Journal of Pharmacy and Pharmacology最新文献

{"title":"UHPLC-MS analysis for bioactive compounds responsible for the anti-inflammation activities of Jiao Mei Gu on lipopolysaccharide-induced acute lung injury in mice.","authors":"Dan Zhou, Kai He, Wei Cai, Bin Li, Zaiqi Zhang","doi":"10.1093/jpp/rgaf063","DOIUrl":"https://doi.org/10.1093/jpp/rgaf063","url":null,"abstract":"<p><strong>Objective: </strong>To identify the anti-inflammatory ingredients of a typical Dong herbal medicine Jiao Mei Gu (JMG) (Cayratia albifolia C.L.Li) and reveal the underlying mechanisms.</p><p><strong>Methods: </strong>For the first time, the chemical constituents in JMG ethyl acetate extract, which showed the highest anti-inflammatory activity, were analyzed by Ultra-performance liquid chromatography-quadrupole-electrostatic field Orbitrap mass spectrometry (UHPLC-Q-Exactive orbitrap MS). The anti-inflammatory activities and the underlying mechanisms of JMG extracts were evaluated in the lipopolysaccharide (LPS)-induced RAW 264.7 cell model and LPS (10 mg/kg) induced acute lung injury model in BALB/c mice.</p><p><strong>Key findings: </strong>Overall, 65 compounds including lignans, apigenin, quercetin, chrysin, phlorizin, and eriodictyol, etc., were identified in JMG ethyl acetate extract. At 200 mg/kg, JMG ethyl acetate extract reversed the structure change of lung alveoli and inflammatory cell infiltration in LPS-induced acute lung injury model. Compared with the LPS group, the serum levels of IL-1β, IL-6, and TNF-α in the 200 mg/kg JMG-treated group were decreased by 58.6%, 56.5%, and 87.6%, respectively. Western blot results revealed that JMG ethyl acetate extract inhibited LPS stimulated p65 and IκBα phosphorylation in mouse lung.</p><p><strong>Conclusion: </strong>The present study demonstrated that the ethyl acetate fraction of JMG could reverse LPS-induced acute lung hemorrhagic necrosis and inflammatory cell infiltration in mice by preventing the phosphorylation of NF-κB p65 and reducing its nuclear translocation.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958478","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":"Folate-chitosan nanoparticle delivery of cannabidiol for targeted triple-negative breast cancer therapy.","authors":"Jia Liu, Yuqian Wang, Lingfeng Xie, Shanghua Xiao, Xueyan Zhang, Wendi Li, Yutao Peng, Ruizhao Cai, Shoukang Qu, Chengyu Huang","doi":"10.1093/jpp/rgaf072","DOIUrl":"https://doi.org/10.1093/jpp/rgaf072","url":null,"abstract":"<p><strong>Objectives: </strong>Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options. Cannabidiol (CBD) has demonstrated anticancer potential, but its clinical application is hindered by poor solubility and nonspecific distribution. This study aimed to develop a folic acid-modified chitosan (FA-CS) nanoparticle system to enhance the targeted delivery and therapeutic efficacy of CBD against TNBC.</p><p><strong>Methods: </strong>FA-CS@CBD nanoparticles were synthesized and characterized for morphology, size distribution, zeta potential, and stability. Their in vitro anticancer effects were evaluated through cytotoxicity, cellular uptake, apoptosis, and reactive oxygen species (ROS) assays in 4T1 breast cancer cells. The in vivo antitumour efficacy and systemic toxicity were assessed using a TNBC mouse model.</p><p><strong>Key findings: </strong>FA-CS@CBD nanoparticles exhibited uniform morphology, stable physicochemical properties, and efficient cellular uptake. Compared to free CBD, the nanoparticles significantly enhanced ROS production, induced apoptosis, and inhibited migration in 4T1 cells. In vivo studies demonstrated strong tumour-targeting capability and a tumour inhibition rate of 68.07%, with minimal systemic toxicity.</p><p><strong>Conclusions: </strong>The FA-CS@CBD nanoparticle system improved the targeted delivery and therapeutic effects of CBD against TNBC while maintaining favorable biocompatibility. These findings highlight the potential of FA-CS-based nanocarriers for enhancing CBD clinical application in breast cancer therapy.