Pharmacognosy Magazine最新文献

{"title":"Therapeutic Effects of <i>Dendrobium</i> Extract on Pathologic Lens Alterations in Diabetic Cataract Patients","authors":"Baoping Duan, Hongyan Ge, Meng Sun, Sheng Su, Shiqiang Zhao, Ping Liu","doi":"10.1177/09731296251325353","DOIUrl":"https://doi.org/10.1177/09731296251325353","url":null,"abstract":"Background Diabetic cataract, an ocular complication arising from diabetes, can lead to damage to ocular tissues, particularly affecting the lens and causing symptoms such as blurred vision. Objectives This work aimed to demonstrate the therapeutic effects of Dendrobium extract (DE) on pathogenic lens alterations in diabetic cataract patients and an ocular complication arising from diabetes, and to comprehensively assess its in vitro and clinical research outcomes. Materials and Methods Initially, a diabetic cataract cell model was established using high glucose (HG)-induced human lens epithelial cells (HLEB3). The cells were categorized into three groups: the untreated control (UC) group, the HG treatment group, and the HG+DE treatment group. Apoptosis status, reactive oxygen species (ROS), superoxide dismutase (SOD), as well as Bcl-2, Bax, and caspase-3 within the cells, were comparatively analyzed to evaluate the impact of DE on diabetic lens epithelial cells. Subsequently, a cohort of 60 diabetic cataract patients were recruited and randomly allocated into Group C (control group, 30 cases), which received conventional ophthalmic medications and blood glucose control, and Group E (experimental group, 30 cases), which received the DE intervention in addition to the Group C regimen. A comparative assessment of visual acuity, intraocular pressure (IOP), and cataract grading before and after treatment was conducted between the two groups to evaluate the therapeutic efficacy of DE on patient lenses. Results In the in vitro study, the HG+DE group exhibited a drastically inferior apoptotic rate compared to the HG group (.05). The production of ROS in the HG+DE group was drastically inferior, and the SOD levels were markedly superior to those in the HG group ( p &lt; .05). The HG group and HG+DE group showed a greater decrease in Bcl-2 protein levels and a greater increase in Bax and caspase-3 protein levels versus the UC group ( p &lt; .05). Moreover, the HG+DE group displayed notably elevated Bcl-2 protein levels and greatly reduced Bax and caspase-3 protein levels versus the HG group ( p &lt; .05). The in vivo study demonstrated that Group E patients exhibited markedly improved visual acuity recovery versus Group C patients ( p &lt; .05), along with more stable IOP. The cataract grading of Group E patients was remarkably superior to that of Group C patients ( p &lt; .05). Conclusion DE may contribute to ameliorating ocular lesions in diabetic cataract patients, mitigating lens damage, and could potentially emerge as a promising therapeutic option.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 1","pages":"80-89"},"PeriodicalIF":0.0,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251325353","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147895730","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":"Biological Activity and Cell Cycle Effects of Natural Extract Kaempferol on Androgen-dependent Prostate Cancer Cells","authors":"Meikang Peng, Tao Chen, Hui-Liu Peng","doi":"10.1177/09731296251325350","DOIUrl":"https://doi.org/10.1177/09731296251325350","url":null,"abstract":"Background There is an abnormal enhancement of androgen receptor activity in prostate cancer cells, leading to increased sensitivity to androgens and the promotion of cancer cell proliferation. Objectives This study aimed to investigate the effects of Eucommia ulmoides leaf-derived kaempferol extract on the biological activity and cell cycle of androgen-dependent prostate cancer cells (LNCaP) through in vitro cell culture experiments. Materials and Methods Kaempferol was isolated and extracted from the hydrolysate of E. ulmoides leaves, and its clearance rates for superoxide anion (O 2 − ) and hydroxyl radical (·OH) were analyzed. Subsequently, LNCaP cells were treated with kaempferol at concentrations of 0.0, 0.5, 1.0, and 2.0 µmol L⁻¹ and grouped accordingly. Changes in cell proliferation inhibition rate, apoptosis rate, cell cycle distribution, and levels of apoptosis-related proteins were assessed. Results The recovery rate of kaempferol from E. ulmoides leaves was approximately 98.23%, with kaempferol contents of 0.008% before hydrolysis and 0.089% after hydrolysis. As the concentration of kaempferol increased, the clearing rate (CR) of O 2 − and ·OH free