Journal of Pharmacy and Pharmacology最新文献

{"title":"Rosavin and salidroside attenuate microglia injury via nuclear factor κ-B signaling pathway.","authors":"Hang Liu, Yandong Ma, Qian Chen, Yuting Dai, Yixuan Wang, Huating Huang, Zihan Yao, Chaoren Yan, Jingming Shi","doi":"10.1093/jpp/rgaf094","DOIUrl":"https://doi.org/10.1093/jpp/rgaf094","url":null,"abstract":"<p><strong>Objectives: </strong>Inflammation, oxidative harm, and degradation of mitochondria ultimately contribute to the initiation neurodegenerative changes. This study investigated the inhibitory effects of rosavin and salidroside on neuroinflammation induced by β-amyloid oligomers using primary microglia derived from the cerebral tissue of C57BL/6 J mice.</p><p><strong>Key findings: </strong>Following β-amyloid oligomers' production, a series of continuous neurological deterioration takes place. Rosavin and salidroside exhibited distinct inhibitory effects on different neurodegenerative damage. Subsequent studies indicated that the protective mechanism of rosavin was associated with nuclear factor к-B phosphorylation.</p><p><strong>Lay summary: </strong>Rhodiola rosea L., with its natural small molecule compounds like rosavin may be potential candidates for the treatment of AD.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Andrographolide attenuates oxidative stress and apoptosis in osteoporosis rats via MEK/ERK and Beclin-1/ATG-5-mediated autophagy pathway.","authors":"Yankun Li, Guomin Li, Rui Luo, Bo Li","doi":"10.1093/jpp/rgaf052","DOIUrl":"10.1093/jpp/rgaf052","url":null,"abstract":"<p><strong>Objectives: </strong>To explore how andrographolide (AG) activates autophagy and reduces oxidative stress in osteoporosis.</p><p><strong>Methods: </strong>An ovariectomized rat (OVX) model was created in vivo. Osteoblasts were obtained from rat skulls in vitro, and an oxidative stress model was induced by H2O2. Masson staining and micro-CT were utilized to assess pathological damage to bone tissue following treatment with AG, 3-MA, or silencing the ATG-5 gene. The kit detected changes in oxidative stress-related indices, flow cytometry detected apoptosis, alkaline phosphatase and Alizarin Red S staining assessed osteogenic differentiation ability, and Western blot detected changes in osteogenic differentiation-related indices and autophagy-related indices.</p><p><strong>Key findings: </strong>AG therapy clearly reduced pathological damage and inhibited oxidative stress in OVX rats. AG also significantly boosted osteoblast viability, reduced apoptosis, and facilitated osteoblast differentiation. Furthermore, AG treatment substantially elevated the expression of Runx, OPG, BMP-2, as well as autophagy-related proteins MEK, ERK, ATG-5, Beclin-1, and LC3.</p><p><strong>Conclusions: </strong>These findings indicate that AG possesses antioxidant and anti-osteoporosis properties, and that its mechanism may be linked to the MEK/ERK and Beclin-1/ATG-5-mediated autophagy pathways. These results establish the groundwork for the development of AG as an osteoporosis treatment, as well as new directions and therapeutic targets for the intervention of oxidative stress and autophagy-related disorders.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1426-1438"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bruceine E attenuates hepatic steatosis through modulation of PI3K/AKT/NFκB signalling pathway.","authors":"Farahdina Man, Neti Eka Jayanti, Chiuan Yee Leow, Chee-Yan Choo","doi":"10.1093/jpp/rgaf016","DOIUrl":"10.1093/jpp/rgaf016","url":null,"abstract":"<p><strong>Objectives: </strong>This study aims to establish the effect of bruceine E in attenuating nonalcoholic steatohepatitis (NASH) through the PI3K/AKT/NFκB pathway.</p><p><strong>Methods: </strong>High-fat-diet (HFD) male Wistar rats were orally administered with glibenclamide (20 mg/kg) or bruceine E (400, 800, or 1600 µg/kg) for 4 weeks. After 4 weeks of treatment, blood serum was analysed for liver markers. Liver histology was used to identify the degree of inflammation. The liver tissue was evaluated on the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) and inflammatory genes (nuclear factor-kappa B [NFκB], tumor necrosis factor alpha [TNFα], interleukin-6 [IL6], and interleukin-10 [IL10]) and protein expressions.