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958302","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":"Unlocking molecular mechanisms of Saussurea costus (Falc.) Lipsch. root extract against experimentally induced hypothyroidism through integrated ultra-performance liquid chromatography-tandem mass spectrometry-based serum metabolomics and network pharmacology approaches.","authors":"Neveen M Barghouth, Hend M Dawood, Nesrine S El-Mezayen, Eman Shawky, Reham S Ibrahim","doi":"10.1093/jpp/rgaf068","DOIUrl":"https://doi.org/10.1093/jpp/rgaf068","url":null,"abstract":"<p><strong>Objectives: </strong>Saussurea costus (Falc.) Lipschitz is traditionally used to manage thyroid disorders; however, the components responsible for its effects on propylthiouracil (PTU)-induced hypothyroidism and their mechanisms remain unclear. This study investigated the effects of S. costus on PTU-induced hypothyroid rats using serum metabolomics, network pharmacology, and in vivo testing.</p><p><strong>Methods: </strong>Hypothyroidism was induced in rats by oral PTU administration. The metabolites absorbed from S. costus were characterized using UPLC-MS/MS and then analysed through network pharmacology to construct a compound-target-pathway network. Biological assays assessed the anti-hypothyroid effects of S. costus through ELISA and qRT-PCR techniques.</p><p><strong>Key findings: </strong>A total of 28 compounds (6 prototypes and 22 metabolites) were identified from the serum of S. costus extracts, including terpenes and phenolic compounds. The component-target network identified 67 nodes with 51 target genes, such as SLC26A4, SLC5A5, Dio1, Dio2, TPO, CTSB, and THR-β. Key compounds like chlorogenic acid-O-methyl and dihydroreynosin glucuronide showed the highest combined scores in the compound-target network. Top KEGG pathways related to these targets included cancer, TNF signalling, apoptosis, NF-kappa B, and cAMP signalling pathways. Gene ontology analysis revealed biological processes like thyroid hormone generation, cell migration regulation, and hormone biosynthesis as key targets. Cellular components such as collagen-containing extracellular matrix and molecular functions like glycine binding and nuclear receptor activity were also associated with hypothyroidism. Administration of S. costus root extract to hypothyroid rats upregulated genes like SLC5A5, TPO, and Dio1, enhancing T4-to-T3 conversion and restoring normal T3 levels. This treatment also significantly activated Dio2 and THR-β, suggesting enhanced T4-to-T3 conversion in the pituitary gland, promoting negative feedback inhibition of TSH production.</p><p><strong>Conclusions: </strong>S. costus root extract may act as a safe, effective alternative or adjunct therapy to the conventional treatments for hypothyroidism.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958450","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":"Ruxolitinib alleviated muscle atrophy in cancer cachexia by inhibiting IL-6/JAK/STAT3 signaling pathway in mice.","authors":"Cong Li, Xiaofan Gu, Zixia Zhu, Xiaojuan Pan, Meng Fan, Xuan Liu, Xiongwen Zhang","doi":"10.1093/jpp/rgaf073","DOIUrl":"https://doi.org/10.1093/jpp/rgaf073","url":null,"abstract":"<p><strong>Objectives: </strong>Ruxolitinib (Rux), an oral Janus tyrosine Kinase (JAK) tyrosine kinase inhibitor, has demonstrated anti-inflammatory properties and the ability to mitigate denervation-induced skeletal muscle atrophy. Here, we checked the potential efficacy of Rux on cancer cachexia and tried to clarified its mechanisms.</p><p><strong>Methods: </strong>The in vitro cell models of C26 or LLC CM-induced C2C12 myotubes were used to check the influence of Rux on myotube atrophy. C26 tumour-bearing mice (male BALB/c mice) were applied as the animal model to examine the effects of Rux in attenuating cachexia symptoms. Western blot analysis was utilized to investigate the potential mechanisms of Rux.</p><p><strong>Key findings: </strong>Rux significantly attenuated C2C12 myotube atrophy in vitro. Rux suppressed the interleukin-6 secretion by inhibiting STAT3 activation in tumour cells and macrophages. The administration of Rux prevented body weight loss and muscle wasting in C26 tumour-bearing mice without affecting tumour growth. At the end of the experiment, mice in the Rux treatment group exhibited a 6.7% increase in body weight compared to the C26 model group. Furthermore, Rux enhanced in gastrocnemius myofibres cross-sectional area and grip strength.</p><p><strong>Conclusions: </strong>Rux ameliorates cancer cachexia muscle atrophy by inhibiting STAT3/Atrogin-1 signaling. Rux may represent a promising therapeutic candidate for the treatment of cancer cachexia.