Pharmacognosy Magazine最新文献

{"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}

{"title":"Kaempferide Inhibits DOX-induced Liver Inflammation by Activating AMPKα/SIRT1","authors":"Qiang Li, Xing Li, Zhenchang Zhou, Pingwei Zhu, Nana Tuo, Jingli Ge, Zhaoyv Liu, Dengke Chen","doi":"10.1177/09731296241228923","DOIUrl":"https://doi.org/10.1177/09731296241228923","url":null,"abstract":"DOX can promote liver cell inflammation and lead to liver cell death. Ka protects and stabilizes liver cells for the treatment of hepatitis, cirrhosis, and other diseases. However, there is no evidence to suggest that Ka is associated with chemotherapy-related liver inflammation. Treat mice with DOX or Ka to induce or treat liver inflammation. Then, the body weight, liver weight, morphological changes, and liver inflammation of the mice were measured. Western blotting and RT-PCR were used to evaluate the AMPKα/SIRT1/NF-κB inflammatory signaling pathway and inflammatory gene expression. Finally, the above signaling pathways were verified in liver cells. DOX causes liver function damage and liver inflammation in mice. The specific manifestations are abnormal liver tissue structure in DOX mice; abnormal elevation of serum liver function markers ALP, ALT, AST, and GGT levels; abnormal elevation of serum inflammatory factors IL-1β, IL-6, IL-10, and TNF-α levels; and increased expression of liver inflammatory genes NF-κB, IL-1β, IL-6, TNF, and VCAM-1. Ka can effectively prevent and treat these changes. However, there was no significant change in the glucose and lipid metabolism levels of each group of mice. Further research suggests that the inhibitory effect of Ka on DOX-induced liver inflammation is mediated by the AMPKα/SIRT1/NF-κB signaling pathway. Primary liver cell studies have also confirmed the involvement of these signaling pathways and proteins. This study demonstrates that Ka can improve DOX-induced liver inflammation, including changes in inflammatory factors or genes in serum and liver tissue. Further research has found that its potential mechanism may be related to the AMPKα/SIRT1/NF-κB signaling pathway.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"115 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140967987","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":"Tibetan-Origin Edible Chinese Herbal \u2028Prescription C18 Protects H9C2 \u2028Cardiomyocytes from Cobalt Chloride-induced Hypoxia Injury Through the PI3K/AKT Signaling Pathway","authors":"Guoxin Chang, Hongyi Xie, Shu Chen, Ruixue Wang, Xuxin Zeng, Dingmei Lin, Zixuan Mo, Jingjing Yu, Xindan Liu, Zhaoguang Zheng, Yan Wang","doi":"10.1177/09731296241252202","DOIUrl":"https://doi.org/10.1177/09731296241252202","url":null,"abstract":"Altitude sickness is often prone to occur during tourism or work in high-altitude areas. In China, traditional Tibetan medicines have a long history of preventing or treating altitude sickness, especially altitude hypoxia, which may lead to myocardial cell apoptosis and myocardial hypoxia-reoxygenation injury. This study investigated the effect of a Tibetan-origin edible Chinese herbal prescription (named C18) on protecting H9C2 cardiomyocytes from cobalt chloride-induced hypoxia injury and its potential mechanism. In this study, a hypoxic injury model of H9C2 cardiomyocytes induced by cobalt chloride was established first. Then the cell viability, relevant antioxidant indicators malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and protein expression (hypoxia-inducible factor 1 alpha (HIF-1α), phosphoinositide 3-kinase (PI3K), phosphorylated protein kinase B (p-AKT)) were measured after pretreatment with or without C18. At last, the specific PI3K/AKT inhibitor LY294002 was applied to verify the antihypoxia signaling pathway. C18 could significantly promote normal H9C2 cardiomyocyte proliferation and inhibit apoptosis of hypoxic H9C2 cardiomyocytes, reduce the release of lactate dehydrogenase and MDA, and increase the levels of SOD and GSH-Px antioxidant enzymes. In addition, C18 could significantly downregulate the expression of HIF-1α protein and upregulate the expression of intracellular p-AKT. Moreover, these effects of C18 can be blocked by the specific PI3K/AKT inhibitor LY294002. C18 protects H9C2 cardiomyocytes from cobalt chloride-induced hypoxia injury through the PI3K/AKT signaling pathway.