Journal of Pharmacy and Pharmacology最新文献

{"title":"Co-administration of Ceratonia siliqua extract nanoparticles promotes the oral bioavailability and neurotherapeutic efficacy of donepezil in a dementia model.","authors":"Sylvia E Shaker, Dalia B Fayed, Heba Shawky, Ebtehal K Farrag","doi":"10.1093/jpp/rgae094","DOIUrl":"10.1093/jpp/rgae094","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to assess the herb-drug interactions between crude/silver nanoparticle (SNP)-loaded carob extract (Car, NCar, respectively) and donepezil-HCl (DPZ) and their impact on neurotherapeutic outcomes in a dementia model.</p><p><strong>Methods: </strong>Carob pods were subjected to ethanol extraction, and their phytoconstituents were chromatographically analysed. SNP-loaded extract was synthesized and characterized, and dementia-like symptoms were induced in Wistar rats by repeated dosing with 175 mg/kg AlCl3 for 60 days, after which the animals were treated with Car, NCar, DPZ, and combinations of Car/NCar-DPZ for 30 days. The effect of carob formulations on DPZ bioavailability was in-silico profiled and the herb-drug interactions were mathematically assessed as combination indices.</p><p><strong>Results: </strong>Different formulations significantly improved cognitive/spatial memory functions, restored dysregulated brain redox and cholinergic functions, and markedly inhibited cholinesterase, as reflected by the reduction/absence of amyloid plaques and neurofibrillary tangles. In silico profiling of the major phytoconstituents revealed their non-P-glycoprotein substrate nature and CYP3A4, 2C19, and 2C9 inhibition, which might have improved the oral bioavailability of DPZ. The combination index calculations revealed strong synergy between DPZ and both carob formulations, with the strongest effect exhibited by the DPZ/NCar combination.</p><p><strong>Conclusion: </strong>The co-administration of carob extract/SNPs represents a promising approach for enhancing the neurotherapeutic efficacy of DPZ.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":"153-169"},"PeriodicalIF":2.8,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759411","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":"Exploring the mechanism of pachymic acid intervention in myocardial ischemia based on network pharmacology and experimental validation.","authors":"Nengpin Yin, Xuan Zhao, Jin Yang, Zongjun Liu","doi":"10.1093/jpp/rgae153","DOIUrl":"https://doi.org/10.1093/jpp/rgae153","url":null,"abstract":"<p><strong>Objectives: </strong>To deeply explore the mechanism of pachymic acid (PA) intervention in myocardial ischemia, providing new ideas and methods for the treatment of myocardial ischemia.</p><p><strong>Methods: </strong>Predict the targets of PA for improving myocardial ischemia, and conduct functional enrichment analysis using databases, such as Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Reactome. To verify these findings, PPI network topology analysis and molecular docking were used to screen key targets and main mechanisms of action and further validated through in vitro experiments on the H9C2 cell line.</p><p><strong>Key findings: </strong>PA can significantly alleviate myocardial damage caused by hypoxia/reoxygenation, effectively reversing the abnormalities of oxidative stress indicators such as LDH, MDA, SOD, and ROS. PA may exert its effects through 39 targets, particularly by regulating the downregulation of autophagy-related proteins LC3-II and Beclin-1 expression via MTOR, thereby inhibiting excessive autophagy in cardiomyocytes.</p><p><strong>Conclusions: </strong>PA protects myocardial cells during myocardial ischemia through various pathways, particularly by regulating mTOR to inhibit excessive autophagy.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932010","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":"Piperlongumine inhibits glioblastoma proliferation by inducing ferroptosis.","authors":"Jianting Qiu, Fangzhou Guo, Ji Shi, Tangjun Guo, Haozhe Piao","doi":"10.1093/jpp/rgae148","DOIUrl":"https://doi.org/10.1093/jpp/rgae148","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to investigate the effects of Piperlongumine on Glioblastoma multiforme.