</p><p><strong>Key findings: </strong>The alanine transferase and aspartate transferase were reduced in HFD rats administered orally with bruceine E. In liver histology, steatosis, ballooning, and lobular inflammation were alleviated in bruceine E-treated HFD rats. The PI3K/AKT genes and proteins were activated while the inflammatory genes and protein expressions were suppressed in the bruceine E-treated HFD rats showing improvement towards insulin resistance (IR), liver steatosis, and inflammation.</p><p><strong>Conclusions: </strong>In conclusion, bruceine E attenuated NASH through activation of the PI3K/AKT/NFκB inflammation pathway and may further delay the progression of NASH to hepatocellular carcinoma .</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1379-1385"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chrysin ameliorates D-galactose-induced liver aging in mice: the impact of targeting Nrf2/AKT and CXCL1/TNF-α/P53 signaling pathways.","authors":"Abeer Salama, Noha N Yassen, Samar S Khalaf, Mohamed I Fahmy","doi":"10.1093/jpp/rgaf054","DOIUrl":"10.1093/jpp/rgaf054","url":null,"abstract":"<p><strong>Objectives: </strong>Liver aging is a major cause of death all over the world. D-galactose (D-gal) induces liver aging via inflammatory pathways in Kupffer cells. Chrysin (CHR) is a flavonoid having anti-inflammatory and antioxidant effects that can protect liver from aging responses. This study aimed to clarify the hepatoprotective activity of CHR in D-gal-induced liver aging.</p><p><strong>Methods: </strong>Four groups of male mice (10 mice each) were used in the study: normal control group, D-gal (200 mg/kg/day) group, D-gal group + 25 mg/kg/day CHR, and D-gal group + 50 mg/kg/day CHR. Treatment continued for 8 weeks.</p><p><strong>Key findings: </strong>Elevation in cytochrome P2E1 (CYP2E1) enzyme, the chemokine (C-X-C motif) ligand-1 (CXCL-1), the cell surface adhesion receptor CD44, and tumor necrosis factor (TNF)-α occurred in D-gal group. Oxidative stress was evident through downregulation of catalase enzymes, nuclear factor erythroid 2-related factor 2 (Nrf2) and protein kinase B (AKT), and an increasing nitric oxide (NO) levels. Consequently, liver injury was evident with elevation of ALT and AST levels. These responses affected the morphology of the hepatic tissues. CHR managed to prevent these pathways and preserved normal morphology of the hepatic tissues.</p><p><strong>Conclusions: </strong>Our study revealed that CHR prevents D-gal-induced liver aging through its anti-inflammatory and antioxidant effects.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1450-1458"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improvement of primary Sjögren's syndrome salivary gland function by Xinfeng capsule and its effect on EGR1-STAT3 signaling pathway.","authors":"Ling Zhu, Beijia Wang, Pingping Li, Gangli Cheng, Su Bu, Sijie Bian, Xiaoting Qiu, Jian Liu, Xingxing Huo","doi":"10.1093/jpp/rgae121","DOIUrl":"10.1093/jpp/rgae121","url":null,"abstract":"<p><strong>Objectives: </strong>The study was aimed to investigate the effects of Xinfeng capsule (XFC) on tissue morphology, and gland function of the salivary gland (SG) in a primary Sjögren's syndrome (pSS) mouse model.</p><p><strong>Methods: </strong>An animal model of pSS was established by inducing SG protein in C57BL/6 mice. SG tissues were collected for tissue sequencing and subsequent experiments to detect the expression of cholinergic receptor muscarinic 3(M3R), early growth response factor 1 (EGR1) and target genes in the SG before and after XFC intervention, with in vitro validation.