radicals also gradually increased ( p &lt; .05). In contrast to the 0.0 µmol L⁻¹ group, the 0.5, 1.0, and 2.0 µmol L⁻¹ groups have exhibited greatly enhanced proliferation inhibition rate and apoptosis rate of LNCaP, a remarkable decrease in the S-phase proportion, a substantial increase in the G2/M-phase proportion, and a significant reduction in Bcl-2 protein. Conversely, expressions of Bax, caspase-3, and caspase-9 were significantly upregulated ( p &lt; .05). Conclusion E. ulmoides leaf-derived kaempferol extract demonstrated a pronounced antioxidant effect. Kaempferol was found to inhibit LNCaP proliferation and promote its apoptosis by modulating the cell cycle and the apoptosis-related proteins.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 1","pages":"194-202"},"PeriodicalIF":0.0,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251325350","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911746","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":"Integrate Molecular Docking and Animal Model Validation into the Research of the Effect and Potential Mechanism of Eupatilin Against Myocardial Ischemia/Reperfusion Injury","authors":"Yulong Li, Xiang Li","doi":"10.1177/09731296251323316","DOIUrl":"https://doi.org/10.1177/09731296251323316","url":null,"abstract":"Background Myocardial ischemia/reperfusion (I/R) injury refers to myocardial tissue damage caused by blood reperfusion after acute heart ischemia caused by coronary artery thrombosis and others. This process is closely related to inflammation and endoplasmic reticulum (ER) stress, and there is currently no ideal prevention means. In recent years, some traditional natural plant products with anti-inflammatory and anti-ER stress properties have been used to counteract myocardial I/R injury. Eupatilin (EPT), a pharmacologically active flavone derived from the Artemisia plant species, possesses significant anti-inflammatory and anti-ER stress activity. Still, its protective effect against myocardial I/R injury in vivo has not been revealed. Objectives This study aimed to evaluate EPT’s effect and potential mechanism against myocardial I/R injury. Materials and Methods The rat myocardial I/R injury model was prepared and treated with EPT. Then, the levels of myocardial injury markers and hematoxylin and eosin staining were used to evaluate the pathological damage of the myocardial tissue. Western blotting was used to detect the expression of key proteins in the potential signaling pathways. Results It was found that EPT could significantly reduce the levels of myocardial injury markers lactate dehydrogenase and creatine kinase, decrease the levels of inflammatory factors, and reduce apoptosis and pathological damage in myocardial tissue. In addition, the expression of key proteins in purinergic P2x7 receptor (P2X7R)/NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3)/suppressor of cytokine signaling 3 (SOCS3) pro-inflammatory pathways, and pancreatic endoplasmic reticulum eIF2alpha kinase (PERK/eIF2α)/activating transcription factor 4 (ATF4)/C/EBP homologous protein (CHOP) ER stress pathway was significantly downregulated in the EPT-treated group. Molecular docking simulations showed that this may be associated with the fact that EPT can bind to P2X7R, PERK, and other proteins in the aforementioned pathways. Conclusion This study demonstrated that EPT could attenuate myocardial I/R injury in rats, and the protective mechanism was related to the ability of EPT to bind to the initiating proteins of the P2X7R/NLRP3 pro-inflammatory pathway and the PERK/eIF2α/ATF4/CHOP ER stress pathway, which inhibited the inflammatory response and ER stress, thus reducing cardiomyocyte apoptosis. Our findings provide some valuable references for the future application of EPT in treating myocardial I/R injury.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 1","pages":"136-146"},"PeriodicalIF":0.0,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251323316","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878772","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":"Chemical Composition and Anti-arthritic Potential of Himalayan Marmot Oil Against Type II Collagen-induced Rat Rheumatoid Arthritis","authors":"Jie Zhou, Weilong Li, Xina Yu, Ye Wu, Pei Luo, Qingquan Kong, Zhifeng Zhang","doi":"10.1177/09731296251322836","DOIUrl":"https://doi.org/10.1177/09731296251322836","url":null,"abstract":"Background Animal-derived remedies are prominent in folk medicine worldwide, and discovering potent anti-inflammatory agents is attractive for rheumatoid arthritis (RA) treatment. Himalayan marmot oil (HMO), a traditional