</p><p><strong>Methods: </strong>The effects of Piperlongumine on the viability and proliferation of glioma cells LN229 and A172 were measured. Changes in mitochondrial structure were observed. Cell proliferative capacity was assessed using immunofluorescence. The levels of glutathione, malondialdehyde, 4-hydroxynonenal, and intracellular reactive oxygen species were detected. The levels of ferroptosis-related proteins were detected. A plasmid transfection was performed to overexpress the nuclear factor erythroid 2-related factor 2 gene; a subcutaneous tumor model was established in nude mice to observe the in vivo inhibitory effects of Piperlongumine on Glioblastoma multiforme and the recovery effect of Fer-1. The expression levels of ferroptosis-related proteins were detected using immunohistochemistry.</p><p><strong>Key findings: </strong>Piperlongumine inhibited the viability of glioma cells, as well as their proliferation. The ferroptosis inhibitors were able to restore the inhibitory effect of Piperlongumine on glioma cell proliferation. Forced overexpression of nuclear factor erythroid 2-related factor 2 partially reversed Piperlongumine-induced ferroptosis; Piperlongumine exhibited a significant inhibitory effect on Glioblastoma multiforme cells in vivo, which could be restored by Fer-1.</p><p><strong>Conclusions: </strong>Piperlongumine inhibits Glioblastoma multiforme proliferation by inducing ferroptosis in vitro and vivo model.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846863","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":"Exploring the molecular mechanism of Taohong Siwu decoction in the treatment of non-small-cell lung cancer based on network pharmacology and molecular docking.","authors":"Yuan Qin, Jia-Ning Lian, Xin Chen, Feng-Yu Huang, Hai-Wen Chen, Tai-Wei Dong, Zuo-Lin Jin","doi":"10.1093/jpp/rgae141","DOIUrl":"https://doi.org/10.1093/jpp/rgae141","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore the mechanism of Taohong Siwu decoction (THSWD) in the treatment of non-small-cell lung cancer (NSCLC) by using comprehensive analysis.</p><p><strong>Methods: </strong>The active components and relevant targets of THSWD were analyzed by network analysis to construct the active component-target-disease network diagram. Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were conducted on the core targets by the Metascape database. Molecular docking verification was used for molecular visualization.</p><p><strong>Key findings: </strong>A total of 69 active compounds and 114 targets were filtered in lung cancer treatment with THSWD. KEGG analysis suggested that tumor necrosis factor (TNF) signaling pathway, and apoptosis pathway played critical roles. The results of molecular docking showed that populoside_qt with IL-6, baicalein with epidermal growth factor receptor (EGFR), and luteolin with MAPK8 had the strongest binding ability. Moreover, experiment validation revealed that THSWD regulated the expression of IL-6, AKT, Cyclin D1, E-cadherin, and LC3A/B, thereby inhibiting the proliferation and migration ability, promoting apoptosis, and blocking the cell cycle of NSCLC cells.</p><p><strong>Conclusions: </strong>The potential targets and molecular mechanisms of THSWD in the treatment of NSCLC were preliminarily revealed by a comprehensive analysis in this study, which will provide new ideas and methods for the study of the mechanism of traditional Chinese medicine in treating lung cancer.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142836980","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":"Capsaicin: pharmacological applications and prospects for drug designing.","authors":"Anshita Gupta, Renjil Joshi, Lokkanya Dewangan, Kamal Shah, Deependra Soni, Umesh K Patil, Nagendra Singh Chauhan","doi":"10.1093/jpp/rgae150","DOIUrl":"https://doi.org/10.1093/jpp/rgae150","url":null,"abstract":"<p><strong>Objectives: </strong>A primary objective of this review is to summarize the evidence-based pharmacological applications of capsaicin, particularly its use to manage pain and treat various health conditions. A second goal of the review is to research how recent technological advances are improving the bioavailability and therapeutic index of capsaicin, as well as the development of novel capsaicin-mimetics that are able to enhance therapeutic responses in various human diseases.