</p><p><strong>Results: </strong>Downstream targets of the EGR1 gene were predicted and analyzed using data analysis. EGR1 showed high expression and was selected for subsequent experiments. Administration of XFC significantly increased saliva production (P < 0.001) and reduced the extent of lymphatic infiltration observed in SG. Furthermore, the expression of EGR1 was increased in the model group with statistical significance in contrast with the control group but decreased after administration of XFC (P < 0.05). Data analysis predicted the downstream target of EGR1 as signal transducer and activator of transcription 3 (STAT3), which was validated in SG tissues of mice (P < .05).</p><p><strong>Conclusions: </strong>XFC demonstrated a significant improvement in the salivary secretion function of the SG in pSS mice. EGR1 can serve as a biomarker and therapeutic target for pSS.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1371-1378"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142468355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Citropten attenuates H₂O₂-induced neurotoxicity by modulating redox balance, inflammation, and apoptotic pathways in SH-SY5Y cells.","authors":"Vikram P Jadhav, Pradeep Kumar Mohanty","doi":"10.1093/jpp/rgaf048","DOIUrl":"10.1093/jpp/rgaf048","url":null,"abstract":"<p><strong>Objectives: </strong>The proposed study explores the neuroprotective potential of Citropten, a natural coumarin derivative, against H₂O₂-induced oxidative stress in SH-SY5Y human neuroblastoma cells. H₂O₂ treatment induced significant cytotoxicity, oxidative damage, mitochondrial dysfunction, and inflammation.</p><p><strong>Methods: </strong>SH-SY5Y cells were exposed to H₂O₂ to induce oxidative stress, followed by treatment with Citropten. Cell viability was measured using the MTT assay, and oxidative damage was assessed via LDH release, ROS generation, lipid peroxidation, and glutathione reductase (GR) activity. Mitochondrial membrane potential (MMP) was evaluated by flow cytometry. Inflammatory markers were quantified using ELISA, and apoptosis was determined by acridine orange (AO)/ethidium bromide (EB) staining and flow cytometry.</p><p><strong>Key findings: </strong>Citropten treatment significantly restored cell viability and reduced intracellular ROS levels by 63%, lipid peroxidation by 36% and LDH release by 44.7%, indicating improved membrane integrity. Citropten also preserved MMP (with a 79% restoration) and elevated GR activity. Inflammatory responses were attenuated with a decrease in NF-κB, IL-1β, IL-6, and TNF-α levels. Apoptotic cell death was markedly diminished, as confirmed by AO/EB staining and flow cytometry.</p><p><strong>Conclusions: </strong>Citropten demonstrated significant antioxidant, anti-inflammatory, and anti-apoptotic properties, highlighting its potential as a promising neuroprotective agent for mitigating oxidative stress-associated neuronal damage and possibly treating neurodegenerative diseases.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1402-1413"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined neuroprotective potential of vitamin E and levodopa/carbidopa in a rat model of rotenone-induced Parkinson's disease: role of AMPK/SIRT1/PGC-1α and HMGB1/RAGE axes.","authors":"Alaa S Wahba, Nehal S Wahba, Ghadir A Sayed, Sara K Hamed, Dina M Abo-Elmatty, Noha M Mesbah, Ahmed M Reda","doi":"10.1093/jpp/rgaf044","DOIUrl":"10.1093/jpp/rgaf044","url":null,"abstract":"<p><p>This study investigated the molecular mechanisms underlying the neuroprotective effects of vitamin E in a rotenone-induced Parkinson's disease (PD) rat model, in comparison to levodopa/carbidopa (LD/CD), and evaluated the benefit of their combined use. PD was induced by rotenone (2.5 mg/kg/day, i.p) for 42 days. On day 14, disease onset was confirmed via behavioral deficits and reduced striatal tyrosine hydroxylase (TH) levels. From day 15 to day 42, Parkinsonian rats received vitamin E (100 IU/kg/day, i.p), LD/CD (20/5 mg/kg/day, i.p), or both. ROT-intoxicated rats exhibited progressive motor dysfunction, striatal neurodegeneration, neuronal loss, reduced TH/dopamine levels, and α-synuclein aggregation. These changes were associated with suppressed AMPK/SIRT1/PGC-1α signaling, impaired mitochondrial biogenesis and