Pharmacognosy Magazine最新文献

{"title":"Functional Recovery and Cellular Damage Mechanism of Mesoporous Silica Nanoparticles/Chitosan Solution/Methylprednisolone-collagen on Nerve Injury Caused by Ketamine Overdose","authors":"Shuangju Liao, Huiqiong Huang, Yuan Tang","doi":"10.1177/09731296251360081","DOIUrl":"https://doi.org/10.1177/09731296251360081","url":null,"abstract":"Background Ketamine, a commonly used anesthetic, plays a significant role during surgery, but its potential risk for neurotoxicity has drawn considerable attention. Objectives This study was aimed to investigate the effects of methylprednisolone (MP) loaded onto mesoporous silica nanoparticles (MSN) based on chitosan solution (CS) in ketamine overdose-induced neurotoxicity, focusing on its effects on neural function recovery and cellular damage. The goal was to provide new strategies and a theoretical foundation for the treatment of neuro injury. Materials and Methods MSN/CS/MP collagen (MP col) was prepared using the sol-gel method and characterized for its drug loading capacity, encapsulation efficiency, and release performance. Forty Sprague-Dawley rats were divided into five groups: control group (CG), ketamine group (KG), low concentration group (LG), medium concentration group (MG), and high concentration group (HG)). Except for the CG, the remaining groups were subjected to a ketamine-induced nerve injury model and received different concentrations of MSN/CS/MP col injections. Subsequently, the expression of key hippocampal proteins, apoptosis levels, and spatial memory were evaluated. Results The drug loading capacity of MSN/CS/MP col was 23.01 ± 0.51%, and the encapsulation efficiency was 95.24 ± 2.36%. Compared to CG, the escape latency was prolonged and exploratory time was shortened in the KG, LG, MG, and HG. The levels of p-Akt/Akt, Bcl-2, and PSD-95 were reduced, while the levels of Cas-3/Cas-3 and Bax were increased in the KG. The density of apoptotic cells was elevated in the KG and HG ( p <0.05). Conclusion MSN/CS/MP col promotes functional recovery by regulating key proteins and reducing neuronal apoptosis, offering a novel approach for the treatment of nerve injury.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 2","pages":"702-713"},"PeriodicalIF":0.0,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147884853","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":"Vicenin-2 Exerts Bidirectional Immunomodulation via p38MAPK Phosphorylation in RAW264.7 Macrophages","authors":"Xi Duan, Shuang Du, Hao Yang, Jia He, Lei Zhang, Yunzhu Mu","doi":"10.1177/09731296251360569","DOIUrl":"https://doi.org/10.1177/09731296251360569","url":null,"abstract":"Background Inflammatory diseases, including autoimmune disorders, and chronic inflammatory conditions, are driven by dysregulated immune responses, particularly involving macrophage activation. Macrophages play a critical role in modulating inflammation through the production of pro-inflammatory mediators such as nitric oxide (NO), reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). Vicenin-2 (VCN-2), a flavonoid with potential immunomodulatory properties, has garnered attention for its therapeutic potential. This study investigates the bidirectional immunomodulatory effects of VCN-2 on lipopolysaccharide (LPS)-induced RAW264.7 mouse macrophage cells to establish a foundation for its development as a novel anti-inflammatory agent. Objectives This study investigates the bidirectional immunomodulatory effects of vicenin-2 (VCN-2) on lipopolysaccharide (LPS)-induced mouse macrophage RAW264.7 cells, aiming to establish a basis for developing VCN-2 as a novel anti-inflammatory agent in diseases such as skin inflammation, autoimmune disorders, and chronic inflammatory conditions. Materials and Methods LPS-induced mouse macrophage RAW264.7 cells were used as an inflammation model. The CCK-8 method was used to detect the activity and toxicity of VCN-2. The neutral red assay was used to measure the phagocytic ability of RAW264.7 cells. The Griess assay was used to detect nitric oxide (NO) levels. Flow cytometry was used to measure reactive oxygen species (ROS) levels. Enzyme-linked immunosorbent assay (ELISA) was used to measure tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 messenger ribonucleic acid (mRNA). Western blot (WB) was used to detect