Pharmacognosy Magazine最新文献

{"title":"Study on the Mechanism of <i>Guizhi</i> Fuling Decoction in Treating Hyperlipidemia Based on Network Pharmacology and Experimental Methods","authors":"Mi Zhang, Yuntian Zhang, Hongyun Wang, Chunlei Fan","doi":"10.1177/09731296241281441","DOIUrl":"https://doi.org/10.1177/09731296241281441","url":null,"abstract":"Background Hyperlipidemia, caused by abnormal lipid metabolism, has become a significant health concern, especially in younger populations. While statins are commonly used for treatment, they often cause severe side effects with long-term use, leading to increased interest in finding natural alternatives. Objectives This study aimed to investigate how Guizhi Fuling Decoction (GZFL) treats hyperlipidemia using network pharmacology and experimental validation. Materials and Methods Network pharmacology analyzed GZFL’s active components, targets, and treatment mechanisms for hyperlipidemia. Hyperlipidemia rat and high-fat cell models were established. Experimental validation included enzyme-linked immunosorbent assay, Western blot, quantitative polymerase chain reaction, Oil Red O staining, and other methods. Statistical analysis was performed using one-way analysis of variance followed by Tukey’s post hoc test for multiple comparisons. Pearson correlation analysis was used to identify correlations between key protein expressions and lipid levels. Results GZFL comprises 85 active components and targets 218 proteins. Hyperlipidemia involves 3,852 targets, with 175 overlapping targets. Key targets included estrogen receptor 1, prostaglandin-endoperoxide synthase 2, interleukin-6 (IL-6), protein kinase B (AKT) 1, tumor necrosis factor, interleukin-1 beta, peroxisome proliferator-activated receptor gamma (PPARG), tumor protein p53 (TP53), and fructo oligosaccharide (FOS). Major active components were quercetin, phytosterols, kaempferol, and baicalein. Enrichment analysis highlighted processes like lipopolysaccharide response and lipid signaling pathways. Animal studies showed GZFL significantly reduced serum total cholesterol, triglycerides, and low-density lipoprotein cholesterol levels, and increased apolipoprotein A1 ( p &lt; 0.05). Western blot indicated that GZFL influenced AKT, TP53, IL-6, PPARγ expression, and mRNA levels in the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway ( p &lt; 0.01). Serum pharmacology experiments demonstrated GZFL-medicated serum reduced lipid droplet formation in high-fat cell models. Conclusion GZFL contains multiple pharmacologically active components, such as quercetin, phytosterols, and kaempferol, which can influence lipid metabolism. It may exert its effects by regulating proteins like AKT, TP53, IL-6, and PPARγ, participating in lipid and atherosclerosis signaling pathways and the PI3K/AKT/mTOR pathway.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 1","pages":"152-160"},"PeriodicalIF":0.0,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296241281441","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902260","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":"Chikusetsusaponin IVa Targets Nrf2 to Inhibit H9N2 Avian Influenza Virus Infection","authors":"Qi Dai, Songtao Wu, Xin Zheng, Pengtao You, Liu Yan-wen, Yuan Zhao, Xiu-Qiao Zhang","doi":"10.1177/09731296241277316","DOIUrl":"https://doi.org/10.1177/09731296241277316","url":null,"abstract":"Background Chikusetsusaponin IVa (CHS) is a triterpenoid saponin that has been demonstrated to possess multiple properties. Objectives This study focused on inhibiting H9N2 avian influenza virus (AIV) by CHS and investigated the underlying mechanisms, specifically targeting the nuclear factor erythroid2-related factor 2 (Nrf2) signaling pathway. Materials and Methods The antiviral activity of CHS was evaluated by determining its half inhibitory concentration and therapeutic index (TI) in vitro . Markers of oxidative stress, encompassing superoxide dismutase, glutathione peroxidase, and malondialdehyde levels, were assessed. Analyses of pathways from the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology were conducted to elucidate the underlying mechanisms, followed by network investigation and simulations of molecular docking. Moreover, the effects of CHS on Nrf2 and mitogen-activated protein kinase (MAPK) signaling pathways were assessed in human lung carcinoma A549 cells and a mouse model of H9N2 AIV infection. Results CHS showed inhibitory effects on H9N2 AIV in vitro , with TI values of 4.00 (co-treatment) and 6.29 (posttreatment). CHS reduced H9N2 AIV-induced oxidative stress and was predicted to target Nrf2, MAPK/phosphoinositide 3-kinase (PI3K)-protein kinase B (Akt) signaling pathways, and oxidation–reduction processes. Molecular docking analysis revealed a high affinity between CHS and Nrf2. In A549 cells, CHS enhanced Nrf2 activation, inhibited MAPK signaling, and reduced H9N2 AIV-induced oxidative stress. The therapeutic mechanism of CHS was found to be mediated by Nrf2. In a mouse model, CHS mitigated pulmonary impairment, improving the organism’s antioxidant activity. CHS also regulated the Nrf2 and MAPK signaling pathways in lung tissue. Conclusion CHS inhibits H9N2 AIV and alleviates virus-induced oxidative stress by targeting the Nrf2 signaling pathway. These observations lay the groundwork for devising prospective therapeutic interventions targeting H9N2 AIV infection.