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958411","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":"Intervention of non-alcoholic fatty liver disease by Ling Gui Zhu Gan Granules and its volatile components through the metabolism of intestinal microbiota and short-chain fatty acids.","authors":"Nan Wang, Jing Li, Ze-Xuan Chen, Jie Tang, Xue-Yee Lim, Ling Li, Tong Zhang","doi":"10.1093/jpp/rgaf070","DOIUrl":"https://doi.org/10.1093/jpp/rgaf070","url":null,"abstract":"<p><strong>Objectives: </strong>Ling Gui Zhu Gan (LGZG) Granules is a marketed traditional Chinese medicine compound granule, which is formulated to be consistent with the key quality attributes of the traditional LGZG Decoction. The volatile components are important parts of its preparation process.</p><p><strong>Methods: </strong>A high-fat diet (HFD)-induced Non-alcoholic fatty liver disease (NAFLD) mouse model was established to evaluate the therapeutic effects of LGZG and preparation of LGZG's volatile components (IC-LGZG). Gut microbiota composition, Short-chain Fatty Acids (SCFA) levels, and intestinal parameters were assessed, and its correlations were analyzed. Lipopolysaccharide-induced RAW264.7 cells tested anti-inflammatory effects.</p><p><strong>Key findings: </strong>LGZG and IC-LGZG significantly reduced HFD-induced body weight gain, improved lipid profiles and liver function, restored gut microbiota balance, increased beneficial bacteria (Akkermansia, Bacteroides, Parabacteroides, Dubosiella, and Bifidobacterium) that produce SCFAs, thereby enhancing SCFA concentrations (acetic acid, propionic acid, and butyric acid), decreased harmful bacteria abundance, and strengthened the intestinal barrier. In vitro studies showed that LGZG, IC-LGZG, and cinnamaldehyde exerted anti-inflammatory effects.</p><p><strong>Conclusion: </strong>LGZG and its volatile components effectively alleviate the progression of NAFLD by modulating the gut microbiota homeostasis and SCFA levels, and can exert anti-inflammatory effects.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958299","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":"Advanced oxidation protein products accelerates paracetamol-induced liver injury through AMPK-mTOR signaling pathway in chronic kidney disease.","authors":"Sui Wei, Huanhuan Liu, Zixi Hong, Mimi Zhang, Zhufen Lin, Haixing Feng, Xiaokang Wang, Jingqian Zhao, Xixiao Yang, Tianrong Xun","doi":"10.1093/jpp/rgaf069","DOIUrl":"10.1093/jpp/rgaf069","url":null,"abstract":"<p><strong>Objectives: </strong>Chronic kidney disease (CKD) is a progressive medical condition marked by a gradual decline in kidney function, leading to an accumulation of waste products and fluids in the body. Drug-induced liver injury (DILI) poses a significant clinical challenge in CKD management, with paracetamol being a commonly used medication. Advanced oxidation protein products (AOPPs) are biomarkers of CKD progression and contributors to DILI. However, the mechanisms behind the increased incidence of DILI in CKD remain unclear.</p><p><strong>Methods: </strong>We developed an adenine-induced CKD mice model, a paracetamol-induced DILI mice model, and an AOPPs-loaded mice model using intraperitoneal injections.</p><p><strong>Key findings: </strong>Declining renal function in the CKD model was associated with a significant weight loss and increased the concentration of serum creatinine and blood urea nitrogen. Following paracetamol administration, the alanine aminotransferase (ALT), aspartate aminotransferase (AST), and N-acetyl-p-benzoquinoneimine and liver tissue necrosis increased significantly in CKD groups. In addition, the expression of cytochrome P450 2E1 (CYP2E1) and thrombospondin receptor (CD36) were upregulated, while the adenylate-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signaling pathway showed significant changes in protein expression and phosphorylation. In AOPPs-loaded model, AOPPs upregulated AMPK and Akt protein expression, along with reduced mTOR levels. In HepG2 and L0-2 cell lines, AOPPs and paracetamol significantly increased the protein expression and phosphorylation of AMPK and Akt, alongside a decreased mTOR expression and phosphorylation. AOPPs and paracetamol significantly induced the apoptosis in HepG2 and L0-2 cells. Notably, the expression of CYP2E1 induced by AOPPs and paracetamol was inhibited by dorsomorphin and corynoxine B.</p><p><strong>Conclusions: </strong>These findings suggest that the AMPK-mTOR signaling pathway mediates the worsening of paracetamol-induced liver injury in CKD, with AOPPs potentially serving as key endogenous factors. This study lays the groundwork for identifying crucial molecules involved in exacerbated paracetamol-induced liver injury in CKD, which may serve as new drug targets and improve the safety profile of paracetamol in patients with CKD.