Tibetan medicine topically or orally used for burns and arthritis, has been common in Tibetan areas for centuries. However, the composition and systematic pharmacological evaluation of HMO are still unclear. Objectives This study focused on the chemical composition and anti-inflammatory effects of HMO in vitro and in vivo to expand the topical value of the application of HMO in RA. Materials and Methods First, the chemical composition of HMO was explored by gas chromatography–mass spectrometry (GC–MS). Then, we established a bioassay system for L929 cells and RAW 264.7 cells to evaluate the effect of HMO on cytotoxicity and inflammatory responses. The anti-arthritic evaluation involved testing for paw swelling, swelling inhibition, and histological analysis in collagen-induced arthritis (CIA) rats. Enzyme-linked immunosorbent assay, Western blot analysis, and quantitative real-time polymerase chain reaction were performed to determine the effect of HMO on the production and secretion of inflammatory cytokines. Results GC–MS results showed that seven categories of chemical substances, including 261 compounds in HMO, and the main components of HMO were saturated fatty acids and unsaturated fatty acids. HMO showed low toxicity in cells according to the CCK-8 tests. In CIA model rats, HMO obviously inhibited hind paw swelling and reduced the arthritis index. Pathological staining results and micro-CT imaging indicated that HMO attenuated synovial hyperplasia and inflammatory cell infiltration in joint tissues. Meanwhile, in vivo and in vitro , HMO significantly inhibited interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels, while the expression of interleukin-10 (IL-10) was increased. Conclusion The current work identified an excellent anti-inflammatory animal-derived medicinal agent, HMO, in alleviating synovial inflammation and joint destruction by regulating IL-6, IL-10, and TNF-α expression with low toxicity, which provides a protective effect against RA. Our study expands the topical value of the application of HMO to inhibit the progression of inflammation, and it could be a safe, novel RA complementary therapy.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1549-1561"},"PeriodicalIF":0.0,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251322836","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147886584","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 Action of Raspberry Natural Extract on Apoptosis in Human Brain Artery Aneurysm Vascular Endothelial Cells","authors":"Junti Lu, Yanhui Zhou, Zhenyu Xia, Bowen Yang, Gao Wu, Hui Gui, Shiwen Guo","doi":"10.1177/09731296251321210","DOIUrl":"https://doi.org/10.1177/09731296251321210","url":null,"abstract":"Background and Objectives Raspberry natural extract exhibits a regulatory effect on apoptosis in human brain artery aneurysm vascular endothelial cells (VECs). This work was to gain deeper insights into the impact of raspberry extract on apoptosis in VECs in the treatment of human brain artery aneurysms, along with the associated molecular mechanisms, thereby providing scientific support for its application in the treatment of human brain artery aneurysms. Materials and Methods High-performance liquid chromatography was employed to determine the primary components of raspberry extract. Human brain artery aneurysm VECs were divided into the following groups: model (M) group, raspberry low-dose (LD) group (50 µg/mL), raspberry medium-dose (MD) group (100 µg/mL), raspberry high-dose (HD) group (150 µg/mL), and normal human brain artery VECs as the control (C) group. Cell viability was assessed under 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide assay. Levels of relevant proteins were measured under Western blot, and related indicators were evaluated in each group. Results Raspberry extract included ellagic acid, rutin, kaempferol-3- O -rutinoside, oleanolic acid, tiliroside, quercetin, and kaempferol. The cell viability of brain VECs in the raspberry extract groups was drastically superior to that in the M group ( p &lt; 0.05). In the HD group, cell viability of brain VECs was drastically superior to that in the LD group ( p &lt; 0.05). Brain VECs in the raspberry extract groups exhibited greatly inferior levels of matrix metalloproteinase-9 (MMP-9), interleukin (IL)-17A, and endothelin (ET)-1 to M group ( p &lt; 0.05). In the HD group, brain VECs showed notably lower levels of MMP-9, IL-17A, and ET-1 versus the LD group ( p &lt; 0.05). PI3K and AKT in brain VECs were substantially superior in the raspberry extract groups to the M group ( p &lt; 0.05). In HD group, levels of Bax, Caspase8, Cleaved-caspase8, Caspase12, Cleaved-caspase12, Caspase3, and Cleaved-caspase3 in brain VECs were markedly inferior to those in LD group ( p &lt; 0.05), while Bcl-2 level in HD group was drastically superior to LD group ( p &lt; 0.05). Conclusion Raspberry natural extract can enhance the survival rate of brain VECs, suppress cell apoptosis, and protect VECs. Raspberry extract can reduce inflammatory factors in brain VECs, activate PI3K/AKT signaling, and modulate apoptosis-related protein levels.