Acta Poloniae Pharmaceutica - Drug Research最新文献

Ginkgolide B Reduces Cartilage Damage in Arthritic Rats by Inhibiting Oxidative Stress and Inflammatory Signaling Pathways 银杏内酯B通过抑制氧化应激和炎症信号通路减少关节炎大鼠软骨损伤

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2026-06-17 DOI: 10.32383/appdr/220635

Huanjiang Liu, Yifeng Wang, Fangcan Hu, Junheng Li, Peng Ren

{"title":"Ginkgolide B Reduces Cartilage Damage in Arthritic Rats by Inhibiting Oxidative Stress and Inflammatory Signaling Pathways","authors":"Huanjiang Liu, Yifeng Wang, Fangcan Hu, Junheng Li, Peng Ren","doi":"10.32383/appdr/220635","DOIUrl":"https://doi.org/10.32383/appdr/220635","url":null,"abstract":"Rheumatoid arthritis (RA) is a chronic inflammatory disease that causing joint damage, persistent pain, and dyskinesia. Previous studies have indicated that RA injury is closely associated with oxidative stress in joint tissues. Ginkgolide B (GB) is a natural terpenoid extracted from the leaves of the Ginkgo biloba tree. It has potent antioxidant and anti-inflammatory properties, but its effect on RA is unclear. This study was designed to investigate GB’s effects on RA in greater depth and uncover potential mechanisms for preventing damage. A rat model of collagen-induced arthritis (CIA) was used to test the effects of treatment with 20 mg/kg GB (CIA+GB-L) or 40 mg/kg GB (CIA+GB-H). Structural and pathological changes in knee joints were identified and potential mechanisms related to oxidative stress and inflammation pathways were examined. Results showed that GB ameliorated the pathological features of knee arthritis in CIA rats, as cartilage damage was reduced in +GB groups, especially CIA+GB-H. The level of MDA, a common oxidative stress product, was significantly reduced by 63.9% and the antioxidant enzymes GSH, SOD remarkably increased by 86.6% and 124.5% in the CIA+GB-H. GB inhibited the oxidative stress-related JAK2/STAT3 pathway and the pro-inflammatory IL-17A/Act1/TRAF6 pathway and promoted the Nrf2/HO-1 antioxidant pathway. These findings provide background for the future application of GB in treating RA.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"84 1","pages":"19-27"},"PeriodicalIF":0.0,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/220635","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148672237","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}

引用次数: 0

Antiviral Mechanism of Gentiopicroside Against Herpes Zoster by Targeting TLR3 龙胆苦苷靶向TLR3抗带状疱疹的机制研究

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2026-03-03 DOI: 10.32383/appdr/216205

Yan Zhou, Jinbao Zhong

{"title":"Antiviral Mechanism of Gentiopicroside Against Herpes Zoster by Targeting TLR3","authors":"Yan Zhou, Jinbao Zhong","doi":"10.32383/appdr/216205","DOIUrl":"https://doi.org/10.32383/appdr/216205","url":null,"abstract":"Herpes zoster (HZ), caused by the reactivation of human herpes virus 3 (HHV-3), is a painful neurological condition with limited treatment options. Gentiopicroside (GPS), a key iridoid compound from the traditional Chinese medicine Gentiana scabra, possesses broad anti-inflammatory and immunomodulatory properties, yet its potential against HHV-3 remains unexplored. Given the critical role of the Toll-like receptor 3 (TLR3) pathway in initiating antiviral innate immunity, this study aimed to investigate the anti-HHV-3 activity of GPS and its dependence on TLR3. We found that GPS treatment significantly reduced viral titers in HHV-3 infection in vitro. Mechanistically, GPS upregulated TLR3 expression and subsequently attenuated the HHV-3-induced production of pro-inflammatory cytokines TNF-α and IL-6. Furthermore, GPS ameliorated HHV-3-induced reduction in cell viability and attenuated apoptosis. Crucially, the antiviral efficacy of GPS was enhanced by a TLR3 agonist and diminished by a TLR3 inhibitor, demonstrating that its action is TLR3-dependent. In conclusion, our findings reveal that GPS exerts its anti-HHV-3 effects by modulating the TLR3-mediated immune response, highlighting its potential as a novel therapeutic candidate for herpes zoster.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"82 5","pages":"757-768"},"PeriodicalIF":0.0,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/216205","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148305794","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}