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873745","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":"Ambroxol mitigates renal ischemia/reperfusion-induced cardiac and renal injury via Nrf2/HO-1 activation and TLR4 pathway inhibition.","authors":"Hadeer A Fayed, Somaia A Abdel-Sattar, Azza S Awad","doi":"10.1093/jpp/rgaf064","DOIUrl":"10.1093/jpp/rgaf064","url":null,"abstract":"<p><strong>Background: </strong>Ambroxol is a mucokinetic drug with antioxidant and anti-inflammatory properties. Renal ischemia/reperfusion (IR) is the cause of acute kidney injury that usually occurs with other comorbidities.</p><p><strong>Objectives: </strong>To explore ambroxol for repurposing against renal IR-induced cardio-renal injury.</p><p><strong>Methods: </strong>Sprague-Dawley rats were assigned into: Sham group (Group I), untreated renal IR group (Group II), and ambroxol-pretreated group (Group III). Cardiac injury parameters, histopathology, and oxidative and antioxidant status, plus signaling molecules related to hypoxia, inflammation, mitochondrial dysfunction, and apoptosis were evaluated.</p><p><strong>Key findings: </strong>Ambroxol administration significantly (P < .001) improved the IR-deteriorated cardiac biomarkers and histopathology and up-regulated the Nrf2/HO-1 pathway to increase antioxidant capacity. The cardio-renal expression of hypoxia-inducible factor (HIF)-1α was significantly (P < .001) attenuated by ambroxol. Ambroxol also attenuated inflammation by significant (P < .001) down-regulation of TLR4, p38 mitogen-activated protein kinase, nuclear factor kappa B, and nod-like receptor protein 3 expression while decreasing IL-1β and TNF-α secretion. Moreover, ambroxol significantly (P < .001) ameliorated mitochondrial dysfunction and apoptosis. Statistical results revealed positive correlations between the expression of TLR4 and HIF-1 and between TLR4 and dynamin-related protein 1.</p><p><strong>Conclusions: </strong>Ambroxol's cardio-renal protecting potential was elicited by inhibiting oxidative stress, inflammation, and mitochondrial dysfunction through activating the Nrf2/HO-1 pathway and inhibiting multiple TLR4-interconnected signaling pathways, thus affording a theoretical base for ambroxol's clinical use in renal IR-induced injuries.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873746","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":"Icariside II: natural occurrence, biotransformation, pharmacological activity, synthetic modification, pharmacokinetics, and bioavailability.","authors":"Huynh Thi Ngoc Ni, Nguyen Ngoc Linh, Phi Thi Tuyet Nhung, Pham Thi Bich Dao, Vu Quoc Manh, Ninh The Son","doi":"10.1093/jpp/rgaf065","DOIUrl":"https://doi.org/10.1093/jpp/rgaf065","url":null,"abstract":"<p><strong>Objectives: </strong>Icariside II (ICS-II), a flavone containing 3-rhamnopyranosyl and 8-prenyl groups, is one of the main natural compounds found in Epimedum species (the family Berberidaceae). The current study aims to provide a systematic review of its natural occurrence, pharmacological value, synthetic modification, pharmacokinetics, and bioavailability.</p><p><strong>Key findings: </strong>Sources such as Google Scholar, Web of Science, PubMed, and journal websites were used to gather references about ICS-II. 'Icariside II' is the most meaningful keyword to seek references, and references have been updated till now.</p><p><strong>Summary: </strong>ICS-II is a characteristic metabolite of various Epimedum plants, and it can be obtained by enzymatic hydrolysis of other flavonoids. It is a promising compound with multiple in vitro and in vivo pharmacological potentials. The studied flavone showed cancer-related biological activity via cell cycle arrest, proliferation inhibition, autophagy, and apoptosis and inhibited cytokines in anti-inflammatory actions. Significantly, the health benefits were accompanied by its role in antidiabetics, sexual reproduction, and protection against harmful effects on the heart, brain, bones, lungs, kidneys, livers, and eyes. Molecular mechanisms of action were deduced from various signaling pathways, such as Akt/NOS/NF-κB, JAK/STAT3/MAPK, and PI3K/Akt/mTOR. Pharmacokinetic evidence involved sugar and methyl removals, hydroxylation, glucuronidation, and glycosylation.