PHYTOCHEMICAL ANALYSIS
·
2021
·Vol. 32
·期 6
·1074-1081
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IF 3.373
Yanfang Wu,Yindi Chu,Qinyu Yang,Mengjia Li,Miao Yu,Ruixue Deng,Kun Liu,Xinsheng Wang,Enguo Fan
Introduction Syringa pubescens Turcz. was reported to be abundant in the Funiu Mountains of Henan Province and can be used to treat hepatitis and cirrhosis. In order to develop and utilise the resource, a fast and simple technique to extract bioactive compounds is needed. Objectives Our aims were to provide an extraction technique of glycosides from S. pubescens and study the antioxidant activity of this material. Methods Box–Behnken design (BBD) was employed with three factors at three levels. The process parameters such as ethanol concentration ( X 1 ), temperature ( X 2 ), and solvent–solid ratio ( X 3 ) could significantly influence efficiency and yield of target compounds. High-performance liquid chromatography (HPLC) was used to determine the content of glycosides. DPPH (α,α-diphenyl-β-picrylhydrazyl), ABTS (2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) and reducing power were used to evaluate the antioxidant activity of S. pubescens extract. Results The optimal parameters for the maximal extraction yield were obtained with ethanol concentration of 68%, temperature of 89°C, solvent–solid ratio of 46 mL/g, and time of 20 min. The S. pubescens extract showed strong antioxidant properties in vitro . Conclusion The findings indicated the potential application of solvothermal extraction method to extract bioactive compounds from S. pubescens Turcz. Furthermore, the S. pubescens extract could be used as an important resource of antioxidant activity.
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高影响因子
INDUSTRIAL CROPS AND PRODUCTS
·
2020
·
IF 4.244
Xinsheng Wang,Yanfang Wu,Jie Li,Aoxiang Wang,Guangyao Li,Xueli Ren,Weiping Yin
In this work, deep eutectic solvents (DESs) were synthesized using ultrasound-assisted and stirring heating methods. DES combined with ultrasonic-assisted extraction (UAE) was proposed for the efficient extraction of glycosides from Syringa pubescens Turcz. A series of DES systems were used to evaluate the extraction efficiency of glycosides in S. pubescens . The DES composed of choline chloride/glycerol extracted higher than those of conventional solvents and other DESs. The extraction procedure of DES-UAE was optimized using response surface methodology. The extraction solvent was choline chloride-glycerol formed a DES with the mole ratio of 1:2 with 20 % of water content. The optimum conditions for echinacoside (ECH) and oleuropein (OLE) were ultrasound power of 200 W, extraction temperature of 68 °C, solvent to solid ratio of 20:1 mL/g and the extraction time of 45 min. Furthermore, the DES with 30 % water content can be used as dilution solvent before HPLC analysis of DES extract. In addition, the enrichment of ECH and OLE from DES extract was achieved using HPD-450 macroporous resin, with the recoveries of 80.04 % and 86.21 %, respectively.
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BIOMEDICINE & PHARMACOTHERAPY
·
2018
·
IF 3.457
Min Chen,Xiaodong Wang,Bo Hu,Jian Zhou,Xin Wang,Wei Wei,Hua Zhou
Echinacoside is a natural ingredient with various pharmacological activities . In this study, we investigated the protective effects of echinacoside on cardiomyocytes (rat H9c2 cells) in an anoxia/reperfusion (A/R) model. Further, the regulatory function of sodium-calcium exchanger protein 3 (SLC8A3/NCX3) as well as the protein kinase B (AKT) signaling were studied. The present results indicated that echinacoside protected against A/R-induced apoptosis in a dose manner, which was characterized by a decrease in the apoptosis and caspase 3 protein levels in H9c2 cells. Further, Ca 2+ uptake were dose-dependently reduced in H9c2 cells by echinacoside under A/R conditions. Whereas, relative mRNA expression of SLC8A3 and protein levels of SLC8A3 and p-AKT showed opposite tendency. On the one hand, the A/R-induced abnormalities in H9c2 cells were remarkably ameliorated by activated p-AKT and over-expression of SLC8A3 but aggravated by inhibited p-AKT, and the aggravated effection were ameliorated by echinacoside. Moreover, protein levels of SLC8A3 were positively regulated by p-AKT signaling. On the other hand, apoptosis and Ca 2+ uptake as well as protein levels of caspase 3 were significantly increased by SLC8A3 silencing in H9c2 cells under normoxic conditions, and this symptom was remarkably reversed by echinacoside or Nimodipine (an antagonis of Ca 2+ ) treatment . Collectively, echinacoside has showed a cardioprotective effect against A/R treatment in a dose dependent manner in vitro, and this cardioprotective effect was potentially achieved via up-regulating p-AKT and SLC8A3.
