. Accumulating preclinical evidence suggests that curcumin can modulate p38 MAPK-associated signaling, attenuate inflammatory mediator production, reduce oxidative damage, and improve histological and functional outcomes in experimental SCI. In addition to p38-related effects, curcumin has also been reported to influence interconnected pathways involved in cell survival, gliosis, and stress responses. However, the available literature remains heterogeneous with respect to injury models, formulations, dosing strategies, and outcome measures. Overall, curcumin appears to be a promising adjunctive candidate for limiting secondary injury after SCI, but further mechanistic clarification and improved delivery strategies will be required to enhance translational relevance and support future clinical application.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6389-6412"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Arbutin mediated neuroprotection in zebrafish model of traumatic brain injury via modulating Nrf2/NF-κB pathway.","authors":"Romanpreet Kaur, Shamsher Singh","doi":"10.1007/s10787-026-02373-5","DOIUrl":"10.1007/s10787-026-02373-5","url":null,"abstract":"","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6849"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phenolic-driven antioxidant activity, metabolite profiling, and in vivo antipyretic effect of Kalanchoe ceratophylla aqueous leaf extract.","authors":"Astuti Astuti, Tika H Siregar, Alyssa Z B Karo, Lamhot P Manalu, Abdullah Bin Arif, Tantry E P Mariastuty, Wahyu Purwanto, Subandrio Subandrio, Maisaroh Maisaroh, Lusiana K Hartono, Bantari W K Wardhani, Nenie Yustiningsih, Taufik Hidayat, Cut Raihanah","doi":"10.1007/s10787-026-02394-0","DOIUrl":"10.1007/s10787-026-02394-0","url":null,"abstract":"<p><p>The plant juice of Kalanchoe ceratophylla has been reported to be traditionally used in fever treatment. Currently, this plant has been claimed to have antioxidant activity due to its flavonoid compound. This study aims to evaluate the correlation between antioxidant activity of the K. ceratophylla aqueous extract with total phenolic and flavonoid content, determine the metabolite profile of the extract, and investigate the antipyretic effect of the extract in vivo. The extract was obtained through maceration method with aquadest 1:5. The total phenolic content (TPC) and total flavonoid content (TFC) were calculated using the Folin-Ciocalteu and aluminum chloride method, respectively. Furthermore, the antioxidant activity was determined by DPPH free radical scavenging procedure. The metabolite profile of the extract was analyzed using GC-MS. The antipyretic assay was conducted in animal model using yeast-induced rat. In general, the antioxidant activity of the aqueous extract of K. ceratophylla more correlated to TPC (r = 0.711) than TFC (r = 0.500), with DPPH scavenging activity was 1.89 ± 0.01%. The metabolite profile supported this finding through dominant compound of the extract including fatty acid, phenolic acid, and carboxylic acid class. K. ceratophylla was revealed the antipyretic activity in animal test with dose of 500 mg/kg bw (AUC_0-180 min = 6547.80 ± 5.87), which comparable to paracetamol as standard drug (AUC_0-180 min = 6555.90 ± 8.40) and similar to the normal group (AUC_0-180 min = 6503.40 ± 3.66). These findings offer the scientifical evidence of empirical information of K. ceratophylla in fever treatment.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6713-6721"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular target for neuroinflammation and pain management: transient receptor potential vanilloid 1.","authors":"Zunera Chauhdary, Muhammad Saad Masood, Muhammad Irfan, Amina Shafi, Duryab Rafique, Abeesha Arif, Maryam Akmal","doi":"10.1007/s10787-026-02385-1","DOIUrl":"10.1007/s10787-026-02385-1","url":null,"abstract":"<p><p>Transient receptor potential vanilloid 1 (TRPV1) is a nonselective cation channel and polymodal sensor of noxious heat, protons, capsaicin and endogenous lipids. The wide variety of functions of TRPV1 in pain transmission, inflammatory pathways and neurological disorders has triggered efforts to understand the molecular mechanisms underlying these functions, particularly pain and neuroinflammation. The molecular structure and its tetrameric structure, temperature and ligand dependent activation and post-translational modification are discussed. It also covers the Ca²⁺-dependent signalling pathways such as CaMKII/Nrf2, MAPK, NF-κB and PI3K/ERK, and the localization of TRPV1 in sensory neurons, microglia, astrocytes, T lymphocytes and brain tissues. Other notable mentions are the involvement of TRPV1 in acute