DALTON TRANSACTIONS
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2022
·Vol. 51
·期 31
·11703-11712
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IF 4.569
Jun Sun,Minghui Zhou,Bei Zhang,Youjie Hua,Feifei Huang,Hongping Ma,Renguang Ye,Shiqing Xu
A series of Rb1−yKyNa3(Li3SiO4)4:Eu2+(0 ≤ y ≤ 1) phosphors were successfully synthesized through a high-temperature solid-state reaction. The introduction of K+ into the RbNa3(Li3SiO4)4:Eu2+ phosphor to partially or completely replace Rb+ allows the emission spectrum to be modulated from blue (λ = 473 nm, FWHM = 22.5 nm) to a narrow cyan band (λ = 485 nm, FWHM = 21.1 nm). As the K+ ion content increases, the space group of the phosphor evolves from I4/M to I41/A. The complete replacement of Rb+ by K+ results in the KNa3(Li3SiO4)4:Eu2+ cyan phosphor, which shows excellent thermal stability (the comprehensive emission loss is only 8% at 150 °C) and can be used to fill the cyan light gap in white LED devices. By adding the KNa3(Li3SiO4)4:Eu2+ cyan phosphor in packaging with yellow and red phosphors, the color rendering index is increased from 90.2 to 97.1 and the correlated color temperature improved to 3658 K. These results indicate that the cyan phosphor has important application value in full-spectrum white LEDs.
研究领域:
材料科学
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光学工程
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无机非金属材料
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发光材料
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半导体照明
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高影响因子
CytoJournal
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2025
·
IF 3.1
Xunjia Li,Zhixin Xu,Ying Li,Yan Luo,Jie Zhou,Deyu Zuo,Weijian Xiong
Objective:
Patients with chronic kidney disease (CKD) exhibit increased vascular calcification (VC) risks, worsened by high-dose erythropoietin (EPO). While EPO treats anemia, its role in VC pathogenesis remains unclear. Ginsenoside Rb1 (Rb1), a Panax ginseng compound with anti-calcification properties, may counteract EPO-induced VC through the GATA binding protein 6 (GATA6)/bone morphogenetic protein 2 (BMP2)/Smad1/5/9 pathway. This article aims to explore whether Rb1 could counteract EPO-induced VC through the GATA6/BMP2/Smad1/5/9 pathway.
Material and Methods:
Adenine-induced CKD rats and b-glycerophosphate-treated vascular smooth muscle cells (VSMCs) received EPO ± Rb1. Calcification was assessed through von Kossa/alizarin red staining. Smooth muscle protein 22-a (SM22a)/a-Smooth muscle actin (a-SMA) expression was measured by immunofluorescence and real-time-quantitative polymerase chain reaction (RT-qPCR). GATA6/BMP2/Smad1/5/9 activation was analyzed using RT-qPCR/Western blot. Rb1-BMP2 interactions were tested through biotin pulldown, micro-thermophoresis, and Co-immunoprecipitation (Co-IP). GATA6 knockdown validated pathway roles.
Results:
High-dose EPO significantly worsened CKD-associated calcification and VSMC calcification (P < 0.01), suppressed SM22a and a-SMA expression levels, and activated the GATA6/BMP2/Smad1/5/9 pathway (P < 0.01). GATA6 knockdown reduced EPO-exacerbated calcification and modulated BMP2/Smad1/5/9 signaling (P < 0.01). Rb1 increased SM22a and a-SMA expression levels and inhibited Smad 1/5/9 phosphorylation (P < 0.01), without affecting GATA6 or BMP2 expression (P > 0.05). Molecular docking and Co-IP experiments revealed that Rb1 binds directly to BMP2, blocking its interaction with bone morphogenetic protein receptor and inhibiting Smad 1/5/9 phosphorylation (P < 0.01).
Conclusion:
Rb1 mitigates EPO-aggravated VC in CKD by disrupting BMP2/Smad1/5/9 signaling, positioning it as a promising molecular intervention strategy to reduce EPO-induced vascular toxicity.
