Pharmacognosy Magazine最新文献

{"title":"The Ethanol Extract of Sugemule-3 Decoction Treats Isoproterenol-induced Heart Failure in Rats via PPARγ/PGC-1 Pathway","authors":"XueDong Pan, Hong‐Yang Wang, Qian Li, Fuli zhang","doi":"10.1177/09731296241312488","DOIUrl":"https://doi.org/10.1177/09731296241312488","url":null,"abstract":"Background The herbs Baidoukou (the fruit of Amomum compactum Sol. ex Maton), Baijusheng (the fruit of Lactuca sativa L.), and Biba ( Piper longum L.) make up the traditional Mongolian medicine known as Sugemule-3 decoction. Objectives Heart failure (HF) is severely impacted; however, the pharmacological mechanism behind it is yet unclear. This investigation looked at the Sugemule-3 ethanol extract’s therapeutic mechanism for isoproterenol-induced HF in rats. Materials and Methods To create a HF model, isoproterenol was administered to Wistar rats. Following the model’s successful establishment, various medications were administered for 4 weeks. The electrical signals of cardiac fluctuations, cardiac morphology, and function were observed using electrocardiogram (ECG) and echocardiography. The rats were killed 4 weeks later, and the hearts were observed using an electron microscope and HE staining. Cardiomyocyte apoptosis was observed using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. The levels of markers in serum were determined using enzyme-linked immunosorbent assay (ELISA). Western blot and immunohistochemistry were used to detect the expression of proteins in rats. Results Our findings show that isoproterenol injection subcutaneously interfered with the structure and function of the left ventricle, particularly during systole. In the model group, the level of oxidative stress index malondialdehyde ( p < 0.01) increased with the decrease in antioxidant enzymes such as superoxide dismutase ( p < 0.01) and glutathione peroxidase ( p < 0.01). Sugemule-3 ethanol extract considerably reduced the harmful effects of isoproterenol on the rat myocardium. Additionally, isoproterenol increased the level of peroxisome proliferator-activated receptor (PPAR), carnitine palmitoyl transferase-1 (CPT-1), phosphoenolpyruvate carboxylase (PEPCK), stearyl CoA desaturase-1 (SCD-1), and ubiquitin-conjugating (UCB) expression while decreasing the level of peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1) expression, leading to cardiometabolic diseases. Sugemule-3 ethanol extract improved cardiac metabolism. Conclusion The findings demonstrate that Sugemule-3 ethanol extract may improve energy metabolism of cardiomyocytes and alleviate isoproterenol-induced HF through inhibiting the peroxisome proliferator-activated receptor gamma (PPARγ)/PGC-1 signaling pathway.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1300-1312"},"PeriodicalIF":0.0,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147900207","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 <i>Curcuma phaeocaulis</i> Extracts on the Proliferation and Apoptosis of Gallbladder Cancer Cells via mTOR/p70S6K Signaling Pathway","authors":"Jiaxuan Yang, Jiawei Tian, Erhao Zheng, Qi Li, Chen Chen, Zhimin Geng, Jigang Bai","doi":"10.1177/09731296251313627","DOIUrl":"https://doi.org/10.1177/09731296251313627","url":null,"abstract":"Background Curcuma phaeocaulis (CP) is utilized as a Chinese herbal medicine to treat abdominal distension and other related ailments. Curcuma phaeocaulis extracts (CPE) are rich in active components and exhibit anti-tumor properties. Objectives Purpose: This work was to assess the impact of CPE on the proliferation, apoptosis, migration, and invasion of gallbladder cancer cells (GCC), aiming to investigate its potential underlying mechanisms of action. Materials and Methods CP was utilized as the raw material to prepare CPE volatile oil via drying and heating processes. Total phenolic content analysis was conducted, assessing its scavenging capacity against 2,2-diphenyl-1-picrylhydrazyl (DPPH•) and •OH free radicals, as well as its inhibitory effects on the growth of Staphylococcus aureus, Escherichia coli , and Pseudomonas aeruginosa . Human GCC line GBC-SD was selected, cultured conventionally as a control, and treated with CP volatile oil at concentrations of 25 µg/mL (Low-CPE group), 50 µg/mL (Middle-CPE group), and 100 µg/mL (High-CPE group). Cell proliferation activity was evaluated using MTT assay, apoptosis rate was assessed via flow cytometry, migration, and invasion were measured using the Transwell chamber assay, and Western blot was performed to assess proteins in the mTOR/p70S6K signaling pathway. Results The total phenolic content in the volatile oil prepared from warm CPE was approximately 30.9 mg/g, consisting of over 20 active constituents. The warm CP volatile oil exhibited scavenging rates of 85.3% for DPPH• radicals and 91.5% for •OH radicals, with minimum inhibitory concentrations against S. aureus, E. coli , and P. aeruginosa at 4.0 mg/mL, 8.0 mg/mL, and 1.0 mg/mL, respectively. Relative to the Ctrl group, Low-CPE, Middle-CPE, and High-CPE groups demonstrated decreased cell proliferation activity, increased apoptosis rates, reduced cell migration and invasion, decreased phosphorylation levels of mTOR and p70S6K proteins ( p &lt; 0.05), exhibiting concentration-dependent characteristics. Conclusion The volatile oil derived from warm CPE exhibited robust anti-oxidant and anti-bacterial activities. The warm CP volatile oil effectively inhibited GCC proliferation, migration, and invasion by suppressing the activation of the mTOR/p70S6K signaling, while promoting apoptosis.