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"7 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140970018","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":"Lentinan Regulates Glioma Cell Proliferation and Apoptosis by Activating p53 and Caspases Pathways","authors":"Ying Sun, Peng Gao, Xilin Wan, Xinze Liu, Fang Xu, Jiaqi Wang","doi":"10.1177/09731296241253125","DOIUrl":"https://doi.org/10.1177/09731296241253125","url":null,"abstract":"Gliomas are highly lethal malignancies that develop in the central nervous system. The primary treatment for gliomas involves surgical resection followed by chemoradiotherapy. However, due to the infiltrative growth nature of gliomas, surgical resection is often incomplete. Moreover, the efficacy of chemotherapeutic drugs is constrained by their ability to cross the blood–brain barrier, and the currently utilized agents can lose effectiveness, particularly with prolonged administration. Lentinan, an active compound in Lentinula edodes, exhibits various pharmacological activities. This study aims to investigate the anti-tumor effects of lentinan on glioma U251 cells. Cell proliferation assays, cell fluorescence staining, scratch healing experiments, and transwell chamber experiments were conducted to assess the anti-tumor activity of lentinan on U251 cells. Additionally, quantitative real-time polymerase chain reaction (qPCR) and Western blot experiments were performed to validate the anti-tumor mechanism of lentinan. The findings revealed that lentinan significantly suppressed the proliferation of U251 cells, induced robust apoptosis, and decreased the cells’ migration and invasion capabilities. Furthermore, lentinan notably influenced the gene and protein expression of P53, Bcl-2, Cyto-c, Bax, Caspases, and MMP-9 in U251 cells. These findings suggest that lentinan may inhibit glioma cells by activating P53 and caspase-related apoptosis pathways.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"30 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140969179","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":"The Hepatoprotective Effect of Trigonelline in Diabetic Rat Through Insulin-related IRS1-GLUT2 Pathway: A Biochemical, Molecular, Histopathological, and Immunohistochemical \u2028Study","authors":"Meizhi Li, Shiqing Li, Shanshan Jiang, Weihong Li","doi":"10.1177/09731296241247365","DOIUrl":"https://doi.org/10.1177/09731296241247365","url":null,"abstract":"Background: Diabetes significantly increases morbidity and mortality rates, causing complications such as cardiovascular disease, kidney failure, and blindness. Purpose: The aim of this study was to investigate the hepatoprotective effects of trigonelline (TRIG) in diabetic rats through the antioxidative, anti-inflammatory, and insulin-related IRS1-GLUT2 pathway. Methods: In this experimental investigation, sixty male Wistar rats (n = 10/group) were randomly divided into six groups: a healthy group (HEL), healthy rats treated with 1500 and 3000 mg/kg of TRIG, a diabetic (D), and diabetic rats treated with 1500 and 3000 mg/kg of TRIG (D+ TRIG). The effects of TRIG on rats with induced diabetes were evaluated by serum biochemical parameters, such as insulin, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), free fatty acids (FFA), nitric oxide, and adiponectin levels. The activities of hepatic carbohydrate metabolic enzymes (hepatic glucokinase, glucose 6-phosphatase, glycogen, and glucose-6-phosphate dehydrogenase) were also measured. Furthermore, the expression levels of genes and proteins associated with carbohydrate/lipid metabolism, including peroxisome proliferator-activated receptor gamma (PPARg), glucose transporter 2 (GLUT2), insulin receptor substrate 1 (IRS1), sterol regulatory element-binding protein 1c (SREBP-1c) were analyzed using real-time PCR and western blotting techniques, respectively. Liver sections were examined using H&E staining and immunohistochemistry targeting the p53 protein. Results: The results showed that 3000 mg/kg TRIG was able to suppress TNF-α, IL-6, and FFA by inhibiting inflammatory pathways along with increasing the activity of antioxidant enzymes. TRIG treatment regulated serum levels of insulin, adiponectin, and hepatic carbohydrate metabolic enzymes as well as glycogen content by regulation of the IRS1/ GLUT2- SREBP-1c/ PPARg pathway. Conclusion: These results provide evidence that TRIG has the potential to protect liver organs from oxidative damage in diabetic patients.