引用次数: 0

Antiviral Mechanism of Quercetin Against Herpes Zoster by Targeting EGFR 槲皮素靶向表皮生长因子受体抗带状疱疹的机制

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2025-11-20 DOI: 10.32383/appdr/210150

Wen Ni, Lingling Yang, Xiaoguo Zhang, Jung-Won Kang, Min You

{"title":"Antiviral Mechanism of Quercetin Against Herpes Zoster by Targeting EGFR","authors":"Wen Ni, Lingling Yang, Xiaoguo Zhang, Jung-Won Kang, Min You","doi":"10.32383/appdr/210150","DOIUrl":"https://doi.org/10.32383/appdr/210150","url":null,"abstract":"Background: Herpes zoster, caused by the varicella-zoster virus (VZV), is an acute vesicular dermatitis with increasing incidence and severity in the elderly due to age-related immune decline. Purpose: This study aims to explore the molecular mechanism of quercetin in treating herpes zoster using a combination of network pharmacology and cell experiments. Methods: The study utilized network pharmacology to predict the targets of quercetin and VZV-related targets. A protein-protein interaction (PPI) network was constructed, and gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Molecular docking was used to validate the interaction between quercetin and core targets. Cell experiments were conducted to verify the antiviral effects of quercetin on VZV in HaCaT cells. Results: Network pharmacology identified 17 common targets between quercetin and VZV, with EGFR emerging as a key target. GO analysis indicated quercetin’s potential to regulate cell cycle progression, membrane-related structures, and enzyme activities. KEGG pathway analysis highlighted pathways like \"EGFR tyrosine kinase inhibitor resistance\". Molecular docking confirmed quercetin’s binding ability to EGFR. Cell experiments showed quercetin significantly inhibited VZV replication in HaCaT cells in a concentration-dependent manner without significant cytotoxicity. Conclusion: Quercetin exhibits promising antiviral activity against VZV through multi-target interactions, particularly by targeting EGFR. These findings suggest quercetin’s potential as a therapeutic candidate for herpes zoster treatment, warranting further in vivo and clinical studies.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"82 3","pages":"513-522"},"PeriodicalIF":0.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/210150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147916439","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}

引用次数: 0

Diammonium glycyrrhizinate attenuates Mycobacterium tuberculosis-induced inflammation by modulating the HMGB1/NF-κB/NLRP3 cascade 甘草酸二铵通过调节HMGB1/NF-κB/NLRP3级联减轻结核分枝杆菌诱导的炎症

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2025-11-20 DOI: 10.32383/appdr/209552

Lei Yi, Chuan-zan Zhao, Yu Yi, Feng Wang, Xiao Chen, Y H Huang, Ting Guo, Z. Ji, Xue-Cheng Ji

{"title":"Diammonium glycyrrhizinate attenuates Mycobacterium tuberculosis-induced inflammation by modulating the HMGB1/NF-κB/NLRP3 cascade","authors":"Lei Yi, Chuan-zan Zhao, Yu Yi, Feng Wang, Xiao Chen, Y H Huang, Ting Guo, Z. Ji, Xue-Cheng Ji","doi":"10.32383/appdr/209552","DOIUrl":"https://doi.org/10.32383/appdr/209552","url":null,"abstract":"Diammonium glycyrrhizinate (DG), derived from glycyrrhizic acid, is recognized for its properties that combat inflammation and oxidative stress. Excessive and persistent inflammation during Mycobacterium tuberculosis (Mtb) infection is detrimental to eliminating the bacteria and instead results in severe lung dysfunction. The aim of this study was to investigate the anti-inflammatory role of DG in Mtb infection. A model of macrophages infected with Mtb was developed. The survival of cells was assessed with the Cell Counting Kit-8, and the release of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β, and IL-18 was checked through enzyme-linked immunosorbent assay. Activation of the high mobility group box 1 protein (HMGB1)/nuclear factor-κB (NF-κB)/NLR family pyrin domain containing 3 (NLRP3) cascade was determined through Western blot analysis. In macrophages, DG suppressed the survival of Mtb and the generation of inflammatory agents TNF-α, IL-6, IL-1β, and IL-18, varying with the dosage. DG's ability to reduce inflammation stemmed from its suppression of the HMGB1/NF-κB/NLRP3 cascade activation. DG mitigates inflammation induced by Mtb through the suppression of the HMGB1/NF-κB/NLRP3 cascade.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"82 3","pages":"503-511"},"PeriodicalIF":0.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/209552","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147904485","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}