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1427-1437"},"PeriodicalIF":0.0,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147910435","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":"Inhibitory Effects of Different Doses of Matrine on Breast Cancer and Its Relationship with miR-188","authors":"Zhao Liu, Jianbin Xu, Heng Xia, Miaofeng Wang, Qianlan Xu","doi":"10.1177/09731296241311986","DOIUrl":"https://doi.org/10.1177/09731296241311986","url":null,"abstract":"Background Malignant tumors represented by breast cancer still have limitations in clinical treatment methods. Matrine is a compound with anticancer activity, but its inhibitory effect on breast cancer and its mechanism for regulating miR-188 are still unclear. Objectives Therefore, it is necessary to explore more effective breast cancer treatment methods and understand the intervention mechanism of matrine and its effect on miR-188. Materials and Methods A nude mouse model of breast cancer was in this study constructed and divided into a model group, 4 mg/kg group, 8 mg/kg group, drug group, and miR-188 mimic group. Different concentrations of matrine were administered intragastrically, and cell proliferation and apoptosis were observed. At the same time, a specific mechanism for miR-188 in the anti-breast cancer effect of matrine was explored by overexpressing miR-188. Results It was found that matrine inhibited the proliferation of breast cancer cells and caused cancer cell apoptosis. In addition, it inhibited cell migration in a dose-dependent manner. At the same time, miR-188 was lowly expressed in breast cancer and significantly increased after matrine treatment. Overexpression of miR-188 enhanced the antitumor effect of matrine. Phosphatase and tensin homolog (PTEN) was also activated in the surface by matrine, and expressions of matrix metalloproteinase-9 (MMP-9) and matrix metalloproteinase-2 (MMP-2) were inhibited. This study shows that matrine has a significant inhibitory effect on breast cancer, and its mechanism is related to upregulation of miR-188, activation of PTEN, and inhibition of MMP-9 and MMP-2 expressions. Conclusion miR-188 is involved in the anti-breast cancer process, which can be used as the theoretical basis of matrine potential drugs for breast cancer treatment. Meanwhile, miR-188 and matrine will also have great potential in developing new breast cancer treatment methods, which can provide ideas and a basis for further development of related studies.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 3","pages":"906-916"},"PeriodicalIF":0.0,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147919864","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":"Hyperoside inhibits Mitochondrial DNA Damage to Reverse Hepatocyte Pyroptosis to Treat Doxorubicin-related Hepatotoxicity","authors":"Qing Liu, Ying Lan, Zhe Bai","doi":"10.1177/09731296241306199","DOIUrl":"https://doi.org/10.1177/09731296241306199","url":null,"abstract":"Background Hyperoside is a potential liver cell and mitochondrial protector, but there is no evidence to suggest that hyperoside can effectively treat doxorubicin (DOX) related liver toxicity. Objectives This study aims to determine the role of hyperoside in DOX related liver toxicity and liver cell damage in vivo and in vitro. Materials and Methods A mouse model of liver toxicity was induced by intraperitoneal injection of DOX, and hyperoside was administered orally for treatment. During this period, the weight and food intake of the mice were recorded. The morphology of mouse liver tissue was observed by hematoxylin and eosin staining. Oxidative stress and inflammatory status in mice were observed through serum inflammatory factors and liver oxidative stress markers. Mitochondrial damage is determined by the degree of mitochondrial DNA damage. Western blotting and reverse transcription polymerase chain reaction (RT-PCR) were used to detect the expression of pyroptosis and genes in the liver and liver cells. Results Hyperoside can effectively treat DOX-induced oxidative stress and inflammatory status, liver function damage, and hepatocyte necrosis in mice. Further research suggests that the beneficial effect of hyperoside is achieved by inhibiting mitochondrial DNA damage in liver cells. Conclusion This study indicates that hyperoside improves DOX-induced liver toxicity by inhibiting mitochondrial DNA damage.