Huan Cheng, Yichun Wang, Chengjian Ji, Yong Wang, Da Zhong, Ninghong Song
{"title":"Vitamin D Regulates Cooperation Between Metadherin and Transcription Factor Lymphoid Enhancer-Binding Factor 1 in Prostate Cancer Development and Progression","authors":"Huan Cheng, Yichun Wang, Chengjian Ji, Yong Wang, Da Zhong, Ninghong Song","doi":"10.37290/ctnr2641-452x.22:1193-1204","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:1193-1204","url":null,"abstract":"The incidence of prostate cancer is increasing, and its poor prognosis is associated with metadherin overexpression; however, its molecular mechanisms are unclear. This study used Western blot, quantitative real-time polymerase chain reaction, immunofluorescence, and tumorigenicity assays to investigate metadherin and epithelial-mesenchymal transition in prostate cancer. We found that metadherin was highly expressed in prostate cancer tissues, especially PC-3 cells. Metadherin overexpression promoted t epithelial-mesenchymal transition and tumor growth. Bioinformatics analysis and assays revealed that lymphoid enhancer-binding factor 1 directly activates the metadherin promoter. The epithelial-mesenchymal transition and tumorigenicity were suppressed by the silencing of lymphoid enhancer-binding factor 1; however, these effects were reversed by metadherin overexpression. Vitamin D treatment downregulated metadherin and lymphoid enhancer-binding factor 1, counteracting lymphoid enhancer-binding factor 1-induced metadherin upregulation. Our findings indicate that metadherin enhances epithelial-mesenchymal transition and tumorigenicity through lymphoid enhancer-binding factor 1, with vitamin D modulating this interaction in prostate cancer.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 4","pages":"1193-1204"},"PeriodicalIF":0.0,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147916490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Magnolol plays a protective role in the kidney of rats with diabetic nephropathy","authors":"Meihua He, Chao Dong, Sha Xiang","doi":"10.37290/ctnr2641-452x.22:8-13","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:8-13","url":null,"abstract":"This study investigated the protective effects of magnolol on the kidneys of diabetic nephropathy (DN) rats via the mitogenactivated protein kinase/nuclear factor-kappa-B (MAPK/NF-κB) signaling pathway. Rats were divided into control, diabetic control, low-dose magnolol, and high-dose magnolol groups. The DN model was induced by a high-glucose/high-fat diet and streptozocin injection. The results showed that in the diabetic control group, various parameters indicative of DN worsened compared to the control group. However, in the magnolol-treated groups, there were improvements in glucose levels, urine volume, proteinuria, kidney function markers, inflammatory factors, and renal tissue morphology. Magnolol treatment also correlated with the decreased activation of extracellular regulated protein kinases, c-jun N-terminal kinase, p38 MAPK, and increased levels of the inhibitor of NF-κB, suggesting inhibition of the MAPK/NF-κB signaling pathway. These findings suggest that magnolol exerts a protective effect on DN rats by inhibiting the MAPK/NF-κB signaling pathway and reducing inflammatory cytokines, such as tumor necrosis factor-α, interleukin-6, and interleukin-1β.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"23 1","pages":"8-13"},"PeriodicalIF":0.0,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147877893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Platycodin D Exerts Anticancer Effects by Promoting Mitochondrial Apoptosis in Laryngeal Squamous Cell Carcinoma","authors":"Meihua Kong, Yanzhi Cai, Qian He","doi":"10.37290/ctnr2641-452x.22:1018-1024","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:1018-1024","url":null,"abstract":"Laryngeal squamous cell carcinoma is a challenging malignancy with increasing incidence globally, necessitating the exploration of novel therapeutic strategies. Platycodin D, a saponin derived from Platycodon grandiflorum, has shown promise in cancer therapy, exhibiting anticancer effects in various tumor types. However, the specific mechanisms of action of Platycodin D in laryngeal squamous cell carcinoma remain poorly understood. Therefore, our study aimed to investigate the anticancer effects of Platycodin D in laryngeal squamous cell carcinoma. We revealed that Platycodin D effectively inhibited the proliferation of laryngeal squamous cell carcinoma cells and induced mitochondrial apoptosis. Furthermore, we found that Platycodin D downregulated the expression of S-phase kinase-associated protein 2, indicating a novel target for PD’s action. Finally, the suppression of S-phase kinase-associated protein 2 by Platycodin D led to cell cycle arrest and enhanced apoptosis in laryngeal squamous cell carcinoma cells. Collectively, these findings underscore the potential of Platycodin D as a novel therapeutic agent for laryngeal squamous cell carcinoma, with implications for targeting mitochondrial apoptosis and S-phase kinase-associated protein 2 in cancer treatment.