引用次数: 0

MiR-204 Inhibits Thyroid Cancer Cell Proliferation, Apoptosis, and Migration Through Targeting HMGB1 Expression MiR-204通过靶向HMGB1表达抑制甲状腺癌细胞增殖、凋亡和迁移

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2025-09-30 DOI: 10.32383/appdr/208304

Min Yu, Yongzhi Liu, Xiaoying Zhou

{"title":"MiR-204 Inhibits Thyroid Cancer Cell Proliferation, Apoptosis, and Migration Through Targeting HMGB1 Expression","authors":"Min Yu, Yongzhi Liu, Xiaoying Zhou","doi":"10.32383/appdr/208304","DOIUrl":"https://doi.org/10.32383/appdr/208304","url":null,"abstract":"Thyroid cancer incidence is rising globally, yet early diagnosis remains challenging due to the lack of initial symptoms, highlighting the need for novel molecular targets. miR-204, a tumor-suppressive microRNA downregulated in various cancers, has unclear mechanisms in thyroid cancer. This study explored how miR-204 affects thyroid cancer cell behavior by targeting high-mobility group protein B1 (HMGB1). Tumor and adjacent tissues from 40 thyroid cancer patients (Feb 2019–June 2021) and multiple thyroid cancer cell lines (TPC-1, NPA87, FTC133) were analyzed. miR-204 was significantly downregulated in cancer tissues and cells (P < 0.05), with the lowest expression in FTC133 cells. These cells were transfected and divided into experimental groups (e.g., miR-204 mimics, inhibitors, si-HMGB1). Overexpression of miR-204 suppressed proliferation and migration and promoted apoptosis in FTC133 cells, while its inhibition had the opposite effect (P < 0.05). Luciferase assays confirmed HMGB1 as a direct target of miR-204. HMGB1 knockdown reduced proliferation and migration and increased apoptosis, effects reversed by miR-204 inhibition (P < 0.05). In summary, miR-204 inhibits thyroid cancer cell progression and promotes apoptosis, likely by directly targeting HMGB1, suggesting its potential as a therapeutic target.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"82 2","pages":"253-262"},"PeriodicalIF":0.0,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/208304","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883368","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}

引用次数: 0

Anti-Inflammatory, Antioxidant, and Analgesic Effects of Nitrophenylthiazole Acetamide in a Papain-Induced Osteoarthritis Rat Model 硝基苯噻唑乙酰胺在木瓜蛋白酶诱导的骨关节炎大鼠模型中的抗炎、抗氧化和镇痛作用

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2025-09-30 DOI: 10.32383/appdr/208363

Xin Feng

{"title":"Anti-Inflammatory, Antioxidant, and Analgesic Effects of Nitrophenylthiazole Acetamide in a Papain-Induced Osteoarthritis Rat Model","authors":"Xin Feng","doi":"10.32383/appdr/208363","DOIUrl":"https://doi.org/10.32383/appdr/208363","url":null,"abstract":"Abstract: Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage degradation, inflammation, oxidative stress, and pain. This study aimed to evaluate the therapeutic potential of a nitrophenylthiazole acetamide, 6a, in a papain-induced OA rat model. OA was induced by intra-articular injection of papain, followed by oral administration of compound 6a at doses of 2.5, 5, and 10 mg/kg. Knee joint diameter and mechanical allodynia were assessed using caliper measurements and the Von Frey pain threshold test, respectively. Oxidative stress markers (MDA, SOD, and GSH), pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), and mRNA expression levels of NLRP3, ASC, and caspase-1 were also evaluated. Results demonstrated that compound 6a significantly reduced joint swelling and increased pain threshold in a dose-dependent manner. Biochemical analysis revealed a marked decrease in MDA levels, along with significant increases in SOD and GSH, indicating strong antioxidant activity. Furthermore, compound 6a suppressed the elevated levels of TNF-α, IL-1β, and IL-6 and downregulated the mRNA expression of NLRP3, ASC, and caspase-1, suggesting inhibition of inflammasome-mediated inflammation. In conclusion, compound 6a exhibited notable anti-inflammatory, antioxidant, and analgesic effects in the OA rat model, highlighting its potential as a promising therapeutic agent for osteoarthritis management.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"82 2","pages":"363-374"},"PeriodicalIF":0.0,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/208363","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902989","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}