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 3","pages":"831-841"},"PeriodicalIF":0.0,"publicationDate":"2025-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147916679","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":"Polystyrene Nanoparticles-coated Astragalus Polysaccharides Affects the Development of Prostate Cancer by Regulating Glycolysis of DAP12/SYK Axis through miR-370","authors":"Gao Cheng, Zixiong Liu, Jiafu Tan","doi":"10.1177/09731296241298361","DOIUrl":"https://doi.org/10.1177/09731296241298361","url":null,"abstract":"Background This study aims to explore the use of polystyrene nanoparticles as a carrier to encapsulate astragalus polysaccharides and regulate the glycolytic pathway of the DNAX-activating protein of 12 kDa/spleen tyrosine kinase (DAP12/SYK) axis through miR-370, thereby affecting the development mechanism of prostate cancer. Materials and Methods Polystyrene nanoparticles coated with astragalus polysaccharide nanoparticles (APS/PDA NPs) were prepared, and PC-3 cell experiments were used for culture and further detection of miRNA and other genes, detection of glycolysis-related proteins and genes, and observation of the biology of PC-3 cells behavioral changes, exploring the mechanism of action of APS/PDA NPs. Results We successfully prepared composite materials of APS/PDA NPs, and found that APS/PDA NPs could inhibit glycolysis and induce apoptosis in PC-3 cells. Further experiments showed that APS/PDA NPs could increase miR-370 expression, inhibit glycolysis, and induce apoptosis. APS/PDA NPs play a strong role in inhibiting the DAP12/SYK axis, inhibiting glycolysis, and causing apoptosis. Combined with biological information and multiple experiments, it was confirmed that miR-370 targeted DAP12, and the inhibition of PCa progression by APS/PDA NPs was achieved through targeting miR-370 and negatively regulating the DAP12/SYK axis. Conclusion As a drug carrier, polystyrene nanoparticles can effectively deliver astragalus polysaccharides to prostate cancer cells, thereby increasing the local concentration of drugs and enhancing the therapeutic effect. More encouragingly, this drug carrier not only performed well in inhibiting glycolysis but also significantly upregulated the level of miR-370, which further inhibits the expression of DAP12, providing a new therapeutic idea for inhibiting the development of prostate cancer.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 3","pages":"974-983"},"PeriodicalIF":0.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878428","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":"Cucurbitacins Loaded in Liposome Nanoparticles Inhibit the Development of Lung Cancer Through BECN1-mediated Autophagy","authors":"Xietian Liu, Peng Diao","doi":"10.1177/09731296241300750","DOIUrl":"https://doi.org/10.1177/09731296241300750","url":null,"abstract":"Background Autophagy has always been a current research hotspot during lung cancer treatment. Objectives This study aimed to explore the molecular mechanism by which cucurbitacins loaded in liposome nanoparticles (Cu B-NPs) inhibit the development of lung cancer through Beclin 1 (BECN1) regulation. Materials and Methods Cu B-NPs were prepared, and the A549 group, Cu B group, and Cu B-NPs group were set up to assess the mechanism of Cu B-NPs in regulating autophagy and inhibiting the development of lung cancer. Cu B-NPs+si-BECN1 group and Cu B-NPs+pc-BECN1 group were also set up to analyze whether Cu B-NPs regulate autophagy through BECN1 to inhibit the development of lung cancer. Results Cu B-NPs were successfully prepared and had good dispersion stability. Cu B-NPs reduced cell viability, promoted apoptosis and the accumulation of autophagosomes, and regulated apoptosis-related proteins, thereby inhibiting lung cancer development. After activating/inhibiting BECN1 expression, Cu B-NPs promoted cell autophagy and apoptosis by upregulating BECN1 expression, thereby inhibiting the development of lung cancer. Conclusion In this study, Cu B-NPs were successfully prepared, and the particles promoted autophagy and induced apoptosis in A549 cells by upregulating BECN1, thereby inhibiting the development of lung cancer. This provides strong evidence and clues for further research and development of lung cancer treatment strategies.