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 2","pages":"584-598"},"PeriodicalIF":0.0,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911627","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":"Research on the Improvement of Endothelial Cell Function and Trophoblast Apoptosis in Rats with Preeclampsia by Tanshinone IIA","authors":"Hui Dong, Jie Song, Yan‐Ju Jia, Hongyan Cui, Xu Chen","doi":"10.1177/09731296241277301","DOIUrl":"https://doi.org/10.1177/09731296241277301","url":null,"abstract":"Background Preeclampsia is a pregnancy complication characterized by high blood pressure and signs of damage to another organ system, often the kidneys. Recent studies suggest that endothelial dysfunction and trophoblast apoptosis are involved in the pathogenesis of preeclampsia. Objectives To investigate the effects of tanshinone IIA (TIIA) on clinical symptoms, vascular endothelial function, and placental trophoblast apoptosis in preeclampsia rats. Materials and Methods Twenty-four pregnant Sprague-Dawley rats, between 8 and 10 weeks old, were randomly divided and allocated into three groups: Control, model, and treatment, with each group consisting of 8 rats. The control group received normal saline injections via the tail vein; the model group received NG-nitro-l-arginine methyl ester (l-NAME) to induce preeclampsia, followed by normal saline injections; and the treatment group received TIIA (10 mg/kg) via tail vein injection after preeclampsia induction with l-NAME. Various parameters were measured, including tail artery systolic pressure, 24-hour proteinuria, offspring and placental weight, levels of endothelial nitric oxide synthase (eNOS), endothelin-1 (ET-1), placental growth factor (PLGF), and soluble FMS-like tyrosine kinase 1 (sFlt-1) in serum, and expression of B-cell lymphoma-2 (Bcl-2) and Bcl-2-related X protein (Bax) in placental trophoblasts. Results TIIA treatment led to decreased tail artery systolic pressure and 24-hour urine protein levels, increased body and placental weights of offspring, and favorable changes in serum levels of ET-1, sFlt-1, eNOS, and PLGF. Moreover, TIIA treatment resulted in decreased Bax levels and apoptosis in placental trophoblasts, along with increased Bcl-2 levels. Conclusion TIIA can improve the clinical symptoms of preeclampsia in rats induced by l-NAME, alleviate the apoptosis of placental trophoblast cells, and improve vascular endothelial function.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 1","pages":"116-123"},"PeriodicalIF":0.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147880111","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 Effect of <i>Cayratia albifolia</i> C. L. Li Extract on LPS-induced Inflammation of RAW264.7 Cells by Regulating the Nrf2/HO-1 Axis","authors":"Yi Tan, Liang Cao, Dan Zhou, Biao Qin, Yanbin Zhang, Jianxin Liu, Kai He, Bin Li, Zaiqi Zhang","doi":"10.1177/09731296241266095","DOIUrl":"https://doi.org/10.1177/09731296241266095","url":null,"abstract":"Background Cayratia albifolia C. L. Li (Jiao Mei Gu (JMG)) has potential therapeutic effects in inflammatory diseases. Objectives The primary goal of the research was to focus on the antioxidant and anti-inflammatory qualities of C. albifolia and the underlying mechanisms that contribute to these benefits. Materials and Methods To explore the anti-inflammatory abilities of JMG, we employed enzyme-linked immunosorbent assay and nitric oxide (NO) assay in a lipopolysaccharide (LPS)-induced macrophage inflammation model. Furthermore, flow cytometry was employed to assess the antioxidant effects of C. albifolia, and Western blotting was used to reveal the underlying mechanisms. Results Ethyl acetate extract of C. albifolia effectively reduced the release of NO, interleukin-6, tumor necrosis factor-α, and prostaglandin E2 in macrophages. Additionally, it prevented the expression of reactive oxygen species. Mechanistically, the extract may downregulate the expression of inducible nitric oxide synthase, cyclooxygenase-2, the nuclear factor-erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) protein expression. Conclusion The ethyl acetate extract of C. albifolia demonstrated remarkable anti-inflammatory and antioxidant effects by modulating the Nrf2/HO-1 axis.