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 1","pages":"265-276"},"PeriodicalIF":0.0,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251321210","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147921654","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>Moringa oleifera</i> Leaf Extract Enhances the Viability and Inhibits Ferroptosis in High Glucose-induced Rat Podocytes by Downregulating ACSL4","authors":"Meixiao Liu, Yue-Lin Sui, Yin Pang, Jianhui Liu, Haifeng Zhang","doi":"10.1177/09731296251322834","DOIUrl":"https://doi.org/10.1177/09731296251322834","url":null,"abstract":"Background Diabetic nephropathy (DN) is a severe complication in patients with diabetes mellitus, which is mainly characterized by glomerular podocyte injury. Ferroptosis is crucial in the pathogenesis of DN. Moringa oleifera leaf extract (MOLE) has attracted attention due to its multiple pharmacological activities, but it is unclear whether it can delay the progression of DN by inhibiting ferroptosis. Objectives To investigate whether MOLE can alleviate podocyte injury and delay the progression of DN by inhibiting ferroptosis. Materials and Methods DN model cells were established using rat podocytes induced by high glucose (HG); the cells were processed with MOLE, dapagliflozin (DAPA, positive control), and acyl-CoA synthetase long-chain family member 4 (ACSL4) overexpression plasmids. Cell viability, Fe 2+ concentration, reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) levels were monitored by Cell Counting Kit-8 (CCK-8) and corresponding kits. Results MOLE treatment markedly enhanced HG-induced rat podocyte viability, decreased intracellular Fe 2+ concentration, ROS level, MDA concentration, and elevated GSH concentration. ACSL4 overexpression reversed the protective effect of MOLE on podocytes. Conclusion MOLE ameliorates rat podocyte injury and delays DN progression by inhibiting ACSL4-mediated ferroptosis. This finding provides a theoretical basis for further developing MOLE-based therapeutic agents for DN treatment.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1574-1584"},"PeriodicalIF":0.0,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/09731296251322834","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147880113","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":"Scutellarin Nanoparticles Inhibit Colon Cancer by Regulating Ferroptosis","authors":"Yuanzhi Li, Chaochi Yue, Yingyin Liao, Weiliang Du","doi":"10.1177/09731296251320700","DOIUrl":"https://doi.org/10.1177/09731296251320700","url":null,"abstract":"Background In our previous research, we addressed the issues of poor stability and water solubility of scutellarin by developing scutellarin nanoparticles. Our findings indicated that these nanoparticles exhibited enhanced anti-colon cancer activity compared to scutellarin alone. However, the underlying mechanisms of scutellarin’s anti-colon cancer effects require further investigation. Scutellarin is known to suppress the proliferation of different tumor cells. In this study, we explored whether scutellarin, encapsulated in nanoparticles, could suppress the proliferation of colon cancer cells by modulating ferroptosis. Objectives In this study, we explored whether scutellarin, encapsulated in nanoparticles, could suppress the proliferation of colon cancer cells by modulating ferroptosis. Materials and Methods SW480 and HCT-116 cells were divided into (a) control group, scutellarin group, and scutellarin nanoparticles group; and (b) control group, scutellarin nanoparticles group, ferrostatin-1 group, and scutellarin nanoparticles + ferrostatin-1 group. First, we determined the half-maximal inhibitory concentration of colon cancer cells by Cell Counting Kit-8 (CCK-8) assay. Then, the ferroptosis of cells in each group was detected, and the levels of oxidative stress-related factors, superoxide dismutase (SOD) and malondialdehyde (MDA), were detected by biochemical kits. Cell death was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay, cell invasion was detected by Transwell assay, and reactive oxygen species (ROS) levels were detected by flow