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TECHNOLOGY AND HEALTH CARE
·
2024
·
IF 1.4
Wang Guoyu,Han Yang,Zhuang Juhua,Mai Zhongchao,Xia Wei,Ye Ying
BACKGROUND: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-attributed mortality and the primary liver malignancy in the world. Echinacoside is a phenylethanoid glycoside derived from traditional Chinese medicinal herbs which possessed multiple health benefits on humans, including anti-tumor effects. OBJECTIVE: This study aimed to demonstrate the function of echinacoside in HCC progression and the involvement of miR-30c-5p/FOXD1/KLF12 axis. METHODS: The HepG2 cells were treated by different dose of echinacoside, miR-30c-5p mimic, miR-30c-5p inhibitor, and FOXD1 overexpression lentiviruses or siRNA individually or simultaneously. The cell invasion and migration were measured by transwell assay. RNA and protein levels were tested by RT-PCR and western blot, respectively. The regulatory function of miR-30c-5p on Forkhead box D1 (FOXD1), FOXD1 on Krüppel-like factor 12 (KLF12) was tested by luciferase reporter assay or/and ChIP assay. Meanwhile, a liver cancer lung metastasis mice model was used to examine the functions of echinacoside and miR-30c-5p on HCC metastasis in vivo. Moreover, the correlations among miR-30c-5p, FOXD1, KLF12, and HCC prognosis was analyzed using clinical sample and TCGA database. RESULTS: Based on both in vitro and in vivo investigations, we found that echinacoside could inhibit HCC cell migration, invasiveness, and tumor metastasis, and associated with the enhanced miR-30c-5p/FOXD1/KLF12 axis. Furthermore, through analyzing the interactions among intermediate molecules, we revealed that miR-30c-5p, FOXD1, and KLF12üere clinically relevant with each other in HCC patients, correlated with HCC prognosis, and regulated by echinacoside to contribute in the inhibition of HCC progression. CONCLUSIONS: These findings suggest that echinacoside could inhibit HCC progression, and the mechanism related to the enhanced miR-30c-5p/FOXD1/KLF12 axis. Moreover, the abovementioned intermediate molecules might serve as prospective biomarkers for HCC prognosis.
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Journal of Natural Medicines
·
2017
·Vol. 72
·期 2
·390-398
·
IF 1.982
Lu Jianrao,Yi Yang,Pan Ronghua,Zhang Chuanfu,Han Haiyan,Chen Jie,Liu Wenrui
Renal ischemia reperfusion injury (RIRI) refers to the irreversible damage for renal function when blood perfusion is recovered after ischemia for an extended period, which is common in clinical surgeries and has been regarded as a major risk for acute renal failures (ARF) that is accompanied with unimaginably high morbidity and mortality. Hypoxia during ischemia followed by reoxygenation via reperfusion serves as a major event contributing to cell apoptosis, which has been widely accepted as the vital pathogenesis in RIRI. Preventing apoptosis in renal tubular epithelial cell has been considered as effective method for blocking RIRI. In this paper, we established a hypoxia/reoxygenation (H/R) injury model in human proximal tubular epithelial HK-2 cells. Here, we found increased SPHK1 levels in H/R injured HK-2 cells, which could be significantly down regulated after berberine treatment. Berberine has been reported to exert a protective effect on H/R-induced apoptosis of HK-2 cells. So, in our present study, we planned to investigate whether SPHK1 participated in the anti-apoptosis process of berberine in H/R injured HK-2 cells. Our study confirmed the protective effect of berberine against H/R-induced apoptosis in HK-2 cells through promoting cells viability, inhibiting cells apoptosis, and down-regulating p-P38, caspase-3, caspase-9 as well as SPHK1, while up regulating the ratio of Bcl-2/Bax. However, SPHK1 overexpression in HK-2 cells induced severe apoptosis, which can be significantly ameliorated with additional berberine treatment. We concluded that berberine could remarkably prevent H/R-induced apoptosis in HK-2 cells through down-regulating SPHK1 expression levels, and the mechanisms included the suppression of p38 MAPK activation and mitochondrial stress pathways.
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Separation Science Plus
·
2024
·Vol. 8
·期 1
·e202400247
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IF 1.3
Zi-Chen Zhang,Yan-Fang Wu,Jian-Sheng Xiong,Xin-Yi Guan,Su-Ya Zhang,Xin-Sheng Wang
Syringa pubescens Turcz. has been universally employed to make flower tea for the treatment of cough in the western part of Henan Province. Many researchers have confirmed that the phenylethanoid glycosides from S. pubescens were bioactive compounds. In this study, various macroporous resins have been employed to evaluate the potential of adsorption and desorption for phenylethanoid glycosides. The HPD-450 resins were appropriate for the purification of phenylethanoid glycosides, and the optimum purification conditions were established. The adsorption properties were well modeled using the pseudo-second-order kinetics. Meanwhile, the adsorption isotherm could be better represented by the Langmuir equation, suggesting that the process was an exothermic reaction. Moreover, the purified sample possessed a stronger antioxidant capacity. The inhibitory activity of the crude extract against α-amylase and α-glucosidase was stronger than that of purified sample. The findings obtained provided a scientific foundation for further research and high-value exploration of this plant and a potential technique for scale-up purification of phenylethanoid glycosides.