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 1","pages":"207-217"},"PeriodicalIF":0.0,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147908135","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":"Ganoderic Acid A Suppresses Androgenindependent Cell Growth via the AKT/GSK-3β/β-catenin Signaling Pathway","authors":"Qiao Lyu, Yuan Qu, Jianfan Chen, Guo Chen, Zheng Chen, Lijun Qu","doi":"10.1177/09731296241262075","DOIUrl":"https://doi.org/10.1177/09731296241262075","url":null,"abstract":"Objectives The primary aim of this study is to investigate the specific effects and mechanisms of ganoderic acid A (GAA) on castration-resistant prostate cancer (CRPC). Materials and Methods We successfully established an androgen-independent prostate cancer cell line (LNCaP-AI). The LNCaP-AI cells demonstrated accelerated growth, elevated levels of androgen receptor and prostate-specific antigen (PSA), and resistance to the drug enzalutamide. Then, we administered LNCaP-AI cells with GAA or a control and determined the cell growth rate. Next, LNCaP-AI cells with and without GAA treatment were subjected to RNA-seq for mRNA sequencing. The genes were subjected to a Kyoto Encyclopedia of Genes and Genomes analysis. We also checked the expression levels of the targeted genes. Finally, normal LNCaP or LNCaP-AI cells were subcutaneously injected into nude mice to further confirm the effect of GAA. Results Experiments showed that GAA effectively suppressed the growth rate, PSA secretion, migration, and invasion of LNCaP-AI cells. The results of a subsequent RNA-seq analysis identified the PI3K/AKT pathway as the key signaling pathway influenced by GAA. Notably, AKT and GSK-3β phosphorylation was decreased, and β-catenin protein levels were also lowered, as a result of GAA treatment. Moreover, we observed decreased activity in crucial genes, including c-Myc, Cyclin D1 , and MMP-2 , which play integral roles in CRPC development. Furthermore, GAA inhibited the tumorigenesis of LNCaP-AI cells in nude mice in vivo . Conclusion GAA effectively suppresses the growth of androgen-independent cells by inhibiting the AKT/GSK-3β/β-catenin signaling pathway. These findings demonstrate the potential of GAA as a therapeutic candidate for CRPC.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 2","pages":"467-479"},"PeriodicalIF":0.0,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296241262075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147880315","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":"Unraveling the Pharmacological Intricacies of Kurarinone in Osteoporosis: Insights from a Network Pharmacology Approach","authors":"Z Xiong, Huawen Yang","doi":"10.1177/09731296241259563","DOIUrl":"https://doi.org/10.1177/09731296241259563","url":null,"abstract":"Background Kurarinone, a compound derived from Sophora flavescens, has been widely studied for its anti-inflammatory properties, as well as its potential in treating autoimmune encephalomyelitis and inflammation-related musculoskeletal diseases. However, the specific molecular mechanisms by which Kurarinone affects osteoporosis are still not fully understood. Objectives To explore the potential pharmacological targets and molecular mechanisms underlying the therapeutic effects of Kurarinone on osteoporosis. Materials and Methods To confirm the impact of Kurarinone on osteoporosis, network pharmacology techniques were used to analyze the mechanisms of Kurarinone on osteoporosis. Molecular docking was performed to examine the binding of Kurarinone to key targets involved in osteoporosis. Then, we conducted TRAcP staining, quantitative polymerase chain reaction (q-PCR), and Western blot experiments to validate the results. Results Utilizing network pharmacology approaches coupled with docking analysis, our investigation revealed that Kurarinone was involved in the osteoclast differentiation and MAPK signaling pathways. According to in vitro experiments, Kurarinone was found to inhibit osteoclast formation through the p38/MAPK pathway. Conclusion This study suggests that Kurarinone may treat osteoporosis by inhibiting MAPK phosphorylation and inhibiting osteoclast formation.