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"24 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140982484","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":"Huanglian Jiedu Decoction Inhibits LPS-induced Neuroinflammation and Attenuates the \u2028Activation of NLRP3 Inflammasome in \u2028BV2 Cells","authors":"Junli Wang, Rui Wang, Yaming Du, Xinzi Xu, Xin Liu, Wei Shao, Guohua Chen","doi":"10.1177/09731296241244575","DOIUrl":"https://doi.org/10.1177/09731296241244575","url":null,"abstract":"Background: Huanglian Jiedu decoction (HLJDD) is a classical herbal formula for treating inflammatory diseases with Traditional Chinese Medicine (TCM). However, the impacts of HLJDD on neuroinflammation and the precise mechanisms involved remain poorly understood. Purpose: In the present study, HLJDD was found to inhibit lipopolysaccharide (LPS) induced neuroinflammatory responses in BV2 microglia via regulating NLRP3 inflammasome activation. Methods: Anti-inflammatory activity was evaluated with ELISA assay and the polarization changes were observed using immunofluorescent staining. The levels of NLRP3 inflammasome activation were determined using qPCR and Western blotting. Results: The administration of HLJDD successfully countered LPS-induced neuroinflammatory responses by attenuating microglial activation and fostering a phenotypic conversion from the pro-inflammatory M1 to the anti-inflammatory M2. . Additionally, HLJDD treatment demonstrated inhibition of NLRP3 inflammasome activation. Conclusion: The findings of the present study may provide insights into how HLJDD could be a therapeutic drug for neuroinflammatory diseases associated with regulating NLRP3 inflammasome and microglial activation.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":" 37","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140997225","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":"Fraxinus excelsior L. for Prevention of \u2028Capecitabine-induced Enterocolitis in Rat: An Integrated Biochemical, Molecular, and Histopathological Study","authors":"Li Li, HaiYan Tan, TianLu Su","doi":"10.1177/09731296241244561","DOIUrl":"https://doi.org/10.1177/09731296241244561","url":null,"abstract":"Background: Chemotherapy drugs damage intestinal cells, weakening the intestinal barrier. This damage results in higher permeability, which enables bacteria and toxins to enter the intestinal tissue. Purpose: This study aimed to explore the protective effects of Fraxinus excelsior L. (F. excelsior) extract against Capecitabine (CT)-induced enterocolitis. Methods: Fifty Wistar rats were divided into five groups: sham, F. excelsior (750 mg/kg orally), CT (500 mg/kg orally), and two co-treatment groups receiving CT with F. excelsior (500 and 750 mg/kg orally). After 50 days, rats were sacrificed, and blood samples were collected for various analyses. Biochemical assessments included measurements of serum nitric oxide, catalase, glutathione peroxidase, and superoxide mutase enzymes. Tissue oxidative stress was evaluated through FRAP, thiol, and TBARS levels. Pro-inflammatory cytokines were quantified using ELISA, and apoptosis was assessed through the evalution of p53/Bax/Bcl-2 pathway. Histopathological examination affirmed the preservation of tissue structure in groups treated with F. excelsior extract. Results: F. excelsior extract reduced intestinal cell apoptosis and elevated the expression of intestinal aquaporin (AQP) genes/proteins by enhancing antioxidant enzymes and diminishing free radicals. Additionally, the extract modulated inflammatory cytokine levels, regulated antidiuretic hormone (ADH) and arginine vasopressin (AVP) levels, maintaining serum and intestinal osmotic balance. The study also revealed decreased expression of pro-inflammatory cytokines and a positive impact on water homeostasis-related genes (AQP3, AQP8, AQP10). Conclusion: The study concludes that F. excelsior extract exhibits potential benefits in treating enterocolitis in individuals undergoing chemotherapy, emphasizing its ability to mitigate oxidative stress, inflammation, apoptosis, and maintain osmotic balance.