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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2025
·
IF 2.2
Yang Han,Junyong Fan,Wei Xia,Xiao Dong,Ying Ye
Primary liver cancer remains a major contributor to global cancer-related mortality. Echinacoside, a bioactive phenylethanoid glycoside isolated from traditional Chinese medicinal herbs, has shown potent anti-tumor effects. In this study, poly (lactic-co-glycolic acid) (PLGA) nanoparticles encapsulating echinacoside (E@PLGA and E@PLGA-FA) were synthesized via the double emulsification method. Their physicochemical properties, drug release kinetics, and anti-cancer efficacy were systematically evaluated through in vitro and in vivo models. Transmission electron microscopy (TEM) and dynamic light scattering (DLS) analyses revealed that the particle sizes of E@PLGA and E@PLGA-FA were approximately 91 nm and 100 nm, respectively, with zeta potentials of -22.50 mV and -31.89 mV. The polydispersity index (PDI) of E@PLGA and E@PLGA-FA was determined to be 0.16±0.01 and 0.19±0.01, respectively. The encapsulation efficiency and drug-loading capacity of echinacoside in E@PLGA-FA were 28.78% and 12.05%, respectively, slightly lower than those in E@PLGA nanoparticles (40.34% and 16.12%), likely due to folic acid modification altering PLGA solubility during formulation. In vitro release profiles demonstrated pH-dependent drug release: 22% at physiological pH (7.4) versus 67% under acidic conditions (pH 5.5) over 12 h, indicating tumor microenvironment-responsive behavior. Furthermore, E@PLGA-FA significantly inhibited the proliferation of HepG2 cells, induced apoptosis, caused cell cycle arrest at the G0/G1 phase, and suppressed cell mobility. Meanwhile, the protein levels of MMP2, MMP9 and Bax were increased after exposure to E@PLGA and E@PLGA-FA, whereas the protein levels of COL-Ⅰ, COL-Ⅱ, Bcl-2, Cyclin D1, and PCNA were decreased. In vivo, E@PLGA-FA effectively inhibited tumor growth, induced tumor cell apoptosis, and exhibited tumor-specific accumulation confirmed by fluorescence imaging. In addition, The E@PLGA-FA nanoparticle intervention did not induce pathological damage or inflammatory responses in murine liver and kidney tissues, suggesting a favorable safety profile for this compound. In conclusion, we engineered a novel tumor-targeted PLGA-based nanoparticle system for echinacoside delivery, which synergizes pH-responsive drug release, multi-mechanistic anti-cancer effects, and biosafety, offering a promising therapeutic platform for hepatocellular carcinoma.
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Chemical Biology & Drug Design
·
2025
·Vol. 105
·期 4
·e70097
·
IF 3.3
Wei-fang Song,Sheng-nan Li,Rui-xin Yao,Qiu-yan Jiang,Ting Shi,Dan-dan Fan,Hai-juan Zhang,Wen-hui Zhang,Rui-jun Wang
The primary objective aims to evaluate the therapeutic efficacy of echinacoside in ameliorating hepatic steatosis and exploring its role in modulating autophagic flux through AMP-activated protein kinase (AMPK) signaling, positioning it as a potential treatment for non-alcoholic fatty liver disease (NAFLD). A well-established NAFLD rat model was employed, administering varying concentrations of echinacoside. Biochemical parameters, including triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), alongside liver enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), were measured to assess liver function. To elucidate the molecular mechanisms, western blot analyses were performed to assess the expressions of p-AMPK, total AMPK, and key autophagy markers LC-3 I/II and Beclin-1. Echinacoside significantly improved the lipid profile by lowering plasma TG, TC, and LDL-C levels while increasing HDL-C. It also reduced serum ALT, AST, and ALP activities, demonstrating hepatoprotective effects. Notably, echinacoside reversed the p-AMPK levels in NAFLD rats in a dose-dependent manner, with the highest dosage showing the strongest effect. This was accompanied by increased expression of LC-3 I/II and Beclin-1. Echinacoside is expected to be a therapeutic drug for NAFLD by activating AMPK activity and enhancing autophagy to improve liver function. These findings suggest its clinical potential, with autophagy modulation via the AMPK pathway as a possible therapeutic mechanism for NAFLD treatment.
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