Keywords: Bone morphogenetic protein 2/Smad1/5/9 signaling pathway, Chronic kidney disease, Erythropoietin, Ginsenoside Rb1, Vascular calcification
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Frontiers in Pharmacology
·
2021
·
IF 5.811
Hao Xincai,Sun Xiaodong,Zhu Haizhen,Xie Lixia,Wang Xuanbin,Jiang Nan,Fu Pan,Sang Ming
Trans-resveratrol (RES) exhibits a wide range of biological activities. Various methodological approaches have been established to improve the pharmacokinetic properties of RES. Moreover, additional in vivo studies are required to support clinical application. In this study, RES/HP-β-CD (RHSD) inclusion complex was prepared and characterized by FTIR, PXRD, DSC and NMR data. The effect and potential mechanism of RHSD against cervical cancer were investigated in a mouse xenograft tumor model by qPCR assay, Western blot assay, and immunohistochemical assay. Results showed that RHSD significantly decreased tumor growth compared with free RES, while the effect of preventing tumor growth was more prominent in vivo. Notably, RHSD could inhibit tumor development by suppressing the expression of HPV E6 and E7 oncogenes and upregulating P53 and Rb1 protein in cervical cancer. These findings demonstrated that RHSD was safe and potential for development of a new oral administration drug to treat cervical cancer.
研究领域:
药理学
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肿瘤学
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药物递送系统
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DOI
PubMed
高影响因子
Scientific Reports
·
2025
·Vol. 15
·期 1
·1-13
·
IF 3.9
Jeong Ji-Soo,Kim Jeong-Won,Kim Jin-Hwa,Kim Chang-Yeop,Chung Eun-Hye,Boo So-Young,Giorgi Mario,Ko Je-Won,Kim Tae-Won
Korean red ginseng (KRG, Panax ginseng C.A. Meyer) contains ginsenosides, which are metabolized into active metabolites with various pharmacological effects. This study assessed the in vivo exposure and accumulation of ginsenosides following single and repeated administration of KRG and its active ingredient, compound K, in experimental rodents. In Study 1, rats received KRG (2 g/kg) orally as a single dose or for 2, 4, and 8 wks. Repeated administration increased the maximum plasma concentrations (C max ) of ginsenosides Rb1 and Rd compared to a single dose (Rb: 23.9 to 68.3 ng/mL; Rd: 8.5 to 30.8 ng/mL over 8 wks). Compound K was detected at 2.9 and 2.3 ng/mL of C max after 4 and 8 wks of continuous KRG administration, with no significant differences. In Study 2, oral administration of compound K (5 or 10 mg/kg) in rats resulted in accumulation factors of 4 and 7, respectively. Study 3 evaluated the oral bioavailability of compound K in mice (intravenous, 2 mg/kg; oral, 10 mg/kg), estimating it at approximately 12%. Additionally, network pharmacology and molecular docking simulation studies supported the clinical potential of compound K against inflammation-related diseases. These findings suggest that for substances like KRG, which undergo in vivo metabolic conversion after administration, repeated KRG administration alters pharmacokinetic profiles and should be taken into consideration in its application.
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REACTIVE & FUNCTIONAL POLYMERS
·
2023
·
IF 5.1
Yu Liu,Xinqi Qiu,Minhui Zhang,Yali Lin,Hui Lan,Xican Li,Quanzhou Wu,Jianfeng He
A novel approach combining boronate affinity with surface molecular imprinting was developed for the specific recognition and separation of ginsenoside Rb1 . Firstly, the boronic acid-functionalized polymer microspheres were prepared as inner cores via suspension polymerization using methyl methacrylate , ethyleneglycol dimethacrylate, and 4-vinylphenyl boronic pinacol ester (4-VBPE) as polymerization monomers . Then, the Ginsenoside Rb1 (GRb1) template was covalently pre-anchored onto the surface of microspheres through boronate affinity binding after the hydrolysis of 4-VBPE. Finally, dopamine and polyethyleneimine were used as co -coating monomers to form a thickness-controllable imprinting layer onto the polymer microspheres via in-water self-copolymerization. The key factors affecting specific recognition, including the boronic acid content, adsorption media, and polymerization time were carefully optimized. The resulting molecularly imprinted microspheres (MIMs) exhibited strong surface hydrophilicity . In the aqueous media, the optimal adsorption capacity for the template reached 81.45 μmol g −1 , and the imprinting factor was 5.32. The specific evaluation showed that the MIMs had a much higher selectivity for GRb1 than its analogues, and the selectivity coefficients were all higher than 2.4. In addition, the MIMs can be applied as adsorbents for solid-phase extraction to selectively separate ginsenosides from American ginseng extract. The eluting recovery ratios of GRb1, GRg2, and GRd reach 92.39%, 88.90%, and 92.49%, respectively.