</p><p><strong>Methods: </strong>In the review, numerous human clinical trials and preclinical studies are examined to determine how effective, safe, and optimal dosages of capsaicin can be used in pain management and therapeutic applications. Furthermore, it discusses capsaicin's mechanisms of action, specifically its interactions with the transient receptor potential vanilloid 1 (TRPV1) channel. As a result of this review, the potential of nanotechnology systems for bypassing the limits of capsaicin's pungency is discussed. The review takes into account individual factors such as pain tolerance and skin sensitivity.</p><p><strong>Key findings: </strong>For topical applications, capsaicin is typically used in concentrations ranging from 0.025% to 0.1%, with higher concentrations being used under medical supervision for neuropathic pain. The formulation can come in the form of creams, gels, or patches, which provide sustained release over the course of time. A condition such as arthritis or neuropathy can be relieved with capsaicin as it depletes substance P from nerves. Neuropathy and osteoarthritis as well as musculoskeletal disorders have been treated successfully with this herbal medicine. A major mechanism through which capsaicin relieves pain is through activating TRPV1 channels, which induce calcium influx and neurotransmitter release. Additionally, it affects the transcription of genes related to pain modulation and inflammation, particularly when disease conditions or stress are present. There have been recent developments in technology to reduce capsaicin's pungency and improve its bioavailability, including nanotechnology.</p><p><strong>Conclusions: </strong>It is proven that capsaicin is effective in pain management as well as a variety of therapeutic conditions because of its ability to deplete substance P and desensitize nerve endings. Although capsaicin is highly pungent and associated with discomfort, advancements in delivery technologies and the development of capsaicin-mimetics promise improved therapeutic outcomes. There is a great deal of complexity in the pharmacological action of capsaicin due to its interaction with TRPV1 channels and its ability to affect gene transcription. There is a need for further research and development in order to optimize capsaicin's clinical applications and to enhance its therapeutic index in a variety of human diseases.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142807440","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":"Decoding the power of saponins in ferroptosis regulation and disease intervention: a review.","authors":"Min Ouyang, Jianhua Wu, Xizhuo Hu, Changfu Liu, Dan Zhou","doi":"10.1093/jpp/rgae144","DOIUrl":"https://doi.org/10.1093/jpp/rgae144","url":null,"abstract":"<p><strong>Objectives: </strong>This review endeavors to elucidate the complex interplay underlying diseases associated with ferroptosis and to delineate the multifaceted mechanisms by which triterpenoid and steroidal saponins modulate this form of cell death.</p><p><strong>Methods: </strong>A meticulous examination of the literature was undertaken, drawing from an array of databases including Web of Science, PubMed, and Wiley Library, with a focus on the keywords \"ferroptosis,\" \"saponin,\" \"cancer,\" \"inflammation,\" \"natural products,\" and \"signaling pathways.\"</p><p><strong>Key findings: </strong>Ferroptosis represents a distinctive mode of cell death that holds considerable promise for the development of innovative therapeutic strategies targeting a wide range of diseases, especially cancer and inflammatory disorders. This review reveals the nuanced interactions between saponins and critical signaling pathways, including system Xc--GSH-GPX4, Nrf2, p53, and mTOR. These interactions highlight the dual capacity of saponins to modulate ferroptosis, thereby offering fresh perspectives for therapeutic intervention.</p><p><strong>Conclusions: </strong>The insights garnered from this review significantly advance our comprehension of the dynamic relationship between saponins and ferroptosis. By shedding light on these mechanisms, this work sets the stage for leveraging these insights in the creation of pioneering approaches to disease treatment, marking a significant stride in the evolution of therapeutic modalities.