function, defective mitophagy, heightened oxidative stress, and upregulation of the pro-inflammatory HMGB1/RAGE pathway. Treatment with either vitamin E or LD/CD significantly ameliorated behavioral, histopathological, and molecular abnormalities. Notably, the combination therapy elicited the most robust neuroprotective effects, exceeding the efficacy of monotherapies. Our data affords the molecular basis for managing PD by vitamin E add-on therapy with LD/CD, a strategy that could potentially reduce the need for higher LD/CD doses to overcome wearing-off and may even imply a dose reduction, thereby minimizing the risks of high-dose LD/CD monotherapy.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1386-1401"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Empagliflozin attenuates pyroptosis by regulating thioredoxin-NLRP3 inflammasome axis in a high fat cholesterol diet/streptozotocin model of atherosclerosis.","authors":"Nevien Hendawy, Sayed M El-Sayed, Doaa M AbdelWahed, Sedra Hesham Salaheldin, Sally A Abuelezz","doi":"10.1093/jpp/rgaf051","DOIUrl":"10.1093/jpp/rgaf051","url":null,"abstract":"<p><strong>Objectives: </strong>Oxidative stress (OS), inflammation, and pyroptosis are hallmarks of atherosclerosis pathogenesis. Thioredoxin-interacting protein (TXNIP) crosslinks them through activating nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome pathway. The current work addresses the potentials of empagliflozin (EMPA) on OS markers, thioredoxin (TRX), and TXNIP, downstream mediators of NLRP3 inflammasome and the executioner of pyroptosis; gasdermin D (GSDMD) in a model of atherosclerosis.</p><p><strong>Methods: </strong>Atherosclerosis was induced by high fat cholesterol diet (HFCD) and streptozotocin (STZ) in male Wistar rats. Five groups were allocated: Control group, HFCD-STZ group, and three orally EMPA treated groups with HFCD-STZ in doses (2.5, 5, and 10 mg/kg/d for 4 weeks). To access the underlying mechanism of EMPA on atherosclerosis, serum glycated haemoglobin, lipid profile, inflammatory cytokines, and aortic OS markers were evaluated. Polymerase chain reaction analysis of NLRP3 inflammasome components, TRX, TXNIP, GSDMD, and vascular cell adhesion molecule-1 (VCAM-1) mRNA expressions were performed. Histopathological studies further confirmed EMPA's effects on atherosclerosis.</p><p><strong>Key findings: </strong>EMPA ameliorates metabolic and histopathological alterations, inflammation, OS, TRRX/TXNIP reversal, VCAM-1, activation of NLRP3 inflammasome, and pyroptosis axis.</p><p><strong>Conclusions: </strong>EMPA displayed antioxidant and anti-inflammatory effects through attenuating the OS/TXNIP/NLRP3/GSDMD axis in an experimental model of atherosclerosis.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1414-1425"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive review of Drynariae rhizoma: botany, traditional applications, and active flavonoid components.","authors":"Guo Jingying, Liang Yonghong, Fan Huawei, Huang Huilian, Liu Jianqun, Peng Caiying, Shu Jicheng","doi":"10.1093/jpp/rgaf050","DOIUrl":"10.1093/jpp/rgaf050","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Objectives: &lt;/strong&gt;Drynaria fortunei, a species within the Drynaria genus, is a widely distributed medicinal plant with abundant resources. Its rhizome, Drynariae rhizoma, has been extensively utilized in traditional Chinese medicine for its therapeutic efficacy in promoting wound healing, alleviating pain, tonifying the kidneys, and strengthening bones. With a well-documented historical presence in classical texts, Drynariae rhizoma has played a significant role in traditional medical systems across various cultures. Recent phytochemical investigations have identified a diverse array of compounds in Drynariae rhizoma, including flavonoids, phenolic acids, lignans, steroids, and glycosides. Among these, flavonoids represent the principal active constituents, attracting considerable research attention due to their extensive pharmacological activities. This review systematically integrates and critically analyzes the recent research progress in this field,providing a comprehensive overview of the current research landscape,with the aim of identifying promising future directions for Drynariae rhizome.