inflammatory, neuropathic, and visceral pain as well as in neuroinflammatory and neurodegenerative diseases like multiple sclerosis, Alzheimer's disease and Parkinson's disease. Evidence that comes from the various studies suggests that TRPV1 may cause a number of different responses depending on the cell and disease context, whether pro-inflammatory or neuroprotective. Therapeutic strategies directed to TRPV1 such as desensitizing agents, allosteric and state-selective modulators, peptide-based and natural-product based ligands, and gene-directed strategies, are also taken into account. To conclude, the context-dependent activity of TRPV1 signalling holds promise for therapeutic applications, and highlights the importance for context-specific, local and precise targeting of TRPV1 in clinical practice.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6347-6362"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Topical selegiline accelerates cutaneous wound healing with phase-specific modulation of MAPK signaling.","authors":"Moein Ghasemi, Sara Ashtari, Mohammad M Mehrabi, Bardia Baik, Ebrahim Alipour Limaee, Amirabbas Mohammadi Hamaneh, Negin Bagheri, Fatemeh Nejati, Seyed Amir Asef Agah, Mostafa Neshat Ghalibaf, Mohsen Hosseini, Seyedeh Elaheh Mousavi","doi":"10.1007/s10787-026-02388-y","DOIUrl":"10.1007/s10787-026-02388-y","url":null,"abstract":"<p><strong>Background: </strong>Persistent inflammation, impaired growth-factor signaling, dysregulated apoptosis, and altered signaling-pathway dynamics contribute to delayed cutaneous wound healing. Selegiline, an irreversible monoamine oxidase-B inhibitor with established transdermal delivery, may favorably modulate these interconnected processes within the wound microenvironment.</p><p><strong>Methods: </strong>Male Wistar rats (n = 90) underwent a full-thickness dorsal excisional wound (~ 25 × 16 mm; ~400 mm²) and were randomly assigned to receive daily administration of vehicle or topical selegiline (0.2%, 0.5%, 1%, or 2% w/w). Wound closure was assessed on Days 3, 8, and 14, and tissues were harvested for hematoxylin and eosin-based histopathological scoring; quantification of interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-β), apoptotic biomarkers, extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK) p38, and c-Jun N-terminal kinases (JNK) transcripts.</p><p><strong>Results: </strong>Topical selegiline accelerated wound closure in a dose-dependent manner, with greatest efficacy at 1-2% (86.18% (1%) and 90.28% (2%)), compared with 70.58% in the vehicle group. Histopathology showed reduced inflammation and more advanced granulation/angiogenesis and collagen organization. Selegiline reduced the injury-associated elevation of IL-1β, IL-6, and TNF-α, particularly at later time points, and was associated with enhanced PDGF and TGF-β during proliferative/remodeling phases, shifted apoptosis toward a pro-survival profile, and produced phase-linked changes in ERK/JNK/p38 transcripts.</p><p><strong>Conclusions: </strong>Topical selegiline was associated with faster excisional wound repair, most consistently at 1-2%, by accelerating closure and coordinating inflammatory resolution, growth-factor recovery, apoptosis balance, and MAPK-related signaling across healing phases. These findings support further preclinical evaluation of topical selegiline, including mechanistic validation, local and systemic safety assessment, pharmacokinetic characterization, and investigation in impaired or chronic wound models.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6663-6677"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arbutin mediated neuroprotection in zebrafish model of traumatic brain injury via modulating Nrf2/NF-κB pathway.","authors":"Shamsher Singh, Romanpreet Kaur","doi":"10.1007/s10787-026-02347-7","DOIUrl":"10.1007/s10787-026-02347-7","url":null,"abstract":"<p><p>Traumatic Brain Injury (TBI) is a major cause of mortality and disability worldwide and is associated with oxidative stress, neuroinflammation, and neurotransmitter imbalance. Arbutin, a naturally occurring glycoside with known antioxidant and anti-inflammatory properties, has the potential to modulate neurochemical alterations following brain injury. The present study was designed to evaluate the neuroprotective effects of arbutin in a zebrafish model of TBI induced by a novel non-invasive mechanical impact method termed \"force-induced TBI.