Pharmacognosy Magazine最新文献

{"title":"Polystyrene Targeting Nanoparticles’ Effect \u2028on Lung Injury in Severe Acute Pancreatitis","authors":"Ming Chen, Zhe Wu, Yiqin Yu, Jinhong Wang","doi":"10.1177/09731296251380005","DOIUrl":"https://doi.org/10.1177/09731296251380005","url":null,"abstract":"Background Severe acute pancreatitis (SAP) has an acute onset and critical condition. It can mainly cause a pulmonary infection in patients. Whether polystyrene targeting nanoparticles play a role in lung injury in SAP remain unclear. Purpose To evaluate polystyrene targeting nanoparticles’ (PTNs) effect on lung injury in severe acute pancreatitis (SAP). Materials and Methods Nanoparticles are characterized by a large unit surface area, high dispersion, tissue affinity, and adhesion, and are more conducive to bringing drugs into contact with tissues. In this study, SAP lung injury cells from alveolar lavage exfoliated cells under bronchoscopy were exposed to PTN to detect the proliferation of SAP lung injury cells, cycle and apoptosis, and nicotinamide adenine dinucleotide phosphate oxidase 2/reactive oxygen species/nuclear factor-kappa B (NOX2/ROS/NF-κB) expression. Results The compound PTN inhibited cell proliferation in SAP, and the degree of inhibition was positively correlated with the dose and the length of time. PTN inhibited the proliferation of SAP lung injury cells dose-dependently (5, 10, and 20 µmol/L) and arrested SAP lung injury cells in G2/M phase and increased cell apoptosis. In addition, PTN reduced NOX2, ROS, and NF-κB in SAP lung injury and downregulated interleukin-6, tumor necrosis factor-alpha, Janus kinase, signal transducer and activator of transcription, and interleukin-10 levels. Conclusion This study shows that polymer-targeted nano-drug systems regulate lung-damaged cell growth in SAP. PTN inhibits inflammation in SAP via regulation of NOX2/ROS/NF-κB.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147890882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liposome Nanoparticles Encapsulating Dehydrocameline Inhibit Cyclooxygenase-2 Expression and Reduce Inflammatory Response in Gastric Cancer Mice","authors":"Chengcheng Xu, Shaoqi Chen, Yunxuan Bo, Qunfeng Gui","doi":"10.1177/09731296251388231","DOIUrl":"https://doi.org/10.1177/09731296251388231","url":null,"abstract":"Background Dehydrokoline has a wide range of pharmacological activities and exhibits anti-tumor potential effects in a variety of cancer types. Whether it plays a role in gastric cancer remains unclear. Purpose This study aims to explore the mechanism by which liposome nanoparticles (Harmine NPs) coated with “dehydrocardamine” inhibit COX-2 expression by regulating the PTEN/Akt signaling pathway, thereby alleviating the inflammatory response in mice with gastric cancer and providing a new strategy for targeted therapy of gastric cancer. Materials and Methods Mice suffering from gastric cancer were used as models, and Harmine NPs were further prepared and used in experiments to observe the anti-inflammatory response in gastric cancer, explore its effect on PTEN/Akt, and analyze its role in the regulation of COX-2. Results We successfully prepared the Harmine NPs nanocomposite, and the model group was raised for 12 weeks for subsequent animal experiments. The inflammatory factor, Harmine NPs, in the group of mice showed a better improvement in inflammation. Their mucosal muscle layer cells were evenly arranged. While the levels of inflammatory response were reduced, their COX-2 expression and genes and proteins related to the PTEN/Akt signaling pathway were also inhibited. Using SF1670 based on Harmine NPs, it was found that the inhibitory effect of Harmine NPs on PTEN protein expression was reversed. VO-OHpic simulated the inactivation of PTEN and found that the anti-inflammatory effect of Harmine NPs was amplified. After celecoxib, it was confirmed that Harmine NPs can inhibit the expression of COX-2 through the PTEN/Akt signaling pathway to reduce the inflammatory response in gastric cancer mice. Conclusion Harmine NPs are a new type of complex with anti-inflammatory and anti-cancer effects and are expected to become an effective strategy for the treatment of gastric cancer by inhibiting the PTEN/Akt signaling pathway and the COX-2 expression. This treatment method shows potential benefits in the management of gastric cancer inflammation and provides an important theoretical basis for the treatment of gastric cancer inflammation.