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"20 4","pages":"1350-1358"},"PeriodicalIF":0.0,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296241259563","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883951","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":"Lijing-Anfei Decoction Attenuates COPD in a Mouse Model: Network Pharmacology Analysis, Molecular Docking, and Experimental Validation","authors":"Jiajia Zhu, Jie Liu, Wei Jia, Guoqiang Shao, H. Eric Xu","doi":"10.1177/09731296241242909","DOIUrl":"https://doi.org/10.1177/09731296241242909","url":null,"abstract":"Background Today, network pharmacology and molecular docking were utilized for investigation and prediction of possible mechanisms in fields such as pharmacognosy and traditional Chinese medicine formulas when treating disease. Purpose Chronic obstructive pulmonary disease (COPD) is caused by exposure to toxic particles and leads to chronic bronchitis and lung dysfunction. Lijing-Anfei decoction (LAD) is a traditional Chinese herbal decoction used to cure COPD. This study explored the effects of this decoction and its intrinsic mechanism in a COPD mouse model. Materials and Methods Possible targets were retrieved from several databases and combined using Veny. Protein-protein interaction (PPI) networks were constructed via STRING database. Gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed via the Metascape database. The COPD model was established by exposing the mice to cigarette smoke for 12 weeks. After the model was established, LAD was administered for four weeks. Enzyme-linked immunosorbent assay (ELISA) was performed, and body weights and lung wet/dry ratios were measured. Lung morphology was observed by hematoxylin-eosin staining. Results After the screening, 32 overlapping targets were used to generate PPI networks and the following hub genes were identified: JUN, IL6, RELA, IL1B, HIF1A, MAPK1, PPARG, PTGS2, MAPK14, and NOS2. The KEGG analysis indicated that hypoxia-inducible factor-1 (HIF-1) and other signaling pathways are possible signaling pathways. The molecular docking results demonstrated tight links between major compounds and their targets. In animal experiments, LAD attenuated body weight loss, downregulated inflammatory cell numbers, and inhibited the enhancement of Fe 2+ levels. The mean linear intercept index changes indicated that LAD ameliorated the lung structural damage. ELISA revealed that it downregulated pro-inflammatory cytokine levels and inhibited excessive oxidant production, TdT-mediated dUTP-biotin nick end labeling assay demonstrated that it alleviated cell death in the lungs, and immunohistochemical staining revealed that it inhibited HIF-1α and PTGS2. ML228—an agonist of HIF-1—blocked the effect of LAD, validating the role of HIF-1-mediated ferroptosis in the pharmacological effects of this decoction. Conclusion This study revealed that LAD was successful in treating COPD.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"20 4","pages":"1100-1113"},"PeriodicalIF":0.0,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296241242909","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147904287","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":"Anti-myocardial Ischaemia by Bioinformatics of Apocynum venetum L.","authors":"Yuan-Jia Yue, Yu Li, Xing Rong, Zhao Ji, Huimin Wang, Lin Jiang","doi":"10.1177/09731296241242178","DOIUrl":"https://doi.org/10.1177/09731296241242178","url":null,"abstract":"Background In recent years, the number of patients with myocardial ischaemia is rising year by year in China. Objectives The study uses network pharmacology to predict targets and pathways of action of Apocynum venetum L. (AVL) for the treatment of myocardial ischemia (MI). Materials and Methods The essential active compounds of AVL were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. The objective of selecting the target genes was achieved through the utilization of GeneCards and Swiss Target Prediction resources. The pool of MI-related targets was obtained from DisGeNET, Online Mendelian Inheritance in Man and the Therapeutic Target Database. The protein-protein interaction network was meticulously constructed using the STRING algorithm. The gene ontology (GO) analysis of AVL-MI targets was performed at Metascape. In addition, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was conducted. Furthermore, molecular docking analysis was conducted to study the interactions of AVL components with estrogen receptor 1 (ESR1), heat shock protein 90 alpha (HSP90A), protein kinase B (Akt1), tyrosine kinase Src (SRC) and phosphatidylinositol 3-kinase (PI3K). Finally, cellular experiments were performed to validate the mechanism of action of AVL. Results The molecular target analysis revealed that AVL has the potential to interact with a total of 147 biomolecules. This comprises ESR1, HSP90A, epidermal growth factor receptor, protein kinase B alpha (Akt1), SRC and PI3K. As indicated by GO and KEGG analyses, AVL’s inhibitory potential against MI may be due to its action on the PI3K-Akt signalling pathway. Furthermore, docking studies conducted to assess the interactions between AVL components and their targets (ESR1, HSP90A, Akt1, SRC and PI3K) confirmed that they have robust binding affinities. Cell experiments also showed that AVL treatment significantly reduced oxidative stress indexes ( p &lt; 0.05). Additionally, the expression levels of Akt1 and PI3K proteins were significantly higher in the AVL group compared to the MI group ( p &lt; 0.05). Conclusion AVL therapy exhibits the potential to alleviate the symptoms of MI by mitigating oxidative stress and by orchestrating the expression of proteins such as PI3K and Akt1.