引用次数: 0

Modulation of Insulin Resistance by Dihydromyricetin in T2DM Rats 二氢杨梅素对T2DM大鼠胰岛素抵抗的调节作用

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2025-06-24 DOI: 10.32383/appdr/204042

Lu Liu, Ziying Liang, Yi Zhu, Yanhong Xu

{"title":"Modulation of Insulin Resistance by Dihydromyricetin in T2DM Rats","authors":"Lu Liu, Ziying Liang, Yi Zhu, Yanhong Xu","doi":"10.32383/appdr/204042","DOIUrl":"https://doi.org/10.32383/appdr/204042","url":null,"abstract":"Endoplasmic reticulum stress (ERS) is an important link leading to the occurrence of insulin resistance (IR). The study aimed to investigate the role of Chinese medicine Dihydromyricetin (DHM) in IR in HepG2 cells and type 2 diabetes mellitus (T2DM) rats and its possible mechanism under the participation of ERS. HepG2 cells were treated with 5×10−6 mol/L insulin to establish an IR cell model. T2DM rats were established through the combination of low-dose streptozocin (STZ) and a high-fat diet. T2DM rats were given low doses (DHM-L) or high doses (DHM-H) of DHM. OGTT was performed for the glucose tolerance evaluation. Western blot was done for the protein detection. DHM improved the insulin sensitivity, lipid levels, and inflammatory response in HepG2 cells induced by IR. DHM decreased the body weight, FBG, FINS, and HOMA-IR of T2DM rats. OGTT test demonstrated the increase of blood glucose and area under the curve (AUC) in T2DM rats, which was reduced by DHM treatment in a dosed manner. The increased TC, TG, LDL, and reduced HDL in T2DM rats were reversed by DHM, which is related to the improvement of lipid metabolism. For mechanism, DHM inhibited the ERS signaling and inflammatory response. DHM attenuates IR and lipid metabolism in a dose-dependent manner in T2DM rats, and the mechanism might be related to improving liver ERS and inhibiting inflammation.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"82 1","pages":"163-171"},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/204042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147920412","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}

引用次数: 0

Renal-Protective Roles of Cornuside in Systemic Lupus Erythematosus Model 角苷在系统性红斑狼疮模型中的肾脏保护作用

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2025-06-24 DOI: 10.32383/appdr/204684

S. B. Wang, Shilei Ding, YULING WANG, CAIYU HE, Yi Jen Jiang, YAO YAO, DI ZHU

引用次数: 0

Protective Effect of Berberine on Atopic Dermatitis by Regulating the lncRNA TTC39A-AS1/hsa-miR-3936/RNASE3 axis 小檗碱通过调控lncRNA TTC39A-AS1/hsa-miR-3936/RNASE3轴对特应性皮炎的保护作用

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2025-04-09 DOI: 10.32383/appdr/199800