the expression of phosphorylated p38MARK (p-p38). Results VCN-2 activates RAW264.7 cells and promotes cell proliferation. As the concentration of VCN-2 increases, its proliferative effect increases. In the resting state, VCN-2 improves cell proliferation by increasing cell number and cell volume. In the inflammation model, VCN-2 repairs cell morphology and restores cell proliferation. VCN-2 promotes phagocytosis of resting cells while attenuating phagocytic activity in inflammatory models. VCN-2 increases ROS levels in resting cells and reduces ROS levels in LPS-induced cells. VCN-2 increases NO, IL-6, and TNF-α content by promoting iNOS, IL-6, and TNF-α gene transcription levels, regulating macrophage immune function. In the inflammation model, VCN-2 significantly downregulates the transcription levels of iNOS, IL-6, and TNF-α genes, reduces NO, IL-6, and TNF-α content, and alleviates the inflammatory response. VCN-2 upregulates macrophage p38 in the resting state. In terms of phosphorylation expression, VCN-2 downregulates the phosphorylation expression of p38 in inflammatory model cells.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 1","pages":"300-310"},"PeriodicalIF":0.0,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251360569","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147881753","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":"<i>Panax notoginseng</i> Saponins Enhance Chemotherapy Carboplatin and Immune Checkpoint Blockades PD1ab by Modulating SERPINE1 Downregulation in LUAD","authors":"Yuhuai Wang, Ping Wang, Jiaqi Liu, Yi Yang, Frederick S. Huang","doi":"10.1177/09731296251355018","DOIUrl":"https://doi.org/10.1177/09731296251355018","url":null,"abstract":"Introduction and Objectives Panax notoginseng saponins (PNS), extracted from Chinese ginseng, exert various pharmacological activities, including anti-tumor effects. Lung cancer remains the malignancy with the highest morbidity and mortality rates. However, the mechanisms underlying PNS’s potential tumor-inhibitory effects on lung adenocarcinoma (LUAD) remain largely unknown and warrant investigation. Purpose This study aimed to explore the PNS’s potential tumor-inhibitory effects and related mechanisms in LUAD. Materials and Methods LUAD cell lines A549 and Lewis were utilized to examine the proliferation, colony formation, and migration of LUAD cells after PNS treatment. WI38 cells were employed to evaluate the toxic impact of PNS on human lung fibroblasts. A Lewis subcutaneous tumor-bearing model was established to assess the combined effects of PNS and carboplatin (CBP) or immune checkpoint blockade with programmed cell death 1 antibody (PD1ab). Lentivirus transfection and quantitative polymerase chain reaction (qPCR) assays were conducted to explore the role of serine protease inhibitor clade E member 1 (SERPINE1) in PNS’s anti-tumor mechanism. Immunohistochemistry was utilized to detect CD8 + T cell infiltration in tumor tissue. Cell counting kit-8 and qPCR assays were applied to determine the specific PNS components exerting anti-tumor effects. Results In vitro and in vivo results indicated that PNS selectively inhibited the proliferation, colony formation, and migration of LUAD cells while promoting CD8 + T-cell infiltration in tumor tissue. Consequently, PNS enhanced the inhibitory effects of CBP and PD1ab on LUAD tumors. Mechanistically, the results preliminarily indicated that PNS might impede tumor progression and enhance CBP and PD1ab effects by downregulating SERPINE1. Five PNS components, including notoginsenoside R1, ginsenoside Rg1, ginsenoside Rd, ginsenoside Re, and ginsenoside Rb1, demonstrated anti-tumor effects. Conclusion PNS suppressed LUAD progression and enhanced CBP and PD1ab therapeutic effects by downregulating SERPINE1 expression, indicating its potential as a promising agent for LUAD therapy.