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 3","pages":"1018-1024"},"PeriodicalIF":0.0,"publicationDate":"2024-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lonicerin Alleviates Interleukin-1β-Stimulated Extracellular Cartilage Matrix Degradation and Inflammation","authors":"Jun Ma, Dong Gong, Xiaotao Chen","doi":"10.37290/ctnr2641-452x.22:1006-1011","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:1006-1011","url":null,"abstract":"This study aimed to investigate the effects of lonicerin on an osteoarthritis model in vitro and determine its mechanism of action. We induced SW1353 cells with interleukin-1β to construct a cell model of osteoarthritis. The effects of lonicerin on cell viability were observed using cell counting kit-8 assays. Quantitative polymerase chain reaction, immunoblot, and enzyme-linked immune-sorbent assays revealed the effects of lonicerin on inflammation. Additionally, quantitative polymerase chain reaction and immunoblot assays showed the degree of extracellular matrix degradation. Immunoblot assays were further performed to confirm the mechanism of action of lonicerin. Lonicerin contributed to interleukin-1β-stimulated SW1353 cell viability. Furthermore, lonicerin restrained the inflammatory response of interleukin-1β-stimulated SW1353 cells, suppressed the extracellular matrix degradation of interleukin-1β-stimulated SW1353 cells, and increased collagen II expression. Mechanically, lonicerin suppressed the nuclear factor-kappa B pathway and prevented osteoarthritis progression. Lonicerin alleviates interleukin-1β-stimulated cartilage extracellular matrix and inflammation.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 3","pages":"1006-1011"},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147893756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cirsilineol Protects Renal Tubular Epithelial Cells from Hypoxia/Reoxygenation Injury by Inhibiting Inflammation and Pyroptosis","authors":"Fei Huang, Zi Liu","doi":"10.37290/ctnr2641-452x.22:882-888","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:882-888","url":null,"abstract":"To investigate the effects of Cirsilineol on cell viability, pyroptosis, and inflammation in hypoxia/reoxygenation-induced renal tubular cells, we utilized the renal tubular epithelial cell line HK2. The in vitro renal injury model was induced by hypoxia/reoxygenation. Cell viability in hypoxia/reoxygenation-induced HK2 cells was determined using a methylthiazolyldiphenyl-tetrazolium bromide assay and lactate dehydrogenase releasing kit. The effects of Cirsilineol on inflammation and pyroptosis in HK2 cells were evaluated using enzyme-linked immunosorbent assay, flow cytometry, and immunoblot assays. Our results demonstrated that Cirsilineol promoted survival in hypoxia/reoxygenation-induced tubular cells, inhibited inflammation, and reduced pyroptosis in these cells. Further investigation revealed that the protective effects of Cirsilineol are mediated by the suppression of the Toll-like receptor 4/nuclear factor kappa B pathway, which mitigates the cellular response to hypoxia/reoxygenation injury. Our study suggests that Cirsilineol protects renal tubular epithelial cells from hypoxia/reoxygenation injury by inhibiting inflammation and pyroptosis, highlighting its potential therapeutic value in renal conditions characterized by ischemic injury.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 3","pages":"882-888"},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147908426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Luteolin Inhibits Lipopolysaccharide-Induced Inflammation and Epithelial–Mesenchymal Transition in Human Nasal Epithelial Cells","authors":"Qin Yang, Nimei Shen, Gang Gao","doi":"10.37290/ctnr2641-452x.22:875-881","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:875-881","url":null,"abstract":"Chronic sinusitis is a persistent inflammatory condition needing better treatment options with fewer side effects to reduce recurrence. Luteolin, a flavonoid found in various plants, exhibits anti-inflammatory and anti-allergic properties. This study explores luteolin’s impact on chronic sinusitis. We isolated human nasal epithelial cells from sinusitis patients and used lipopolysaccharide-induced cells as a model. High-mobility group box 1 protein was notably elevated in these patients. Our findings suggest that luteolin can suppress the expression of inflammatory cytokines induced by lipopolysaccharide in these cells. Additionally, luteolin was able to inhibit the epithelial–mesenchymal transition in the treated cells. This inhibitory effect on high-mobility group box 1 expression led to reduced inflammation and transition processes. Overall, luteolin could potentially be an effective treatment for chronic sinusitis, minimizing inflammation and cellular transition in nasal epithelial cells.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 3","pages":"875-881"},"PeriodicalIF":0.0,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M.J. Fu, Jinhuan Chen, Xiaoqian Che, Lu Huang, Yuping Mo
{"title":"Bergamottin Attenuates Mitochondrial Activity and Oxidative Stress in Oxygen-Glucose Deprivation and Reperfusion-Induced Cardiomyocytes","authors":"M.J. Fu, Jinhuan Chen, Xiaoqian Che, Lu Huang, Yuping Mo","doi":"10.37290/ctnr2641-452x.22:901-907","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:901-907","url":null,"abstract":"The aim of this study was to investigate the precise effects and mechanisms of bergamottin in heart failure. Oxygen-glucose deprivation and reperfusion was used to simulate H9C2 cell injury in heart failure. Cell Counting Kit-8 and lactate dehydrogenase kits were used to assess cell viability. JC-1 stain, reactive oxygen species, and adenosine triphosphate kits were utilized to probe mitochondrial status. In addition, oxidative stress indicators were analyzed by enzyme-linked immunosorbent assay. Bergamottin treatment reduced lactate dehydrogenase and enhanced cell survival. Furthermore, oxygen-glucose deprivation and reperfusion-induced mitochondrial function was recovered, and oxidative stress levels were decreased by bergamottin therapy. Finally, mechanistic research showed that the SIRT1/AMPK pathway was activated by bergamottin. Bergamottin could be a potential drug for the clinical treatment of heart disease.