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859267","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":"Application of zebrafish (Danio rerio) as a model organism for central nervous system disorders screening of natural products.","authors":"Ayla Winnie Ramos da Silva, Lorena Batista da Silva, Douglas Fernando Rambo, Renata Biegelmeyer","doi":"10.1093/jpp/rgaf067","DOIUrl":"https://doi.org/10.1093/jpp/rgaf067","url":null,"abstract":"<p><strong>Objectives: </strong>Natural products (NP) play a crucial role in the development of new compounds, due to their complex chemical structure and pharmacological diversity. Neurodegenerative diseases and other disorders in the central nervous system (CNS) have become a significant problem in the world due to the increase in life expectancy of the elderly population. This increases the risk of developing diseases, such as Parkinson's disease, Huntington's disease, Alzheimer's disease. Therefore, this exploratory review aims to show the applications of zebrafish for NP research and how they can be used in CNS's in vivo studies.</p><p><strong>Methods: </strong>The present review covers the literature survey until 2023, including the descriptors for zebrafish, natural product and neurodegenerative diseases. The databases used were PubMed, Scopus, Cochrane and Lilacs.</p><p><strong>Key findings: </strong>For the development of new medicines, an efficient animal model is required, and the zebrafish has stood out as a promising model due to its small size, low cost of maintenance, ease of handling, and transparency of embryos, which allows real-time observation of development and pathological processes. They possess conserved neurotransmission systems such as glutamatergic, cholinergic, dopaminergic, serotonergic, histaminergic, GABAergic, and purinergic pathways, making them especially relevant for modelling CNS disorders. From literature survey, flavonoids, alkaloids, and phenolic compounds were the most frequently studied, indicating that its influence the pathophysiological mechanisms associated with neurodegenerative diseases.</p><p><strong>Conclusions: </strong>This current review offers data for further research work with natural products aiming treatment for CNS disorders.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859266","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":"Protective effect of pirfenidone against ovarian ischemia/reperfusion injury in rats via modulation of TLR4/p38 MAPK/IL-1β and HIF-1α/VEGF-A signaling pathways.","authors":"Asmaa Mohamed Abdel-Aziz, Marwa Hassan, Dina Moustafa Thabit, Safaa Said, Heba A Shawky, Samar Hisham Elsayed, Hanaa Mohamed Khalaf","doi":"10.1093/jpp/rgaf066","DOIUrl":"https://doi.org/10.1093/jpp/rgaf066","url":null,"abstract":"<p><strong>Objective: </strong>Ovarian ischemia/reperfusion (I/R) injury is a common gynecological emergency, typically caused by ovarian torsion. Pirfenidone (PFN) has demonstrated potential therapeutic benefits due to its antioxidant, anti-inflammatory, and antiapoptotic properties. This research aimed to investigate the protective effects of PFN in alleviating ovarian I/R injury in female rats.</p><p><strong>Methods: </strong>Female rats received PFN (300 mg/kg/day) for 3 consecutive days, either with or without the induction of ovarian I/R. The study assessed markers of ovarian oxidative stress, inflammation, apoptosis, and the levels of hypoxia-inducible factor-1 alpha and vascular endothelial growth factor-A (VEGF-A). Ovarian histology was analyzed, along with immunohistochemical staining for Toll-like receptor 4 (TLR4) and p38 mitogen-activated protein kinase (p38 MAPK).</p><p><strong>Key findings: </strong>I/R injury resulted in increased oxidative stress, inflammation, apoptosis, and a significant reduction in ovarian VEGF-A levels. Histological examination revealed ovarian damage, with increased expression of TLR4 and p38 MAPK. PFN treatment significantly improved the hormonal balance and mitigated oxidative stress, inflammatory, and apoptotic markers to normal levels. In addition, PFN improved ovarian tissue morphology and decreased TLR4 and p38 MAPK expression.</p><p><strong>Conclusions: </strong>The findings suggest that PFN may offer protective effects against ovarian I/R injury through its antioxidant, anti-inflammatory, and antiapoptotic properties, as well as by promoting angiogenesis in the ovary.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835474","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}