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823545","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":"Activation of HSPA5 contributes to pazopanib-induced hepatotoxicity through l-ornithine metabolism pathway and endoplasmic reticulum stress.","authors":"Jian Chen, Tieming Zhu, Yaping Deng, Jinliang Chen, Guojun Jiang, Qiaojun He","doi":"10.1093/jpp/rgae130","DOIUrl":"https://doi.org/10.1093/jpp/rgae130","url":null,"abstract":"<p><strong>Objectives: </strong>The clinical application of Pazopanib (Paz) is often accompanied by hepatotoxicity. However, the mechanisms of hepatic toxicity induced by pazopanib are not entirely clarified.</p><p><strong>Methods: </strong>Male C57BL/6J mice were treated with pazopanib every day for 2, 4, or 8 weeks. Transcriptomics and metabolomics analyses of liver tissues were performed. In vitro experiments were carried out to estimate cell viability, apoptosis, and autophagy in L02 cells after Paz treatment. We also examined apoptosis and autophagy-related genes under 4-PBA, l-ornithine, nor-NOHA treatments, and HSPA5 knockdown.</p><p><strong>Key findings: </strong>Repeated Paz treatment for 8 weeks resulted in more severe hypofunction of the liver in mice. Moreover, Paz treatment inhibited L02 cells cell viability in a dose-dependent manner. We also discovered activation of endoplasmic reticulum stress, apoptosis, and autophagy in Paz-treated L02 cells, as evidenced by the boosted expression of HSPA5, p-IRE1α, ATF4, ATF6, p-eIF2α, LC3, Beclin-1, and a decrease of phosphorylated PI3K, AKT, and mTOR levels. Moreover, 4-PBA, l-ornithine, and HSPA5 knockdown inhibited apoptosis and autophagy, while nor-NOHA weakened the effects of HSPA5 knockdown on apoptosis in Paz-treated L02 cells.</p><p><strong>Conclusions: </strong>In summary, our study revealed that Paz-induced liver toxicity is related to HSPA5 expression and l-ornithine metabolism pathway in mice.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824285","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":"Modulation of PPAR-γ/Nrf2 and AGE/RAGE signaling contributes to the chrysin cardioprotection against myocardial damage following ischemia/reperfusion in diabetic rats.","authors":"Neha Rani, Dharamvir Singh Arya","doi":"10.1093/jpp/rgae140","DOIUrl":"https://doi.org/10.1093/jpp/rgae140","url":null,"abstract":"<p><strong>Objective: </strong>Advanced glycation end products/receptor for AGEs (AGE/RAGE) signaling has a well-established role in the etiology of diabetic-related cardiovascular disorders. The purpose of the study was to elucidate the role of chrysin, a peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist, against ischemia/reperfusion (IR) injury in diabetic rats and its functional interaction with the AGE/RAGE signaling pathway.</p><p><strong>Methods: </strong>A single intraperitoneal injection of streptozotocin (STZ, 70 mg/kg) was administered to rats for induction of diabetes. Rats having blood glucose levels more than 300 mg/dl following a 72 hr STZ injection were classified as diabetic. PPAR-γ antagonist GW9662 (1 mg/kg, i.p.), chrysin (60 mg/kg, p.o.), or both were administered to diabetic rats for 4 weeks. On the 29th day, rats were given ischemia for 45 min and then reperfusion for 1 hr to induce myocardial infarction (MI).</p><p><strong>Key findings: </strong>Pretreatment with chrysin significantly improved hemodynamic status, ventricular functions, and cardiac injury markers in diabetic myocardium. Increased PPAR-γ/Nrf2 and decreased RAGE protein expressions were linked to this improvement. Chrysin pretreatment resulted in the upregulation of endogenous antioxidants and reduced TBARS levels. Moreover, chrysin significantly decreased inflammation and apoptosis in diabetic myocardium.</p><p><strong>Conclusion: </strong>PPAR-γ/Nrf2 co-activation by chrysin ameliorated IR-induced MI in diabetic rats, possibly via modulating AGE/RAGE signaling.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823497","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":"Ginsenoside Rb1 ameliorates hippocampal neuroinflammation in rats after intracerebral hemorrhage by inactivating the TLR4/NF-kB pathway.","authors":"Xi Liu, Yuying Wang, Ling Han, Xing Li, Yan Zhong, Jilin Zhou, Xiyun Fei, Min Peng, Jixin Duan, Zhijun Zhong","doi":"10.1093/jpp/rgae145","DOIUrl":"https://doi.org/10.1093/jpp/rgae145","url":null,"abstract":"<p><strong>Purpose: </strong>This work elucidated the therapeutic effect and mechanism of ginsenoside Rb1 on intracerebral hemorrhage (ICH).