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JOURNAL OF CONTROLLED RELEASE
·
2024
·
IF 10.5
Zhi Zheng,Jian Sun,Jun Wang,Suisui He,Zhenqiu Liu,Jiahao Xie,Cui-Yun Yu,Hua Wei
Myocardial infarction (MI)-induced impaired cardiomyocyte (CM) mitochondrial function and microenvironmental inflammatory cascades severely accelerate the progression of heart failure for compromised myocardial repair. Modulation of the crosstalk between CM mitochondrial DNA (mtDNA) and STING has been recently identified as a robust strategy in enhancing MI treatment, but remains seldom explored. To develop a novel approach that can address persistent myocardial injury using this crosstalk, we report herein construction of a biomimetic hydrogel system, Rb1/PDA-hydrogel comprised of ginsenoside Rb1/polydopamine nanoparticles (Rb1/PDA NPs)-loaded carboxylated chitosan, 4-arm-PEG-phenylboronic acid (4-arm-PEG-PBA), and 4-arm-PEG-dopamine (4-arm-PEG-DA) crosslinked networks. An optimized hydrogel formulation presents not only desired adhesion properties to the surface of the myocardium, but also adaptability for deep myocardial injection, resulting in ROS scavenging, CM mitochondrial function protection, M1 macrophage polarization inhibition through the STING pathway, and angiogenesis promotion via an internal-external spatial combination. The enhanced therapeutic efficiency is supported by the histological analysis of the infarcted area, which shows that the fibrotic area of the MI rats decreases from 58.4% to 5.5%, the thickness of the left ventricular wall increases by 1-fold, and almost complete recovery of cardiac function after 28 days of treatment. Overall, this study reported the first use of a strong adhesive and injectable hydrogel with mtDNA and STING signaling characteristics for enhanced MI treatment via an internal-external spatial combination strategy.
研究领域:
心脏病学
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生物材料
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分子生物学
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治疗学
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American Journal of Cancer Research
·
2022
·
IF 5.942
Guangyu Cheng,Lin Li,Qingjie Li,Shulin Lian,Hongbo Chu,Yunlu Ding,Chikun Li,Yan Leng
Multi-drug resistance remains a critical issue in cancer treatment that hinders the effective use of chemotherapeutic drugs. The active components of traditional Chinese medicine have been applied as adjuvants to accentuate the anticancer properties of conventional drugs such as cisplatin. However, their application requires further validation and optimization. This study explored the anticancer activity of β-elemene, a natural component of traditional Chinese medical formulations. The effect of β-elemene on the anticancer properties of cisplatin was evaluated in A549 and NCI-H1650 lung cancer cells. Cell apoptosis, stem-like properties, glucose metabolism, multi-drug resistance, and PI3K/AKT/mTOR activation were assessed via flow cytometry, tumorsphere formation, and western blotting. The target genes of β-elemene were predicted using bioinformatics tools and validated in both cell lines. A xenograft model of lung cancer was established in nude mice to evaluate the combined effects of β-elemene and cisplatin in vivo . We found that β-elemene acted synergistically with cisplatin against non-small cell lung cancer cells by promoting apoptosis and impairing glucose metabolism, multi-drug resistance, and stemness maintenance. These effects were mediated by the inhibition of PI3K/AKT/mTOR activation. Bioinformatics analysis revealed that RB1 and TP53 are common target genes associated with lung cancer and β-elemene. The anti-tumorigenic properties of β-elemene were confirmed in vivo , wherein β-elemene, along with cisplatin, significantly suppressed tumor growth in a mouse xenograft model of non-small cell lung cancer. As such, β-elemene acted as an inhibitor of PI3K/AKT/mTOR signaling and enhanced the anticancer effect of cisplatin by targeting tumor metabolism, chemoresistance, and stem-like behavior. Thus, β-elemene is an effective anticancer adjuvant agent with potential clinical applications.
研究领域:
肿瘤学
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药理学
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分子生物学
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生物信息学
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Chinese Journal of Natural Medicines
·
2025
·
IF 4.9
Yongsheng Fang,Zhiyun Zhu,Chun Xie,Dazhen Xia,Huimin Zhao,Zihui Wang,Qian Lu,Caimei Zhang,Wenyong Xiong,Xiaodong Yang
Saponins associated with Panax notoginseng ( P. notoginseng ) demonstrate significant therapeutic efficacy across multiple diseases. However, certain high-yield saponins face limited clinical applications due to their reduced pharmacological efficacy. This study synthesized and evaluated 36 saponin-1,2,3-triazole derivatives of ginsenosides Rg1/Rb1 and notoginsenoside R1 for anti-adipogenesis activity in vitro . The research revealed that the ginsenosides Rg1-1,2,3-triazole derivative a17 demonstrates superior adipogenesis inhibitory effects. Structure-activity relationships (SARs) analysis indicates that incorporating an amidyl-substituted 1,2,3-triazole into the saponin side chain via Click reaction enhances anti-adipogenesis activity. Additionally, several other derivatives exhibit general adipogenesis inhibition. Compound a17 demonstrated enhanced potency compared to the parent ginsenoside Rg1. Mechanistic investigations revealed that a17 exhibits dose-dependent inhibition of adipogenesis in vitro , accompanied by decreased expression of preadipocytes. Peroxisome proliferator-activated receptor γ (PPARγ), fatty acid synthase (FAS), and fatty acid binding protein 4 (FABP4) adipogenesis regulators. These findings establish the ginsenoside Rg1-1,2,3-triazole derivative a17 as a promising adipocyte differentiation inhibitor and potential therapeutic agent for obesity and associated metabolic disorders. This research provides a foundation for developing effective therapeutic approaches for various metabolic syndromes.