\" Adult zebrafish were randomly divided into seven groups (n = 14 per group): normal control, TBI control, arbutin per se, arbutin-treated groups (25, 50, and 100 mg/kg, i.p.), and a co-treatment group receiving arbutin (100 mg/kg) co-administrated with chrysin (25 mg/kg), a known modulator of the Nrf2/NF-κB signaling pathway. Behavioural assessments, including the open field test, novel tank diving test (NTDT), T-maze, and novel object recognition test (NORT), were conducted on days 1, 4, and 7 to evaluate locomotion activity, anxiety-like behaviour, spatial memory, and recognition ability, respectively. Following behavioural evaluation, brain tissues were analysed for oxidative stress markers (MDA, nitrite, GSH, and SOD), neurotransmitter levels (GABA and glutamate), pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), and histopathological alterations. Immunohistochemical analysis of Nrf2 and NF-κB was also performed. The results demonstrated that arbutin significantly improved behavioural performance, restored oxidative balance, normalized neurotransmitter levels, and attenuated neuroinflammatory responses. Furthermore, arbutin treatment was associated with increased Nrf2 immunoreactivity and reduced NF-κB immunoreactivity in a dose-dependent manner. The co-treatment with chrysin also exhibited protective effects, supporting its potential modulatory role in oxidative stress and these effects are associated with modulation of oxidative stress, neuroinflammation, neurotransmitter imbalance, and Nrf2/NF-κB immunoreactivity. These findings suggest that arbutin possesses neuroprotective potential against secondary brain injury and is associated with modulation of oxidative stress, inflammatory responses, and Nrf2/NF-κB immunoreactivity.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6751-6769"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated network pharmacology and experimental investigation of the potential therapeutic effect of β-sitosterol in systemic lupus erythematosus.","authors":"Rikngam Gibo, Purbajit Chetia, George Hmangte Kom, Apurba Talukdar","doi":"10.1007/s10787-026-02375-3","DOIUrl":"10.1007/s10787-026-02375-3","url":null,"abstract":"<p><strong>Background: </strong>Systemic lupus erythematosus (SLE) is a chronic autoimmune condition characterized by immunological dysregulation, inflammation, and oxidative stress, affecting multiple organs. The need for safer therapeutic alternatives is highlighted by the substantial side effects and inconsistent effectiveness of current treatments. The current study employed integrated computational and experimental methods to examine the potential effects of β-sitosterol against pristane induced SLE.</p><p><strong>Methods: </strong>Network pharmacology, Molecular docking and MD simulations were conducted to discover possible molecular targets of β-sitosterol in SLE. Antioxidant and anti-inflammatory assays were assessed though in vitro experiments. SLE was induced in BALB/c mice by administration of pristane, followed by treatment with β-sitosterol (100, 200, and 400 mg/kg, p.o.) or prednisone (10 mg/kg). Progression of the disease was evaluated through proteinuria, behavioral assessment, paw edema, hematological parameters, cytokine quantification, radiographic and histopathological analysis.</p><p><strong>Results: </strong>68 common BS-SLE targets were identified by network pharmacology, where TNF-α, PPARG, and MAPK3 emerged as major hub proteins with stable interaction demonstrated by docking and molecular dynamics. β-sitosterol demonstrated considerable antioxidant and anti-inflammatory properties in vitro and showed a favorable acute safety profile at 300 mg/kg, while one mortality was observed at 2000 mg/kg. In in vivo experiments, β-sitosterol substantially diminished proteinuria, serum creatinine, BUN, TNF-α, IL-6, paw oedema, and joint inflammation, while improving anxiety-like behavior, motor coordination, and hematological parameters. Considerable protection against kidney, brain and joint tissue injury was demonstrated by histopathological investigations, especially at 400 mg/kg.</p><p><strong>Conclusions: </strong>These findings suggest that β-sitosterol may mitigate lupus-associated inflammation and multiorgan injury through the modulation of inflammatory and metabolic pathways predicted by network pharmacology. The integrated computational and experimental evidence supports further mechanistic investigation and translational studies rather than establishing β-sitosterol as a definitive therapeutic agent for SLE.