</p><p><strong>Methods: </strong>ICH rat models were treated by ginsenoside Rb1. Modified neurological deficit score, and Y-maze and Morris water-maze tests were performed on rats. Hippocampal neuronal damage was observed by Nissl staining. Rat primary astrocytes were exposed to ginsenoside Rb1, Hemin, and lipopolysaccharide (LPS). TNF-α, IL-1β, and IL-6 levels were assessed via enzyme-linked immunosorbent assay. TLR4/NF-kB pathway activity was appraised by Western blot. Immunofluorescence staining was for hippocampal glial fibrillary acidic protein (GFAP) expression and P65 protein location in hippocampus and astrocytes.</p><p><strong>Results: </strong>In rats after ICH, ginsenoside Rb1 ameliorated neurological impairment and hippocampal neuronal damage; improved learning and memory ability; reduced brain water content; decreasedhippocampal TNF-α, IL-1β, and IL-6; inactivated TLR4/NF-kB pathway; and declined hippocampal GFAP expression. In rat primary astrocytes exposed to Hemin, ginsenoside Rb1 declined TNF-α, IL-1β, and IL-6; inactivated TLR4/NF-kB pathway; and hindered P65 protein entry into nucleus. However, these functions of ginsenoside Rb1 on the Hemin-induced astrocytes were abolished by LPS.</p><p><strong>Conclusion: </strong>Ginsenoside Rb1 has promising future for clinical ICH treatment, which exerts therapeutic effect on ICH by ameliorating hippocampal neuroinflammation via inactivating the TLR4/NF-kB pathway.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142729722","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":"GC-MS- and LC-TOF-MS/MS-based ginger volatile oil serum analysis and the potential mechanism of the anticancer effect of serum component citral on MCF-7 breast cancer cells.","authors":"Wenkai Zhang, Zhiyong Liu, Liming Luo, Lei Xu, Qiuting Ma, Shuai Huang, Tao Hong","doi":"10.1093/jpp/rgae116","DOIUrl":"https://doi.org/10.1093/jpp/rgae116","url":null,"abstract":"<p><strong>Background: </strong>To explore the blood components of ginger volatile oil (GVO) after gastric perfusion in rats and its different metabolites from blank serum and the network pharmacological analysis and preliminary verification of the main components against breast cancer.</p><p><strong>Methods: </strong>A total of 20 male rats were randomly allocated to 10 control groups and 10 experimental groups. The administration group was given diluted GVO and the blank group was given the same amount of soybean oil (weigh 12 g of GVO diluted to 100 ml with soybean oil), the serum of rats in the given and blank groups was analyzed by gas chromatography-time-of-flight mass spectrometry, and the differential metabolites were screened and enriched, and the blood components were analyzed by ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS).</p><p><strong>Results: </strong>A total of 34 different metabolites were screened, and 31 original components were identified. The content of citral in volatile oil and serum is high, and the pathway of action is also closely related to the results of network pharmacology. Cell experiments showed that both drug-containing serum and citral significantly inhibited the proliferation and lateral transfer ability of breast cancer MCF-7 cells in a concentration and time-dependent manner, flow cytometry was used to measure apoptosis, and the experimental results showed that the proportion of early and late apoptosis was significantly increased in each group compared with the control group, and the proportion of total apoptosis showed a certain concentration-dependent trend.</p><p><strong>Conclusions: </strong>A combination of serum metabolism, network pharmacology, and experiments was employed; this study offers a significant contribution to the clarification of the material basis and molecular mechanism of GVO- medicated serum against breast cancer.</p>","PeriodicalId":16960,"journal":{"name":"Journal of Pharmacy and Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716344","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}