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polydopamine Nanoparticle-encapsulated Psoralen Promotes Motor Function Recovery from Spinal Cord Compression Through Regulating Phosphatidylinositol 3-kinase/Protein Kinase B Signaling Through miR-140-5p","authors":"Jian Deng, Zongyao Duan, Hao Deng, Lü Y","doi":"10.1177/09731296251385791","DOIUrl":"https://doi.org/10.1177/09731296251385791","url":null,"abstract":"Background Psoralen is a biomaterial that promotes bone growth and repair and has been widely used in clinical orthopedic surgeries. Purpose This study aims to explore the role and mechanism of polydopamine nanoparticle-encapsulated psoralen (PSO/PDA NPs) in the recovery of motor function after spinal cord compression. Materials and Methods A Compressive Spinal Cord Injury (CSCI) rat model was constructed to explore the effects of PDA NPs and PSO/PDA NPs on spinal cord compression, and how PSO/PDA NPs regulate miR-140-5p, improve motor function of spinal cord compression, and 740 Y-P and LY294002 were used to explore the mechanism of PI3K/Akt signaling in PSO/PDA NPs to promote the recovery of motor function of spinal cord compression. Further experiments were conducted on CSCI rats to verify its mechanism through the combined intervention of miR-140-5p inhibitor and 740 Y-P. Results PSO/PDA NPs have a good effect in the rehabilitation after spinal cord compression, and can inhibit miR-140-5p expression, upregulate PI3K/Akt signal, inhibit the apoptosis rate of neurons in CSCI rats, and inhibit the expression of platelet activating factor (PAF), promote Bcl-2 expression, thereby reducing Bax expression. Conclusion PSO/PDA NPs downregulate miR-140-5p and promote PI3K/Akt pathway, thereby accelerating the recovery of related functions after spinal cord compression, laying the foundation for the development of drugs targeting CSCI.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147879249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin Loaded with Ferric Oxide Nanoparticles Reduces Hypoxic Injury in Myocardial Infarction by Regulating miR-208 and Activating SIRT1 Signaling Pathway","authors":"Dandan Wei, Lei Zhao","doi":"10.1177/09731296251388232","DOIUrl":"https://doi.org/10.1177/09731296251388232","url":null,"abstract":"Background Curcumin has antioxidant and anti-myocardial ischemic effects, but its low water solubility and bioavailability limit clinical application. Purpose This study aims to explore whether curcumin-loaded ferric oxide nanoparticles alleviate hypoxic injury in myocardial infarction. Materials and Methods Preparation of ferric oxide (Fe 3 O 4 ) nanoparticle-loaded curcumin complex. A cardiomyocyte hypoxia model was established using ligation surgery. The complex, Fe 3 O 4 nanoparticles, and curcumin were applied to the hypoxia model, respectively, and a blank control group was established. The expression of microRNA-208 (miR-208) in cells in each group was detected by fluorescence quantitative polymerase chain reaction. Western blot was used to detect the expression of sirtuin 1 (SIRT1), p53, and hypoxia-inducible factor 1-alpha proteins in cells in each group. The cell counting kit-8 was used to detect cell proliferation in each group. Results The Fe 3 O 4 nanoparticle-loaded curcumin complex was successfully prepared, and the myocardial infarction rat model was successfully constructed. In vivo experimental results show that Fe 3 O 4 nanoparticles loaded with curcumin complex can significantly reduce the expression level of miR-208 and increase the activity of SIRT1. After hypoxic treatment of myocardial cells, adding composite nanoparticles can reduce cell damage, reduce the cell apoptosis rate, significantly reduce the size of myocardial infarction, and improve myocardial function, and the effect is stronger than curcumin alone. Conclusion Fe 3 O 4 nanoparticles loaded with curcumin activate the SIRT1 signaling pathway by downregulating miR-208, and inhibit the expression of p53 and HIF-1α, and ultimately reduce hypoxic injury in myocardial infarction. This provides new ideas and methods for the treatment of myocardial infarction.