cytometry. Western blotting was used to detect ferroptosis-related glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), and ferroportin 1 (FPN1) expression levels. Results We found that in SW480 and HCT-116 cells, the IC50 of scutellarin nanoparticles cells was lower, cell apoptosis and invasion were more obvious, the oxidative stress level was also higher, Fe 2+ content was increased, and the expression of GPX4, SLC7A11, and FPN1 was decreased. These results were changed after the addition of ferrostatin-1. Conclusion Scutellarin nanoparticles have a better anti-tumor effect than the same dose of scutellarin. Scutellarin nanoparticles can inhibit the proliferation, migration, and invasion of cancer cells by promoting ferroptosis, as well as cell apoptosis.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1510-1518"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147887578","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>Astragalus</i> Polysaccharide Regulates Epithelial-mesenchymal Transition in HepG2 Liver Cancer Cells by Inhibiting NLRP3 Inflammasome Activation","authors":"Hongtao Sui, Hai Yang, Zongyuan Huang, Caihua Zhang","doi":"10.1177/09731296251318411","DOIUrl":"https://doi.org/10.1177/09731296251318411","url":null,"abstract":"Background Epithelial-mesenchymal transition (EMT) is crucial in liver cancer progression. Developing novel medicines to disrupt the progression of EMT might be a novel approach in managing liver cancer. Objectives This study investigates the protective role of Astragalus polysaccharide (APS), a bioactive compound derived from Astragalus membranaceus , in modulating EMT in HepG2 liver cancer cells. Materials and Methods The effects of APS on EMT progression were evaluated by assessing cell viability, proliferation, invasion, migration, cell cycle, and apoptosis in HepG2 cells. Furthermore, the involvement of the NOD-like receptor protein 3 (NLRP3) inflammasome in this process was explored. Results APS treatment significantly inhibited the viability, proliferation, invasion, and migration of HepG2 cells while promoting cell cycle arrest and apoptosis. Notably, APS reduced the expression of NLRP3 inflammasome components, including NLRP3, apoptosis-associated speck-like protein, and caspase-1, while decreasing the levels of inflammatory cytokines. In addition, the activator Nigericin dampened the effect of APS by partially rescuing the activity of NLRP3. Specifically, Nigericin promoted the development of EMT inhibited by APS and exacerbated the malignant transformation of HepG2 cells improved by APS. Conclusion Our findings demonstrated the function of APS in liver cancer and the process by which APS inhibits NLRP3 inflammasome activation to protect the EMT of HepG2 cells. Our results showed that by targeting NLRP3, the application of APS appears to be a viable tactic for preventing the progression of liver cancer.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1267-1277"},"PeriodicalIF":0.0,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911933","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 Ginkgo Diterpene Lactone Meglumine Injection Promoting Angiogenesis and Improving Cerebral Perfusion in Cerebral Infarction Rats","authors":"Tao Zhan, Ruixia Li, Jiahui Shen, Xinya Chen, Pingguo Liu","doi":"10.1177/09731296251313639","DOIUrl":"https://doi.org/10.1177/09731296251313639","url":null,"abstract":"Background In recent years, traditional Chinese medicine has shown advantages in treating ischemic cerebrovascular diseases, including multi-component, multi-target, and low toxicity effects. Objectives The aim of this study was to clarify the impact of ginkgo diterpene lactone meglumine injection (GDLMI) on promoting microvascular neovascularization and improving cerebral perfusion after cerebral infarction (CIF) in rats and to explore its underlying mechanisms in promoting angiogenesis. Materials and Methods Seventy-five rats were randomly rolled into Sham (sham surgery) group, Model (acute CIF model) group, low-dose (LD) (1 g/kg bw GDLMI) group, medium-dose (MD) (3 g/kg bw GDLMI) group, and high-dose (HD) (5 g/kg bw GDLMI) group. The neurological function of rats was evaluated using the Longa method. Micro-PET was performed to evaluate brain metabolism status at 7 days post-reperfusion. Serum expression levels (ELs) of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were measured. Brain tissue samples were collected to assess cerebral infarct volume and to measure oxidative stress (OS) markers, including superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA). TdT-mediated dUTP nick end labeling (TUNEL) was