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This review leveraged a wide range of online databases, including SciFinder, PubMed, SpringerLink, Baidu Scholar, Google Scholar, ScienceDirect, American Chemical Society (ACS) Publications, Web of Science, and China National Knowledge Infrastructure (CNKI), to collect relevant literature. Comprehensive searches were conducted using keywords such as \"Drynariae Rhizoma\", \"flavonoids\", \"extraction\", \"chemical constituents\", \"analytical characterization\". To ensure the scientific accuracy of this study, the botanical name of the plant was meticulously cross-verified using authoritative platforms such as \"World Flora Online\" and \"The Plant List.\"&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Key findings: &lt;/strong&gt;This article provides a comprehensive overview of the botany (including characteristics, distribution, and origin) and traditional applications (such as its historical evolution, botanical sources, and multi-ethnic as well as cross-national therapeutic practices) of Drynariae rhizoma. Additionally, it highlights the latest research advancements on its flavonoid compounds, encompassing extraction methods (e.g. solvent extraction, ultrasound-assisted extraction, and microwave-assisted extraction), analytical characterization (e.g. ultraviolet spectroscopy, high-performance liquid chromatography, and nuclear magnetic resonance), chemical constituents (with 60 flavonoid compounds identified to date), biological activities (e.g. anti-osteoporosis, anti-osteoarthritis, renal protection, dental health promotion, neuroprotection, lipid-lowering, and immunomodulation), and clinical applications. Furthermore, the review discusses current quality control strategies, highlighting the impact of geographical origin and processing methods on flavonoid content. Further in-depth studies are essential to comprehensively explore these areas, paving the","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1319-1337"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive review of scientifically reported phytochemicals to manage allodynia in chronic diabetes complications.","authors":"Piyali Devroy, Dorothy Das, Asis Bala, Ashis Kumar Mukherjee","doi":"10.1093/jpp/rgaf012","DOIUrl":"10.1093/jpp/rgaf012","url":null,"abstract":"<p><strong>Background: </strong>The global prevalence of diabetes mellitus and its associated complications is increasing, impacting both developed and developing nations. One common complication is neuropathy and neuropathic pain, which often manifests as symptoms such as allodynia-a condition where patients experience pain from non-painful stimuli.</p><p><strong>Objective: </strong>This review seeks to explore scientifically validated medicinal plants and phytochemicals, presenting the findings in an organized format based on published literature.</p><p><strong>Methodology: </strong>Data were searched in pubmed literature and only the scientifically reported phytochemicals were considered to include in this review.</p><p><strong>Key findings: </strong>The U.S. Food and Drug Administration (FDA) has not approved many medications targeting the root causes of neuropathy. Instead, various strategies are employed to manage the symptoms of allodynia. Research on plant-based ethno-pharmaceuticals aims to address the symptoms without affecting the disease's progression, which involves the gradual loss of nerve fibres from the extremities. This article delves into allodynia's different forms, implications, and underlying signalling mechanisms.</p><p><strong>Conclusion: </strong>The hope is that further research on phytochemicals could lead to the development of therapies for managing various forms of allodynia in diabetic patients.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"1338-1370"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}