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on the Mechanism of Berberine Based on PI3K/mTOR/Autophagy Pathway to Ameliorate Sepsis-associated Encephalopathy Injury","authors":"Yu Li, Wei Du, Shijun Tang, Yuan-Jia Yue, Xing Rong, Hongxiang Wang, Dugujia Gaerma, Lin Jiang","doi":"10.1177/09731296251384399","DOIUrl":"https://doi.org/10.1177/09731296251384399","url":null,"abstract":"Background Sepsis-associated encephalopathy (SAE) is a major cause of high mortality, and no specific therapeutic drugs are currently available. Berberine has been well-documented for its neuroprotective effects, but its mechanism of action remains unclear. Purpose Use of network pharmacology to study the mechanism of action of berberine (BER) in the treatment of sepsis-associated encephalopathy (SAE). Materials and Methods Application of network pharmacology to predict the signalling pathway of BER in the treatment of SAE. The mouse model of SAE was constructed, and determination of tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-10 (IL-10) was done by enzyme-linked immunosorbent assay (ELISA). The effects of BER on neuronal damage in SAE mice were examined by haematoxylin-eosin (HE) staining and Nissl staining. Transmission electron microscopy was used to observe neuronal autophagy formation, and Western blot analysis was employed to explore the mechanism of action. Results Based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, BER is most likely to treat SAE via the phosphatidylinositol-3 kinase (PI3K)-Akt pathway. TNF-α, IL-1β, IL-6 and IL-10 levels were significantly lower in the BER group than in the SAE group, and the opposite trend was shown in the 3MA group. HE staining and Nissl staining BER were found to significantly reduce SAE injury; terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) and transmission electron microscopy visualised under the microscope that the injured cells were shrunken and apoptosis occurred. Western blotting experiments revealed that PI3K, mammalian target of rapamycin (mTOR), matrix metalloprotein-9 (MMP-9) and p62 were reduced in the BER group as compared to the SAE group; Beclin1 and light chain 3 (LC3) were elevated; the opposite trend was shown in the 3MA group. Conclusion This study predicted the mechanism of action of BER acting on the PI3K/mTOR signalling pathway for the treatment of SAE and linked more potential therapeutic targets.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plumbagin Attenuates Periodontitis by Inhibiting the PI3K/AKT Pathway and Enhancing Autophagy: A Potential Therapeutic Strategy","authors":"Shiya Li, Qian Fang, Huili Wu, Chen Tang, Lijuan Wang","doi":"10.1177/09731296251384058","DOIUrl":"https://doi.org/10.1177/09731296251384058","url":null,"abstract":"Background and Purpose Plumbagin (PLB), a natural compound derived from Plumbago zeylanica L., exhibits potent antioxidant, anti-inflammatory, antibacterial, and anticancer properties. However, its role in modulating periodontitis via the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway and autophagy remains unclear. This study explores PLB’s therapeutic potential in periodontitis, focusing on these mechanisms. Materials and Methods In vitro , Cell Counting Kit-8 was used to examine cell viability, and LysoTracker Red was used to assess the degree of autophagy activation. The effects of PLB on periodontitis and the PI3K/AKT signaling pathway in vitro were detected by real-time quantitative polymerase chain reaction and Western blot. In vivo , we established rat models of periodontitis to validate the efficacy of PLB. Results PLB exhibited a dose-related suppressive influence on periodontitis progression. Notably, PLB significantly downregulated the components of the PI3K/AKT pathway and modulated autophagy. In rat models, PLB treatment effectively alleviated periodontal inflammation and alveolar bone resorption. Conclusion PLB exhibits anti-inflammatory properties in periodontitis by suppressing the PI3K/AKT pathway and enhancing autophagy. Our results offer a scientific basis for using PLB in the treatment of periodontitis, emphasizing its promise as an innovative remedy for this dental condition.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147920193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Curcumin-loaded Polystyrene Nanoparticles on Inhibiting the Generation of Lymphatic Vessels in Gastric Cancer Nude Mice Under Hypoxic Microenvironment","authors":"Yingjie Long, Xin Kang, Bin Li, Tiansheng Yin, Yajun Zhang","doi":"10.1177/09731296251371477","DOIUrl":"https://doi.org/10.1177/09731296251371477","url":null,"abstract":"Background In the treatment of gastric cancer, lymphangiogenesis under a hypoxic microenvironment has always been a current research hotspot. Purpose This study aimed to explore the mechanism of curcumin-loaded polystyrene nanoparticles (CUR/PS NPs) inhibiting the generation of lymphatic vessels in a hypoxic microenvironment of gastric cancer nude mice by interfering with phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling and reducing vascular endothelial growth factor (VEGF) expression. Materials and Methods CUR/PS NPs were prepared, a gastric cancer nude mouse transplanted tumor model was established, and the A549 group, Cu B group, and the Cu B-NPs group were set up to explore the molecular mechanism of Cu B-NPs in regulating autophagy and inhibiting the development of lung cancer; in addition, the Cu B-NPs+si-BECN1 group and the Cu B-NPs+pc-BECN1 group were used to analyze whether Cu B-NPs regulate autophagy through Beclin-1 (BECN1) to inhibit the development of lung cancer. Results (a) A subcutaneous transplanted tumor model was successfully constructed, a CUR/PS NPs composite material was successfully prepared, and the composite material had good dispersion stability. (a) CUR/PS NPs can significantly inhibit the formation of lymphatic vessels in the hypoxic microenvironment of gastric cancer nude mice transplanted tumors, and have an inhibitory effect on the development of gastric cancer. (c) CUR/PS NPs can inhibit the formation of lymphatic vessels in the hypoxic microenvironment of gastric cancer nude mice transplanted tumors by inhibiting PI3K/Akt/mTOR signaling, thereby delaying gastric cancer progression. Conclusion This study successfully prepared CUR/PS NPs, and the particles can reduce the expression of VEGF by inhibiting PI3K/Akt/mTOR signaling, thereby inhibiting the generation of lymphatic vessels in the hypoxic microenvironment of gastric cancer nude mice, delaying cancer progression.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251371477","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maprotiline Attenuates Isoflurane-induced Microglial Inflammation","authors":"Tianyu Lu, Qibin Li, Zengtao Wang","doi":"10.1177/09731296251367865","DOIUrl":"https://doi.org/10.1177/09731296251367865","url":null,"abstract":"Background Maprotiline intervention is noted to alleviate the body’s inflammatory response effectively, but its specific molecular mechanism remains elusive. Objectives This study aimed to investigate the impact of maprotiline on the inflammatory response caused by isoflurane. Materials and Methods Microglia BV-2 cells were grouped into control group, isoflurane group, maprotiline group, and positive control group, and were respectively receiving treatment of isoflurane (10 µg/mL) alone, isoflurane and maprotiline (10 µg/mL), and isoflurane and oxymethylene ketone (10 µmol/L), with cells of control group cultured alone. After treatments, the enzyme-linked immunosorbent assay (ELISA) assay detected BV-2 cell activity, BV-2 cell inflammatory response expression (interleukin 1 beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor (TNF)-α), ionized calcium-binding adapter molecule 1 (Iba-1) protein expression, toll-like receptor 4 (TLR4) protein, p-inhibitor of nuclear factor kappa B (p-IκBα) expression, nuclear P65, and cytoplasmic P65 expression. Results The isoflurane group had the lowest BV-2 cell viability and the highest content of lactate dehydrogenase (LDH), followed by the maprotiline group and the positive control group ( p < .05). As isoflurane induced the contents of IL-1β, IL-6, TNF-α, and Iba-1, the addition of maprotiline or oxymethylene ketone decreased the expressions of the inflammatory cytokines ( p < .05) without significant difference between the maprotiline group and the positive control group ( p > .05). The isoflurane group and the positive control group had the highest expression of TLR4 p-IκBα and nuclear P65 and the lowest expression of cytoplasmic P65, followed by the maprotiline group ( p < .05). There was no significant difference between the isoflurane and positive control groups ( p > .05). Conclusion Maprotiline may enhance microglia activation and alleviate and reduce the isoflurane-induced inflammation of microglia through inhibition of TLR4/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway, P65 nuclear translocation, and IκBα phosphorylation.