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"20 4","pages":"1322-1330"},"PeriodicalIF":0.0,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296241242178","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147880290","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":"Nerolidol Alleviates Oxidative Stress and Inflammation in Diabetic Retinopathy \u2028Mediated by High Glucose Through \u2028Ameliorating Nrf2/HO-1 Pathway","authors":"Changhong Li, Buchao Shi, Dong Li, Hui Li","doi":"10.1177/09731296241247922","DOIUrl":"https://doi.org/10.1177/09731296241247922","url":null,"abstract":"Diabetic retinopathy (DR) is the foremost microvascular problem that causes drastic visual impairment in diabetes patients. Hyperglycemia-triggered reaction cascade of inflammation and oxidative stress constitute the DR pathogenesis. The existing treatment options are not completely satisfactory. We investigated the cell viability by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, inflammatory mediators, lactate dehydrogenase (LDH), superoxide dismutase, glutathione, and malonaldehyde (MDA) levels by ELISA and qRT-PCR assay, protein expression of Nrf2 and heme oxygenase-1 (HO-1) by western blotting assay were analyzed. According to our research, nerolidol (NRD) increases the proliferation and antioxidant activity of human retinal endothelial cells (HRECs) by inducing Nrf2/HO-1 signaling, while attenuating MDA, an oxidative stress marker, LDH, and inflammatory mediators. These outcomes suggest that a substantial reaction of inflammation and oxidative stress injury happened in DR, which might be correlated to the instigation of the signaling Nrf2/HO-1. NRD effectively suppresses oxidative stress and inflammation in HG-induced HRECs. The primary mechanism of NRD on DR may be linked to the activation of the Nrf2/HO-1 pathway and may give a useful medicine for DR treatment.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"33 40","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140966600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Tanshinone IIA on Cognitive Impairment in Alzheimer’s Disease Rats Via Oxidative Stress, Inflammatory Responses and Apoptosis","authors":"Wujiang Ren, Xiaoxiao Li, Tingqiao Wang, Yanxia Liu, Xueling Dai, Qing Huo, Shuo Wang, Qiusheng Zheng, Yaxuan Sun","doi":"10.1177/09731296241246632","DOIUrl":"https://doi.org/10.1177/09731296241246632","url":null,"abstract":"The rationale for the pathogenesis of Alzheimer’s disease (AD) is the production of amyloid-beta (Aβ) and its resultant toxic effects. In this work, rats with AD were used as models to assess the modulatory effects of tanshinone IIA (tan IIA) in alleviating cognitive impairment, oxidative damage, inflammation and apoptosis. Aβ1–42 was injected bilaterally in the hippocampus to establish an AD rat model. The effects of tan II A on the learning and memory capacities of AD rats were detected by ethological experiments. Tan IIA’s anti-inflammatory and antioxidant capacities were examined in this study using biochemical and immunohistochemical methods on rat hippocampus tissues. The experimental data showed that the cognitive ability of rats could be significantly improved by tan IIA. Furthermore, fewer injured neuron apoptosis was demonstrated in the tan IIA rats than in the AD group. More importantly, on the one hand, we discovered that the tan IIA group had considerably lower levels of interleukin 1 beta, tumour necrosis factor-alpha and inducible nitric oxide synthase. On the other hand, tan IIA was discovered to prevent oxidative stress by raising glutathione and superoxide dismutase activity and lowering malondialdehyde, protein carbonyl and 8-hydroxy-2′-deoxyguanosine levels. Tan IIA can alleviate cognitive impairment and neuronal cell damage by inhibiting oxidative stress and inflammatory responses during AD.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"13 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140969068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}