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147331092","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":"<i>Ziziphora clinopodioides</i> Flavonoids Exert a Protective Effect Against MPP ⁺ /MPTP-induced Cell Damage in Parkinson’s Disease Model Through Activating the AMPK/miR-181b Axis","authors":"Xiong-Bin Cao, Jun Cai, Bo Liu, Xiang-Feng Wu, Zhiqiang Wei, Han Luo, Zeng-Xia Zhao, Yong-Zhen Chen, Shuai Li, Li Gong","doi":"10.1177/09731296251346308","DOIUrl":"https://doi.org/10.1177/09731296251346308","url":null,"abstract":"Background and Objectives Parkinson’s disease (PD) is a common age-related neurodegenerative disorder. Mitochondrial dysfunction is considered an important initiating factor for the lack of dopaminergic (DA) neurons. Therefore, identifying drugs that effectively protect DA neurons from mitochondrial damage represents a promising therapeutic strategy. Materials and Methods In this study, an anti-atherosclerosis (AS) drug, Ziziphora clinopodioides flavonoids (ZCF), was shown to inhibit 1-methyl-4-phenylpyridinium (MPP + )-induced DA neuron damage in vitro and in vivo and this was verified by a variety of experimental methods. Cell viability assays, cell fluorescence staining, Western blot experiments, flow cytometry analysis, and quantitative real-time polymerase chain reaction (qPCR) experiments were conducted to assess the protective effect and mechanism of ZCF on SH-SY5Y cells. Additionally, behavioral tests and immunohistochemistry (IHC) were performed to validate the protective effect of ZCF in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD animal model. Results ZCF significantly ameliorated MPP + -induced cell viability loss and elevated lactate dehydrogenase (LDH) in SH-SY5Y cells. Moreover, ZCF treatment improved mitochondrial morphological abnormalities, reduced adenosine triphosphate (ATP) content, attenuated mitochondrial membrane potential loss, cell apoptosis, mitoROS levels, and increased the level of tyrosine hydroxylase (TH). Further results indicate that ZCF treatment significantly stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and its downstream target miR-181b. Additionally, the blockage of the level of AMPK with Compound C or knocking down the expression of miR-181b significantly attenuated the protective effect of ZCF. These results indicate that the AMPK/miR-181b axis plays a vital role in the protective effect of ZCF. Moreover, ZCF treatment alleviated MPTP-induced motor dysfunction and loss of TH-positive neurons in the PD mice model. Conclusion In brief, our findings suggest that ZCF may have potential applications for the treatment and prevention of PD.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 2","pages":"497-508"},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147909710","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":"Paeonol-modified Polydopamine Nanoparticles Promote Colitis-associated Cancer Cell Apoptosis via Regulating the IL-6/STAT-3 Signaling Pathway and Downregulating the Expression of Bcl-2","authors":"Xinchun Zhang, Yin Gao, Yonghua Ma, Xuerong Han, Zhibin Liu","doi":"10.1177/09731296251348012","DOIUrl":"https://doi.org/10.1177/09731296251348012","url":null,"abstract":"Background Polydopamine (PDA) shows promising potential in disease diagnosis and targeted drug delivery. Objectives This study aimed to investigate the role of Paeonol (PAE)-modified PDA nanoparticles (NPs) in the treatment of colitis-associated cancer (CAC). Materials and Methods First, PAE-modified PDA NPs were prepared, and then the mouse model of the CAC model was set up. The mice were divided into a blank control group, a CAC model group, a PAE group, and PAE + nano group ( n = 10). After treatment, cell apoptosis was detected by flow cytometry, and staining was conducted to observe tissues. Additionally, to explore the interaction between signal transducer and activator of transcription 3 (STAT-3) and the effect of PAE-modified PDA NPs, the WP1066 (STAT-3 inhibitor) group and PAE + nano + WP1066 group were established. Results PAE alleviated the pathological injury of colonic tissue in CAC mice and promoted the apoptosis of CAC cells, and a PDA NPs carrying PAE exhibited a greater curative effect when dramatically decreasing IL-6 and STAT-3 expression. The presence of STAT-3 inhibitors decreased the CAC cell proliferation and induced apoptosis. A combination of PAE + nano and WP1066 resulted in the most significant difference. Conclusion PAE-modified PDA NPs can attenuate injuries of the colon tissue in CAC mice and promote the apoptosis of CAC cells by inhibiting the IL-6/STAT-3 pathway and increasing the expression level of Bcl-2, thereby improving the condition of CAC.