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 3","pages":"901-907"},"PeriodicalIF":0.0,"publicationDate":"2024-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147885520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Enrichment of Sodium Alginate-Gum Arabic Composite Films with Oregano/Citronella Essential Oils for Fresh Goji Berry (Lycium Barbarum L.) Preservation","authors":"Zi-Jing Guan, Wang-Wei Zhang, Jingjing Wang, Kiran Thakur, Fei Hu, Jian‐Guo Zhang","doi":"10.37290/ctnr2641-452x.22:657-671","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:657-671","url":null,"abstract":"This study reported the preparation of composite sodium alginate-gum Arabic films by incorporating nano emulsions and pickering emulsions loaded with mixed oregano and citronella essential oils. Nano emulsions and pickering emulsions were prepared with Tween 80 and whey protein isolate/inulin. The results of Fourier transform infrared, X-ray diffraction, thermo-gravimetric analysis, field emission scanning electron microscopy, and atomic force microscopy demonstrated that sodium alginate-gum Arabic and the emulsion-loaded mixed oregano and citronella essential oils were biocompatible. The mixed oregano and citronella essential oils was enclosed in Pickering emulsions in the film samples, which also improved the mechanical and water barrier qualities, slowed the release of the active components. The composite film was applied to the storage experiment of goji berries at 25°C. In comparison to the control group, the composite film containing 0.4% Pickering emulsions significantly decreased weight loss and fruit deterioration while also extending shelf life by 3 days. In conclusion, produced Pickering emulsions laminate film loaded with mixed oregano and citronella essential oils may be a viable material for the food packaging sector.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 2","pages":"657-671"},"PeriodicalIF":0.0,"publicationDate":"2023-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147877263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of Individualized Nursing Based on Stress Adaptation Theory on Nutritional Status and Gastrointestinal Motility of Preterm Infants","authors":"Huimin Li","doi":"10.37290/ctnr2641-452x.21:502-508","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.21:502-508","url":null,"abstract":"We have compared the effect of stress adaptation theory-based nursing care with routine nursing care on the nutritional status and gastrointestinal motility of preterm infants. The results show an improvement in fetal growth and development after delivery, the physiological and neurological functions of babies, an increase in head circumference, body length, and weight and gastrointestinal function after stress adaptation theory-based nursing care (P < 0.05). However, there was no evidence for an intergroup difference in the incidence of adverse reactions (P > 0.05). These results suggest that stress adaptation theory-based nursing care is conducive to enhancing the nutritional status and gastrointestinal function of preterm infants and ensuring their healthy growth.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"57 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2023-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139316769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wang Tianyu, Xu He, Sun Yue, Hou Jumin, Yin Liying
{"title":"Synergistic Effects of Chlorogenic Acid and Ganoderma Lucidum Polysaccharide on Hepatic Fat Accumulation","authors":"Wang Tianyu, Xu He, Sun Yue, Hou Jumin, Yin Liying","doi":"10.37290/ctnr2641-452x.22:792-802","DOIUrl":"https://doi.org/10.37290/ctnr2641-452x.22:792-802","url":null,"abstract":"This study aimed to investigate the impact of different doses of chlorogenic acid and Ganoderma lucidum polysaccharide on lipid accumulation using an obese rat model. We utilized blood glucose assays, oil red O staining, and triglyceride content analysis to examine the effects of chlorogenic acid combined with G. lucidum polysaccharide on fat metabolism in rats. We found substantial potential in using chlorogenic acid combined with G. lucidum polysaccharide for weight control and metabolic regulation in obese rats. After a long-term dietary intervention, chlorogenic acid and G. lucidum polysaccharide markedly inhibited the expression of proteins related to fatty acid synthesis, including AMP-activated protein kinase, fatty acid synthase, and SREBP-1c, leading to reduced body weight and decreased hepatic fat deposition. Additionally, the combined treatment substantially affected enzymes and proteins involved in glucose metabolism, reducing glycogen synthase expression and indicating a potential mechanism for weight reduction through glycogen synthesis inhibition. Furthermore, elevated glucose kinase levels indicated that chlorogenic acid and G. lucidum polysaccharide may enhance hepatic glycogen degradation, thereby reducing hepatic fat accumulation. These findings reveal that chlorogenic acid combined with G. lucidum polysaccharide has a synergistic impact, providing a theoretical basis for their potential as a combined therapeutic approach for obesity.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 2","pages":"792-802"},"PeriodicalIF":0.0,"publicationDate":"2023-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}