performed to detect the apoptosis rate of cortical neurons. Western blotting was conducted to determine brain tissue’s ELs of vascular endothelial growth factor (VEGF), angiopoietins-1 (Ang-1), p-PI3K, and p-AKT proteins. Results Rats in Model group exhibited higher Longa scores and increased cerebral infarct volume, decreased brain 18 F-FDG content, elevated serum ELs of IL-1β, IL-6, and TNF-α, reduced SOD and CAT activities, increased MDA content in brain tissue, elevated apoptosis rate of cortical neurons, and elevated protein ELs of VEGF and Ang-1 in brain tissue, accompanied by decreased ELs of p-PI3K and p-AKT proteins compared to the Sham group ( p &lt; 0.05). Rats in the LD, MD, and HD groups showed decreased Longa scores and cerebral infarct volume, increased brain 18 F-FDG content, decreased ELs of IL-1β, IL-6, and TNF-α, increased SOD and CAT activities, decreased MDA content in brain tissue, decreased apoptosis rate of cortical neurons, and increased protein ELs of VEGF, Ang-1, p-PI3K, and p-AKT in brain tissue versus Model group ( p &lt; 0.05). The effects on all indicators in rats showed a dose-dependent trend. Conclusion GDLMI has a protective effect against acute CIF/reperfusion injury (RI), which may be attributed to its ability to suppress inflammation and OS damage by activating PI3K/AKT signaling.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"22 1","pages":"277-288"},"PeriodicalIF":0.0,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147919521","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":"Astragaloside IV Alleviates Myocardial Fibrosis After Myocardial Infarction through SIRT3/β-catenin/PPARγ Signaling Pathway","authors":"Jinghu Liu, Haokun Zhou, Zhitao Hu, Xiang-Di Tan, Yan Yao","doi":"10.1177/09731296251313634","DOIUrl":"https://doi.org/10.1177/09731296251313634","url":null,"abstract":"Background Myocardial fibrosis following myocardial infarction (MI) is linked to decreased cardiac function and heart failure. Astragaloside IV (AST IV), a component of traditional Chinese medicine, has shown promise in animal studies for improving cardiac function. Objectives This study intends to investigate the role of AST IV in MI and its correlation with the sirtuin-3 (SIRT3)/β-catenin/peroxisome proliferator-activated receptor gamma (PPARγ) signaling pathway. Materials and Methods After the establishment of an animal model of MI, 60 rats were divided into a control group, model group (MI group), positive control group (sham group), low-dose AST IV group (0.8 mg/100 g), and high-dose AST IV group (3 mg/100 g). The animals were injected once a day for 4 consecutive weeks. To further investigate the mechanism of action of AST IV, another nine rats from the model group were randomly divided into the 3TYP group (5 mg/100 g), SKL2001 group (20 µmol/L, 10 mL/kg), and T0070907 group (0.15 mg/100 g), with three rats in each group. The rats in each group were intervened once a day by intraperitoneal injection and once a day by gavage for 4 consecutive weeks. Hemodynamics, cardiac function, ventricular weight, and infarct area were assessed at 1, 2, and 4 weeks post-surgery. Myocardial collagen content in the non-infarcted area was measured, the expression rate of transforming growth factor-beta and ED-positive cells was calculated, and reverse transcription polymerase chain reaction was used to detect SIRT3, β-catenin, and PPARγ mRNA expression. Results The left ventricular ejection fraction, short-axis shortening rate, and left ventricular mass in the model group were decreased obviously. AST IV treatment decreased systolic blood pressure, +dp/dtmax, –dp/dtmax, and left ventricular end-diastolic pressure, as well as reduced myocardial collagen deposition in rat hearts ( p &lt; 0.05). AST IV inhibited the SIRT3/β-catenin/PPARγ signaling pathway when alleviating myocardial fibrosis. Intervention with SIRT3 blocker 3-TYP, β-catenin agonist SKL2001, and PPARγ blocker T0070907 reversed the inhibitory effect of AST IV on the signaling pathway. Conclusion AST IV exhibits significant anti-fibrotic effects, effectively reducing collagen deposition in the MI model, improving cardiac function parameters, and decreasing markers such as creatine kinase-MB. It significantly regulates SIRT3, β-catenin, and PPARγ to exert cardioprotective effects. The key mechanism involves inhibiting the SIRT3/β-catenin/PPARγ, offering an innovative strategy for post-MI treatment.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"21 4","pages":"1323-1333"},"PeriodicalIF":0.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147879110","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}