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 2","pages":"541-551"},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147880389","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":"Rhaponticin Reverses the Hypoxia-mediated Sorafenib Resistance of Hepatocellular Carcinoma Cells by Inhibiting Epithelial–Mesenchymal Transition","authors":"Shunxin Li, Fanchen Zeng","doi":"10.1177/09731296251348093","DOIUrl":"https://doi.org/10.1177/09731296251348093","url":null,"abstract":"Background Hepatocellular carcinoma (HCC) is a major global health threat with a high mortality rate. Sorafenib, the standard treatment for advanced HCC, is often rendered ineffective by tumor drug resistance, particularly under hypoxic conditions that promote resistance and epithelial–mesenchymal transition (EMT) in cancer cells. Traditional Chinese medicine (TCM), with its anti-tumor components, offers a potential avenue for overcoming resistance and inhibiting EMT. Objectives Rhaponticin (RA), an active compound from TCM, is investigated in this study for its ability to counter hypoxia-induced sorafenib resistance and EMT in HCC cells. Materials and Methods HepG2 and Huh7 cells were cultivated under hypoxic conditions to evaluate sorafenib resistance, with cell proliferation assessed using 5-ethynyl-2′-deoxyuridine (EdU) staining and EMT markers analyzed post-treatment. Then, RA’s capacity to diminish cell viability, enhance sorafenib sensitivity, and reverse EMT was examined. The EMT inhibitor C19 was employed to verify the EMT-dependent nature of RA’s effects. Results Hypoxia increased sorafenib half maximal inhibitory concentration (IC 50 ) values in HCC cells, indicating sorafenib resistance. Its inhibitory effect on EMT was reduced under hypoxia, as shown by altered EMT marker expression. RA treatment decreased HCC cell viability without toxicity to normal liver cells, enhanced sorafenib’s sensitivity, and reversed EMT under hypoxia, evidenced by increased E-cadherin and decreased Vimentin and N-cadherin. The EMT inhibitor negated the nullified RA effect on sorafenib sensitivity, confirming RA EMT-dependent action. Conclusion RA can re-sensitize HCC cells to sorafenib by inhibiting hypoxia-mediated EMT, presenting a promising therapeutic approach for HCC.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 2","pages":"583-593"},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147888607","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":"Antithrombic Mechanisms of Viper Venom Platelet Inhibitory Factor in the Rat Myocardial Ischemia-Reperfusion Injury Model","authors":"Juan Wu, Gui-lin Feng, Wei Li, Xue Zhao, Nengsheng Bao, Tianyu Ge, Xi Huang, Qing-quan Xue, He Zhang","doi":"10.1177/09731296251340845","DOIUrl":"https://doi.org/10.1177/09731296251340845","url":null,"abstract":"Background Myocardial ischemia-reperfusion injury (MIRI) exacerbates thrombosis and platelet hyperactivation post-revascularization, with limited therapeutic efficacy of existing antiplatelet agents. Agkistrodon halys venom platelet inhibitor (AHVPI) shows uncharacterized antithrombotic potential. This study evaluates AHVPI’s mechanistic regulation of key platelet biomarkers and hemostatic parameters in a rat MIRI model. Objectives To explore the antithrombic mechanisms of AHVPI in a rat model of MIRI. Materials and Methods Thirty male Sprague-Dawley rats were randomized to the sham operation ( n = 6), MIRI ( n = 6), and AHVPI groups ( n = 18). The left anterior descending coronary artery was ligated to form the MIRI model. The AHVPI group included three subgroups (low-dose, medium-dose, and high-dose groups), which were sublingually administered AHVPI at doses of 0.05, 0.1, and 0.2 mg/kg body weight, respectively (six rats per subgroup). Electrocardiographic changes were monitored via the RM6240 biological signal acquisition system. An enzyme-linked immunosorbent assay was used to measure the plasma levels of platelet membrane glycoprotein VI (GPVI) and P-selectin. Thromboelastography (TEG ® 5000) was used to assess the clot formation time ( K ), coagulation time ( R ), α angle ( A ), and maximum amplitude (MA) in the rat blood. Whole-blood and plasma viscosity was measured using a cone-plate viscometer, whereas turbidimetry was used to determine the platelet aggregation rate. Results Compared with those in the MIRI group, A and MA values ( p &lt; .05), blood viscosity, aggregation amplitude, platelet aggregation rate ( p &lt; .05), and the GPVI and P-selectin expression levels ( p &lt; .05) were prominently lower, and both the K and R values were markedly greater in the medium-dose and high-dose AHVPI groups. Conclusion AHVPI considerably inhibits platelet activity, alleviates MIRI-associated hemorheological properties, and mitigates the adverse effects of MIRI in the MIRI rat model.