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 3","pages":"1055-1063"},"PeriodicalIF":0.0,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878814","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":"Proliferative Effects of <i>Curcuma zedoaria</i> Extract on Ovarian Tumor Cells","authors":"Na Song, Xiuyun Wang, Mingxing Yuan","doi":"10.1177/09731296241298344","DOIUrl":"https://doi.org/10.1177/09731296241298344","url":null,"abstract":"Background Curcuma zedoaria is a common traditional herbal medicine that contains mainly curcumin and volatile oils with antioxidant, anti-inflammatory, and antitumor properties. Objectives This study aimed to investigate the effects of C. zedoaria extract on the biological behavior of ovarian cancer (OC) cells. Materials and Methods Active compounds were extracted from C. zedoaria , and the content of different active compounds was quantified. Their scavenging abilities against DPPH and -OH free radicals were analyzed, and the minimum inhibitory concentrations (MICs) against different bacterial strains were determined. The human OC cell line SK-OV-3 was divided into four groups and cultured in media containing C. zedoaria extract at concentrations of 0.0, 0.3, 0.6, and 1.2 g/L. The proliferation, inhibition, migration, and apoptosis of primary OC cells were then assessed using the methyl tetrazolium (MTT) assay, the scratch-healing assay, and flow cytometry. Tumor cell invasion and clonogenicity were also assessed. Finally, the status of MEK/ERK signaling in the cells was examined by protein imprinting. Results C. zedoaria extract contained 0.18% curcumin, 0.04% demethoxycurcumin, and 0.02% bisdemethoxycurcumin. When the concentration of C. zedoaria extract was ≥10 mg/mL, it exhibited a scavenging rate of over 85% for DPPH and -OH free radicals. In addition, C. zedoaria extract effectively inhibited the growth of Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus , and Staphylococcus epidermidis , with lower MICs observed for gram-positive bacteria. MTT cell proliferation and scratch assay results showed significant inhibition of SK-OV-3 cell proliferation and migration by C. zedoaria extract. Flow cytometry results indicated that the extract strongly promoted apoptosis in SK-OV-3 cells. Compared with the control group, the invasive and clonogenic abilities of SK-OV-3 cells decreased with increasing concentration of the extract. Protein imprinting results showed that treatment with C. zedoaria extract led to a concentration-dependent decrease in p-MEK1/2 and p-ERK1/2 protein levels in SK-OV-3 cells. Conclusion C. zedoaria extract possesses potent antioxidant, antibacterial, and antitumor properties. In addition, C. zedoaria extract can suppress the activation of MEK/ERK signaling, thereby inhibiting the proliferation and migration of SK-OV-3 cells, inducing apoptosis, and reducing the invasive and clonogenic potential of SK-OV-3 cells. It provides a theoretical basis for the discovery of novel drugs using C. zedoaria extract and its clinical applications in the treatment of OC.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 3","pages":"959-973"},"PeriodicalIF":0.0,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147330642","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":"Cinnamon Polyphenols Ameliorate the Dysregulation of Cardiac Energy and Autophagic Homeostasis in Rats with Diabetic Cardiomyopathy via the mTOR/PGC1α Pathway","authors":"Xu Zhang, Xiaoting Zhang, Shiyu Wu, Mengting Hu, Xu Xu, Jian-Ping Gao","doi":"10.1177/09731296241289678","DOIUrl":"https://doi.org/10.1177/09731296241289678","url":null,"abstract":"Background Inflammation mediated by hyperglycemia, lipid metabolism disorders, abnormal myocardial energy metabolism, myocardial cell damage, and changes in ventricular structure are important mechanisms in the occurrence and development of diabetic cardiomyopathy (DCM). Cinnamon polyphenols (CP) are extracted from the traditional Chinese medicine cinnamon, which is believed to have cardioprotective effects and has been used in China for hundreds of years. Objectives This study aimed to investigate the therapeutic effects of CP on DCM and its possible mechanisms. Materials and Methods The DCM model was established by a single intraperitoneal injection of 85 mg/kg 1% streptozotocin in rats. The treatment group was orally administered 135 mg/kg CP for 28 consecutive days, a dosage verified by experiments on AC16 myocardial cells and detecting liver and kidney injury markers. Results CP could reduce high blood sugar, high blood lipids, left ventricular mass index, levels of myocardial injury markers, adenosine diphosphate (ADP), and cyclic adenosine monophosphate (cAMP) in the model group. It also improved weight loss, and increased myocardial adenosine triphosphate (ATP), adenosine monophosphate (AMP), phosphocreatine (PCr), and ATP/ADP, AMP/ATP, and PCr/ATP ratios. The expression of p-mTOR/mammalian target of rapamycin (mTOR), p62, and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) in the myocardium of the CP group was enhanced, while the expression of LC3II/LC3I was inhibited. Conclusion CPs can alleviate myocardial damage by reducing blood sugar, blood lipids, and abnormal autophagy levels while promoting the restoration of myocardial energy metabolism homeostasis.