研究领域:
药物化学
·
药理学
·
天然产物
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生物有机化学
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代谢性疾病研究
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2024
·
IF 5.7
Wenqi Xu,Cuicui Duan,Fumin Ma,Dan Li,Xiaolei Li
To convert ginsenosides Rb1, Rb2, Rb3, and Rc into Rd by a single enzyme, a putative β-glycosidase (Pxbgl) from the xylan-degrading bacterium Petroclostridium xylanilyticum was identified and used. The kcat/Km value of Pxbgl for Rb3 was 18.18 ± 0.07 mM–1/s, which was significantly higher than those of Pxbgl for other ginsenosides. Pxbgl converted almost all Rb3 to Rd with a productivity of 5884 μM/h, which was 346-fold higher than that of only β-xylosidase from Thermoascus aurantiacus. The productivity of Rd from the Panax ginseng root and Panax notoginseng leaf was 146 and 995 μM/h, respectively. Mutants N293 K and I447L from site-directed mutagenesis based on bioinformatics analysis showed an increase in specific activity of 29 and 7% toward Rb3, respectively. This is the first report of a β-glycosidase that can simultaneously remove four different glycosyls at the C–20 position of natural PPD-type ginsenosides and produce Rd as the sole product from P. notoginseng leaf extracts with the highest productivity.
研究领域:
生物化学
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生物技术
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药理学
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微生物学
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JOURNAL OF ETHNOPHARMACOLOGY
·
2022
·
IF 5.195
Tingting Wang,Xiaoting Huang,Kefeng Zhai,Jialin Yu,Jiaxi Li,Hong Duan,Jinhong Liu,Zhuojian Lu,Jia Guo,Fei Li
Ethnopharmacological relevance Panax japonicus C. A. Meye (PJ) has unique effects on diseases by “qi” stagnation and blood stasis in ancient. Modern studies have shown that PJ can treat diabetic kidney disease (DKD) caused by deficiency and blood stasis. Aim of the study This study evaluated the potential effects of PJ on DKD, a microvascular complication, and investigated its possible mechanisms. Materials and methods In this study, the chemical constituents of PJ were analyzed by HPLC. In vivo studies, we constructed a diabetic mice model by HDF combined with STZ , then administered PJ to diabetic mice for 6 weeks. Blood lipid, BUN, 24h urine protein, and renal tissue HE staining were detected to comprehensively evaluate the protective effect of PJ on DKD. Metabolomics investigated the metabolic pathways influenced by PJ in the treatment of DKD. Moreover, the potential targets and signal pathways were investigated using network pharmacology . Finally, molecular docking predicts affinity of active compounds and core targets, and western blotting was used to detect core target expression levels. Results In vivo study, PJ can reduce hyperlipidemia , serum BUN, and 24-h urinary protein in diabetic mice, and protect the pathological changes in renal tissue. Metabolomics results showed that PJ had significant regulatory effect on unsaturated fatty acids , glycerophospholipid metabolism, and purine metabolism. Network pharmacology showed that MAPK1, MAPK8, Bcl-2, and Caspase 3 were the core targets in PJ against DKD. Molecular docking revealed that Bcl-2 and Caspase 3 have a strong affinity for Chikusetsusaponin Iva , Ginsenoside Rb1 , and Ginsenoside Rg1 . Moreover, when compared to the model group, the PJ group had higher levels of anti-apoptosis protein Bcl-2 and lower levels of pro-apoptosis protein Caspase 3. Conclusion PJ can reduce blood lipids, regulate the biosynthesis of unsaturated fatty acids and purine metabolism, thereby alleviating the renal injury of diabetic mice. Moreover, it can regulate the Bcl-2/caspase 3 apoptosis signaling pathway to prevent the apoptosis of renal cells and protect the renal function of diabetic mice.
研究领域:
药理学
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代谢组学
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糖尿病研究
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分子生物学
·
病理学
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危险品化学品经营许可证（带存储）