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6579-6603"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Large-scale comparative virtual screening identifies novel molecular targets underlying the multi-target activity of quercetin in psoriasis.","authors":"Mina Barhoon, Hamid Mahdiuni, Ali Ebrahimi, Reza Khodarahmi","doi":"10.1007/s10787-026-02364-6","DOIUrl":"10.1007/s10787-026-02364-6","url":null,"abstract":"<p><p>Psoriasis is a chronic inflammatory skin disorder arising from immune dysregulation, cytokine storms, and excessive keratinocyte proliferation. Because single-target therapies often show limited efficacy, drug resistance, high costs, and long-term safety concerns, we performed the first large-scale comparative virtual screening of 32 dietary flavonoids against 20 psoriasis-related protein targets to identify safe and cost-effective multi-target therapeutic candidates. Consensus docking predicted quercetin as the top hit, exhibiting a broad binding profile across 11 targets, including previously reported ones (PI3Kδ, the JAK family, PDE4D, and p38α-MAPK) and four newly predicted putative targets (BTK, RORγt, CTSS, and PKCθ). Duplicate molecular dynamics simulations with principal component analysis, free energy landscape, and clustering analyses further characterized these interactions. RORγt and PI3Kδ exhibited the most favourable binding characteristics, followed by the JAK family, whereas PDE4D and PKCθ showed comparatively weaker yet promising interactions. Although quercetin has previously been associated with psoriasis through its antioxidant and immunomodulatory properties, its direct molecular targets and binding mechanisms have remained largely unresolved. Here, quercetin consistently outperformed the other 31 flavonoids while maintaining relative target selectivity. The predicted interaction of quercetin with RORγt provided computational structural support for modulation of the IL-23/IL-17 axis and helped explain quercetin effects on Th17-cell differentiation. Similarly, computationally predicted interactions provided a structural rationale for several other well-documented yet mechanistically unresolved anti-inflammatory and immunomodulatory effects of quercetin, indicating that its therapeutic activity may extend across multiple disease-relevant cell types and signalling pathways. Furthermore, this study presents the atomic-level structural characterization of quercetin binding to newly predicted putative targets and previously known targets lacking complex structural data. Collectively, these findings expand the molecular understanding of quercetin in psoriasis, provide a computational framework for multi-target drug discovery, and highlight the need for experimental validation and enhancement of bioavailability as essential next steps toward clinical translation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6605-6642"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Properties of Persea americana Mill (Lauraceae) kernels aqueous extract on acetic acid-induced ulcerative colitis in rats.","authors":"Estelle Flora Gaffo, Magni Sadi Debsoua Zahara, Larissa Vianney Ngachili Chinda, Sefirin Djiogue, Michel Archange Fokam Tagne","doi":"10.1007/s10787-026-02399-9","DOIUrl":"10.1007/s10787-026-02399-9","url":null,"abstract":"<p><p>Ulcerative colitis is a chronic inflammatory bowel disease characterized by uncontrolled inflammation of the gastrointestinal tract, which is difficult to treat. The aim of this study was to evaluate the effects of Persea americana kernels aqueous extract on acetic acid-induced ulcerative colitis in rats. Thirty-six (36) male and female rats, divided into six (6) groups of six (6) rats each, were anesthetized with a ketamine (50 mg/kg)/valium (10 mg/kg) mixture after eighteen (18) hours of fasting with free access to water. Colitis was induced by the intrarectal administration of 1 mL of acetic acid (4%) in all animals except the control group, which received 1 mL of distilled water. Five (5) hours later, the normal control and the colitis control received distilled water (1 mL/kg), the positive control received prednisolone (20 mg/kg), and the three other groups received Persea americana kernels aqueous extract at 100, 200, and 400 mg/kg for seven (7) days. During treatment, stool quality and changes in body weight were assessed. At the end of treatment, the animals were anesthetized and then sacrificed. The colon, liver, spleen, kidneys, heart, lungs, and blood were collected for the analysis of inflammatory and hematological parameters. During treatment, the Persea americana extract reduced the number of diarrheal stools and maintained a nearly constant weight change. Persea extract significantly reduced (P ≤ 0.01) MPO activity, interleukin-6 levels, and TNFα. Based on these results, the aqueous extract of Persea americana kernel possesses anti-inflammatory and antioxidant effects and could therefore be used in the treatment of chronic inflammatory bowel diseases.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6739-6749"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}