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":" 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140995717","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":"A Review of a Traditional Chinese Medicine Formula for Treating Insomnia with \u2028Depression: Wendan Decoction","authors":"Lingyuan Kong, Xinyi He, Xiuyang Li","doi":"10.1177/09731296241246313","DOIUrl":"https://doi.org/10.1177/09731296241246313","url":null,"abstract":"Background: The relationship between insomnia and depression is complex and two-way. Long-term insomnia may cause, maintain, and aggravate depression, and with the development of the disease, depression patients will also experience insomnia symptoms. Oral medication is currently the main treatment for insomnia with depression (ID). Drugs such as Estazolam have good anti-anxiety and insomnia effects, high safety, and relatively small side effects. They are widely used in the treatment of ID in clinics, but some patients still have adverse reactions or low efficacy when taking Estazolam and other drugs. In recent years, Chinese herbal medicine and TCM prescriptions for the treatment of mental illness have been more and more accepted and studied by international scholars. The efficacy of Wendan Decoction (WDD) has been tested by ancient China for nearly 1,400 years, and with the development of modern pharmacological research, it is widely used in the treatment of insomnia and depression. Purpose: Therefore, based on the understanding of ID in TCM, this article discusses the pharmacodynamic effect of WDD, and based on existing clinical and experimental studies, comprehensively analyzes the clinical observation, mechanism of action, and pharmacological effect of WDD in the treatment of ID, to provide more clinical experience and experimental theoretical support for WDD in the treatment of ID. Methods: Retrieve Chinese and English literature on the treatment of ID with WDD from databases such as Web of Science, etc. Conclusion: WDD has good therapeutic effects on ID.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":" 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140996571","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":"Investigating the Anti-adipogenic Potential of Xanthium strumarium Linn. Leaves Fractions: HPTLC-MS Characterization, Enzymatic Analysis, and 3T3-L1 Adipocyte Differentiation Assay in Oxidative Stress-modulated Adipogenesis Cascade","authors":"Nikita Nayak, A. Pattnaik","doi":"10.1177/09731296241242842","DOIUrl":"https://doi.org/10.1177/09731296241242842","url":null,"abstract":"Background: Molecular pathogenesis of obesity is initiated by cellular oxidative stress along with increased adipogenesis. For the search of better alternatives of synthetic molecules in terms of their adverse events, naturally, existing compounds are now a research focus. In this context, Xanthium strumarium ( X. strumarium) Linn. exhibited anti-diabetic activities and proved to have efficacy in neutralizing very near pathological targets to obesity. Purpose: This study is aimed toward bioactivity-guided fraction isolation of methanolic leaves extract, where bioactivity refers to anti-adipogenesis and anti-oxidant efficacy in in vitro enzymatic and three-day transfer, inoculum 3×105 cells (3T3-L1) adipocyte differentiation assay. Materials and method: Collection and drying of the raw leaves followed by cold extraction in methanol and flash chromatography for bioactive fraction isolation. 3T3-L1 cell line was utilized for adipocyte differentiation assay of those and on the other hand in vitro pancreatic lipase, α-glucosidase, and α-amylase enzymatic assays were analyzed. Based on exhibited activities, selected fractions are further characterized by high-performance thin-layer chromatography-mass spectrometry (HPTLC-MS). Results: The most active fractions from these assays underwent characterization via HPTLC-MS. Fractions 2 and 3 exhibited potent activities in all enzymatic assays (α-glucosidase IC50: 2.48 ± 0.015, 2.84 ± 0.030 µg/mL; α-amylase IC50: 1.98 ± 0.050, 1.79 ± 0.045 µg/mL; pancreatic lipase IC50: 3.16 ± 0.030, 3.18 ± 0.040 µg/mL) and displayed significant inhibition of adipocyte differentiation in 3T3-L1 cell line. These fractions further identified through HPTLC-MS, contained compounds like β-sitosterol and quercetin, affirming their potential bioactivity. Conclusion: The study underscores the potential of X. strumarium Linn. fractions as promising natural alternatives for combating obesity-related pathways, highlighting their significance in developing future anti-obesity therapeutics.","PeriodicalId":508089,"journal":{"name":"Pharmacognosy Magazine","volume":"7 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141018821","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}