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 2","pages":"640-650"},"PeriodicalIF":0.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892448","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":"Simultaneous Determination of Amino Acids, Nucleosides, and Nucleobases in <i>Schisandra chinensis</i> Fructus from Different Regions Based on Liquid Chromatography Coupled with Q-trap MS/MS","authors":"Ya-Yun Chen, Xiang Bi, Huanhuan Li, Yuming Wang, Li‐Zhong Wang","doi":"10.1177/09731296251329984","DOIUrl":"https://doi.org/10.1177/09731296251329984","url":null,"abstract":"Background Schisandra chinensis is a traditional Chinese medicine and is widely consumed as a health food due to its immune-enhancing properties. However, limited research has been done on its nutrient composition. Objectives In this study, liquid chromatography-tandem triple quadrupole mass spectrometry (LC-QTRAP-MS/MS) was developed for quantitative analysis of nucleosides, nucleobases (NNs), and amino acids (AAs) in 16 batches of S. chinensis samples collected from Liaoning, Jilin, and Heilongjiang provinces. Materials and Methods A Waters X-Bridge Amide column (2.1 × 100 mm, 3.5 µm) was used for analysis. The mobile phase consisted of A (water with 0.2% formic acid) and B (acetonitrile with 0.2% formic acid) with a flow rate of 0.6 mL/min. The column temperature was maintained at 30°C. The mass spectrometry was equipped with an electrospray ionization source and operated in positive ion multiple reaction monitoring (MRM) modes. Results The method demonstrated acceptable linearity within the tested concentration range. The average recovery of the 30 components ranged from 96.55% to 103.85%, with relative standard deviations (RSD) ranging from 1.02% to 2.88%. The quantitative data indicated that differences in the contents of NNs and AAs in S. chinensis from different regions were evident. The analysis of clustering heat maps revealed that the 16 batches of S. chinensis samples could be grouped into five categories. Stacked bar chart analysis showed that the levels of arginine and uridine were higher in most regions. Correlation analysis indicated strong correlations among the 14 AAs, with 42 groups showing significant relationships. Additionally, seven robust correlations were observed among the 16 NNs. Conclusion This established method provides essential data for the quality assessment and utilization of S. chinensis resources.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1608-1618"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878750","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":"Mechanism of Alginate-Collagen Hydrogel in the Repair of Rat Cartilage Injury","authors":"Yezhou Li, Chengjian Tang","doi":"10.1177/09731296251323311","DOIUrl":"https://doi.org/10.1177/09731296251323311","url":null,"abstract":"Background and Objectives Alginate and gelatin have biocompatibility and biodegradability for drug formulations or carriers, but the roles and mechanisms in cartilage injury (CI) repair remain unclear. This research investigated the application of alginate-collagen hydrogel (ACH) in rat CI repair and its related mechanisms through in vitro and in vivo experiments. Materials and Methods Alginate and modified collagen solutions were mixed to prepare the ACH. The obtained samples were characterized, and their sustained release properties were determined. L929 mouse fibroblasts were assigned into a blank control group (BC group, untreated), a positive control group (PC group, treated with 6.4% phenol), a negative control group (NC group, treated with tissue culture polystyrene), and an ACH group (treated with ACH). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay assessed cell viability. Meanwhile, the cytotoxicity of the ACH and its impact on cell proliferation and cell attachment capabilities were analyzed. Thirty 4-week-old specific pathogen-free Sprague-Dawley rats were randomly grouped into a chondrocyte group (chondrocytes collected and cultured), a cPAGE group (chondrocytes treated with ACH), a model group (CI model), and an mPAGE group (CI model treated with ACH). The influence of ACH on chondrocyte proliferation and type II collagen (COL-II) expression were assessed via cell counting kit 8 (CCK-8) assay and immunofluorescence staining. Furthermore, the impacts of ACH on chondrocyte tissue and COL-II expression were analyzed using Safranin O-Fast Green staining, the International Cartilage Repair Society (ICRS) score, and COL-II tissue staining. Immunoblotting was utilized to detect tumor necrosis factor alpha (TNF-α), nuclear factor kappa-B (NF-κB), matrix metalloproteinase 13 (MMP-13), and COL-II proteins in cartilage tissue. Results The release rate of the constructed ACH reached over 85% within 72 h and achieved degradation equilibrium within 5 days with a weight loss rate of over 60%. L929 fibroblast culture results showed that the ACH posed no significant cytotoxicity, and cell attachment results were not obviously different from those on tissue culture plates ( p &lt; .05). MTT assay results demonstrated that the ACH exerted no adverse effects on L929 cell proliferation and growth, indicating good biocompatibility. CCK-8 and COL-II results indicated that chondrocyte proliferation in the cPAGE group was markedly higher versus that in the chondrocyte group ( p &lt; .05). Besides, animal experiments unveiled that, relative to the CI group, the mPAGE group had more chondrocytes, upregulated COL-II, and higher ICRS scores ( p &lt; .05). MMP-13, NF-κB, and TNF-α were downregulated, and COL-II was upshifted in the mPAGE group, with remarkable differences ( p &lt; .05). Conclusion ACH exhibited excellent biocompatibility and low cytotoxicity, promoted cell proliferation and growth, and facilitated chondrocyte prolif","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 1","pages":"67-79"},"PeriodicalIF":0.0,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251323311","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147906269","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":"Investigating the Protective Mechanism of the Zha-Chong-Shi-San-Pill Ethanol Extract on Cerebral Stroke Based on Network Pharmacology, Molecular Docking, and <i>in vitro</i> Experiments","authors":"Hua Jin, Hua Jin, Na Ta, Yuehui Liu, Qianqian Ma, Mingqi Liu, Ruo-shui Zhou, Wei Liang, Hong-quan Jin, Hong-quan Jin, Dong-wei Zhang","doi":"10.1177/09731296251324721","DOIUrl":"https://doi.org/10.1177/09731296251324721","url":null,"abstract":"Objectives To study the antioxidant effects of the traditional Mongolian medicine Zha-Chong-Shi-San-Pill ethanol extract (EEZC) on cerebral stroke for future clinical use. Materials and Methods Active components and mechanisms of EEZC against cerebral stroke were predicted and analyzed via ultra-performance liquid chromatography-electrospray ionization tandem mass spectrometry (UPLC-ESI-MS/MS), network pharmacology, and molecular docking. Next, an oxidative damage model was established in bEnd.3 cells using H 2 O 2 to simulate cerebral stroke damage. Multiple cellular tests were performed to verify the mechanisms, including cell counting kit-8 (CCK-8), flow cytometry, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, enzyme-linked immunosorbent assay (ELISA), and Western blotting. Results It was found that EEZC conferred protection against cerebral stroke H 2 O 2 -treated bEnd.3 cells. Moreover, in vitro experiments revealed that EEZC increased cell survival rates and suppressed cell apoptosis and reactive oxygen species (ROS) release. Moreover, EEZC reduced the levels of interleukin-6 (IL-6) and MMP-9, and increased the levels of interleukin-10 (IL-10), superoxide dismutase (SOD), glutathione (GSH), vascular endothelial growth factor (VEGF), phospho-endothelial nitric oxide synthase (p-eNOS), phospho-phosphatidylinositide 3-kinases (p-pi3k), and phospho-protein kinase B (p-AKT). Conclusion These results strongly suggested that EEZC might protect against cerebral stroke via the PI3K/Akt/eNOS signaling pathway.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1597-1607"},"PeriodicalIF":0.0,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251324721","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147916588","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}