Ying Guo, Guoying Miao, Xiaoxiao Liu, Tingting Jing, Lefan Fu, Jianzhou Ye

{"title":"Protective Effect of Berberine on Atopic Dermatitis by Regulating the lncRNA TTC39A-AS1/hsa-miR-3936/RNASE3 axis","authors":"Ying Guo, Guoying Miao, Xiaoxiao Liu, Tingting Jing, Lefan Fu, Jianzhou Ye","doi":"10.32383/appdr/199800","DOIUrl":"https://doi.org/10.32383/appdr/199800","url":null,"abstract":"Colonization of Staphylococcus aureus (S. aureus) is a crucial factor aggravating atopic dermatitis (AD). Berberine (BBR) is the main effective component of Coptis chinensis against bacteria. To explore the potential mechanism by which BBR inhibits the progression of AD caused by S. aureus. S. aureus was cultured with a BBR-added medium to verify the bacteriostatic effect of BBR. Effects of BBR on the expressions of TTC39A-AS1, hsa-miR-3936, and RNASE3 were detected by qPCR, and the dual luciferase assay and overexpression assay were used to demonstrate the regulation among them. The roles of them in S. aureus-induced injury of human primary epidermal keratinocytes (HEKs) were evaluated by their exogenous expressions. The growth, inflammation, and tight junction were evaluated by CCK-8 assay, detection of inflammatory factors, and measurement of transepithelial electrical resistance (TEER) value, to evaluate the impairment of HEKs. BBR significantly inhibited the reproduction of S. aureus and improved the damage to HEKs function caused by it. The stimulation of S. aureus significantly inhibited the growth and tight junction function of HEKs and induced the inflammatory response. These changes were exacerbated by overexpression of TTC39A-AS1 or RNASE3, and reversed by upregulation of hsa-miR-3936. TTC39A-AS1 promoted RNASE3 expression by targeting hsa-miR-3936. Moreover, BBR visibly inhibited the expressions of TTC39A-AS1 and RNASE3 and up-regulated hsa-miR-3936. In conclusion, BBR has the potential to alleviate AD by modulating the TTC39A-AS1/hsa-miR-3936/RNASE3 axis.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 6","pages":"993-1002"},"PeriodicalIF":0.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/199800","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147921045","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}

引用次数: 0

Salvianolic Acid B Represses Cervical Cancer Cell Malignant Biological Behaviors via Modulating PI3K/AKT Signaling Pathway 丹酚酸B通过调节PI3K/AKT信号通路抑制宫颈癌细胞恶性生物学行为

Acta Poloniae Pharmaceutica - Drug Research Pub Date : 2025-04-09 DOI: 10.32383/appdr/200569

Jie Yuan, Yanfei Wu, Yuqi Qiao, Y P Lin, Qian Zhang, Xu Zhang

{"title":"Salvianolic Acid B Represses Cervical Cancer Cell Malignant Biological Behaviors via Modulating PI3K/AKT Signaling Pathway","authors":"Jie Yuan, Yanfei Wu, Yuqi Qiao, Y P Lin, Qian Zhang, Xu Zhang","doi":"10.32383/appdr/200569","DOIUrl":"https://doi.org/10.32383/appdr/200569","url":null,"abstract":"Objective: This study aimed to uncover the functions of salvianolic acid B (SalB) on biological behavior of cervical cancer cells and associated mechanisms. Methods: Human Hela cervical cancer cells were exposed to 0, 0.5, 1, 2.5 µmol/L SalB, respectively, and divided into control group, SalB low-dose group, SalB middle-dose group and SalB high-dose group. CCK-8, colony-formation, scratch test, Transwell and flow cytometry experiments were implemented for functional test. Glucose detection kit, lactic acid detection kit, ELISA detection kit to detect glycolysis index. Western blotting was utilized to observe PI3K/AKT expressions. Results: The effect of SalB on Hela cells was concentration-dependent, with a significant reduction in growth, invasion, migration ability and glycolysis metabolism, as well as a significant enhancement in the level of apoptosis observed in the SalB medium-dose group and the SalB high-dose group. The levels of P-PI3K and P-AKT were markedly declined after SalB administration, revealing that SalB administration depleted PI3K/AKT activity. Conclusion: SalB was observed to exert a repressive effect on Hela cell growth, invasiveness, migrating capacity and glycolysis, while simultaneously promoting apoptosis. It is postulated that these functional mechanisms may be linked to the inactivation of PI3K/AKT signalling.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 6","pages":"973-979"},"PeriodicalIF":0.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/200569","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147919642","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}

引用次数: 0