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 3","pages":"781-792"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296241289678","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147879114","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 Neuroprotective Mechanism of Salidroside Modified with Polydopamine Nanoparticles in Regulating Notch Pathway by Inhibiting miR-155 in Stroke Rats","authors":"Song Liu, Lv Xiaomeng, Dong Wang","doi":"10.1177/09731296241282387","DOIUrl":"https://doi.org/10.1177/09731296241282387","url":null,"abstract":"Background and Objectives Stroke threatens neurological function. Salidroside is widely used to treat neurological diseases such as stroke. Previous studies have shown that miR-155 plays an important regulatory role in the pathogenesis of stroke and that the Notch pathway plays an important role in nervous system development and regeneration. Materials and Methods PDA NPs-SAL complex was prepared, a stroke rat model was constructed, and the cerebral infarction area of rats was measured. Analyze the changes of PDA NPs-SAL on rat brain tissue and evaluate the neuroprotective effect. Detect the changes in miR-155 and Notch pathway-related proteins in stroke rat models to further understand the role of miR-155 and Notch pathway in the pathogenesis of stroke and their relationship. Results Salidroside had certain protective effects on the nerves of stroke rats, and the effect of PDA NPs-SAL was more prominent. At the same time, PDA NPs-SAL promotes the Notch pathway by inhibiting miR-155, thereby exerting a neuroprotective effect on stroke rats. Conclusion Under the intervention of PDA NPs-SAL, the neurological function scores of rats were reduced, and the effect of PDA NPs-SAL was more significant. In addition, PDA NPs-SAL inhibited miR-155 and activated the Notch pathway, thereby reducing the water content of rat brain tissue and cerebral infarction area, thereby exerting a neuroprotective effect on stroke rats.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1176-1186"},"PeriodicalIF":0.0,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296241282387","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147880443","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":"Identification of <i>Astragalus</i> Polysaccharide as a Neuroprotective Agent via Activating Klotho-mediated Nrf2 Pathway","authors":"Kuo Liu, Nannan Ding, Mengying Han, Shen Shuping, Li Lin, Fang Bian, Li Chen, Ji Zhang, Lailiang Qu, Dan Yang","doi":"10.1177/09731296241279103","DOIUrl":"https://doi.org/10.1177/09731296241279103","url":null,"abstract":"Background Neurodegenerative diseases (NDs) have become a significant public health problem, and oxidative stress (OS) serves as a pivotal factor in the pathological progression of NDs. Pharmacological research indicates that Astragalus polysaccharide (APS, extract of Astragalus membranaceus) has antioxidant and antiaging effects, closely related to NDs. Objectives The potential of APS in treating NDs remains uncertain. Herein, the neuroprotective effect of APS was evaluated. Materials and Methods The H 2 O 2 -induced PC12 cell damage model was established to assess the neuroprotection of APS. Cell viability was determined by MTT. Cell images were observed using ImageXpress Micro Confocal analysis. Apoptosis of the cells and intracellular levels of reactive oxygen species (ROS) were detected using flow cytometry. The expression of Klotho, nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), thioredoxin reductase 1 (TrxR1), and NAD(P)H quinone oxidoreductase 1 (NQO1) was determined by Western blot (WB). Results APS exerted significant protection against H 2 O 2 -caused cell death dose-dependently, and APS could significantly reduce the intracellular ROS and relieve cell apoptosis. Furthermore, we found that APS could upregulate the expression of Klotho and Nrf2 dose-dependently, and the expression levels of Nrf2-mediated antioxidant proteins increased significantly, including HO-1, TrxR1, and NQO1. Moreover, we found that APS upregulated Klotho and Nrf2-mediated antioxidant proteins time-dependently. The expression of klotho peaked at 6 hours after treatment with APS (400 mg/L). Subsequently, the protein level of Nrf2 reached the maximum at 12 hours, and the downstream NQO1, HO-1, and TrxR1 levels peaked at 24 hours. Conclusion This study demonstrates that APS is promising for further development against oxidative stress-related NDs.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 1","pages":"161-169"},"PeriodicalIF":0.0,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296241279103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147914807","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}