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 2","pages":"794-801"},"PeriodicalIF":0.0,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251367865","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147886528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Qibai Pingfei Capsules on the HMGB1/TLR4/NF-κB Signaling Axis in CSE-induced Inflammation of 16HBE Cells","authors":"Fang Li, Lu Zhang, Mengyao Shi, Cheng Yang, Jiabing Tong, Yating Gao, Zegeng Li","doi":"10.1177/09731296251364981","DOIUrl":"https://doi.org/10.1177/09731296251364981","url":null,"abstract":"Background and Purpose Chronic inflammation resulting from cigarette smoke extract (CSE) is frequently driven by activation of the high mobility group box 1 (HMGB1)–toll-like receptor 4 (TLR4)–nuclear factor kappa B (NF-κB) signaling cascade. This study was designed to explore the regulatory influence of Qibai Pingfei Capsules (QBPF) on inflammation-related pathways in 16HBE cells, a human bronchial epithelial cell line, following CSE treatment. We also assessed the impact of QBPF on NF-κB signaling dynamics and cytokine production using a co-culture model with THP-1-derived macrophages. Materials and Methods Levels of inflammatory mediators were quantified via enzyme-linked immunosorbent assay and quantitative reverse transcription polymerase chain reaction, while protein expression and intracellular localization were analyzed through Western blotting and immunofluorescence. NF-κB activity was further verified by RNA interference and overexpression techniques. Results QBPF markedly mitigated the inflammatory responses induced by CSE, as evidenced by decreased cytokine output and reduced transcription of HMGB1, toll-like receptor 2, TLR4, and myeloid differentiation primary response gene 88. Furthermore, QBPF hindered the nuclear translocation of NF-κB and disrupted upstream molecular events linked to its activation. Conclusion QBPF demonstrates potent anti-inflammatory potential through modulation of NF-κB-associated signaling networks. The current findings emphasize QBPF’s value as a prospective therapeutic candidate for controlling smoke-induced airway inflammation and suggest its broader applicability to respiratory disorders characterized by chronic inflammation.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147879267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Motherwort Regulates PI3K/Akt Pathway in the Treatment of Spinal Tuberculosis Through miR-432-5p","authors":"Chengliang Zhang, Lidong Zhang, Lei Liu, Dajiang Song, Baolin Zhu","doi":"10.1177/09731296251365003","DOIUrl":"https://doi.org/10.1177/09731296251365003","url":null,"abstract":"Background Spinal tuberculosis involves many complex mechanisms. Motherwort has anti-inflammatory, antioxidant, and anti-tumor activities, but its effect on spinal tuberculosis is unclear. Objectives In this study, motherwort was prepared to explore the therapeutic effect and regulatory mechanism of this nano-complex on spinal tuberculosis. Materials and Methods 0.1 mL of H37Rv standard strain suspension (concentration: 10 8 CFU/mL) was used to establish a spinal tuberculosis model. The model mice were orally administered 50 mg kg –1 Ajugol to form the Ajugol group, and the same doses of mesoporous silica nanoparticle (MSN) and Ajugol were orally administered to form the Ajugol group. After continuing to feed for 8 weeks, four groups of mice were used for experiments. To analyze whether the mechanism of Ajugol in treating spinal tuberculosis is related to its regulation of phosphoinositide 3-kinase/protein kinase (PI3K/Akt) pathway activity through microRNA-432-5p (miR-432-5p). Results No mice died during the modeling period of this study, and the modeling success rate was 100%. An animal model of spinal tuberculosis was successfully established. The bone tissue pathology, bone trabecular number, and thickness of mice were found to be affected by Ajugol and can delay the progression of spinal tuberculosis. This process is related to changes in miR-432-5p and the PI3K/Akt pathway. Under the intervention of Ajugol+miR-432-5p mimic, the number and thickness of bone trabeculae were significantly increased. The above phenomenon was significantly reversed after combining Ajugol with the miR-432-5p inhibitor. Verification test of PI3K/Akt pathway using LY294002 and 740 Y-P further confirmed that Ajugol inhibits the PI3K/Akt pathway by promoting miR-432-5p expression. Conclusion Ajugol promotes the high expression of miR-432-5p and inhibits the PI3K/Akt pathway, thereby reducing the activity of this pathway, inhibiting inflammatory responses, reducing cell proliferation and survival, and thus helping to treat spinal tuberculosis, which is essential for clinical practice and has a potential positive impact on public health. Further future research may focus on developing drugs or new treatments.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 2","pages":"745-753"},"PeriodicalIF":0.0,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251365003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}