SEPARATION AND PURIFICATION TECHNOLOGY
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2024
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IF 8.1
Chengling Bai,Zhengyang Gu,Xuerui Gao,Ruijun Zhang,Jingwen Tang,Qian Xiao,Shuili Yu,Rongsheng Ning
Piperazine (PIP)-based polyamide (PA) nanofiltration (NF) membranes exhibit limited rejection of divalent cations due to their negatively charged surfaces and insufficient compactness, restricting their broader application in various water treatment processes. To overcome this challenge, a novel strategy—stepwise increasing TMC concentration (SITC) during the interfacial polymerization (IP)—was proposed to optimize the PA layer structure. Conventional PA layer demonstrates a vertical diffusion structure: a compact barrier region underneath a thick and loose region. The regulatory goal of SITC is to enhance compactness while minimizing the increase in hydraulic resistance. The regulatory mechanism suggested SITC could regulate the IP reaction in both over time (throughout the IP process) and across the reaction region. During the initial IP stage, SITC reduced the reaction rate and increased PIP/TMC ratio in the bottom reaction zone, thereby improving the compactness and potential of final bottom barrier region. Thus, SITC can effectively restrict the permeation of cations, significantly increasing MgCl 2 rejection from 33.70 % to 92.12 %. In the subsequent diffusion-limited stage, SITC enhanced the restriction on PIP diffusion, decreasing the thickness of the final upper loose region and surface potential. Those advantageous characteristics allowed the membrane to maintain a high rejection for Na 2 SO 4 (>98.44 %). Concurrently, the membrane maintained a high water permeance (13.00 L·m −2 ·h −1 ·bar −1 ), attributed to the thin (16.69 nm) and optimized compactness distribution of its PA layer. This study provided a novel mechanism insight into the functional customization of NF membranes by decoupling the synthesis-property-performance relationship.
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Membranes
·
2021
·Vol. 11
·期 9
·699
·
IF 4.106
Shuai Liu,Xiaofeng Fang,Mengmeng Lou,Yihan Qi,Ruo Li,Gang Chen,Yonglian Li,Yanbiao Liu,Fang Li
The effective separation of dyes and inorganic salts is highly desirable for recycling inorganic salts and water resource in printing and dyeing wastewater treatment. In this work, tannic acid (TA) and polyethyleneimine (PEI) were grafted on the PES/Fe ultrafiltration membrane via the coordination assembly and Michael addition strategy to fabricated a loose nanofiltration membrane (LNM). The effect of PEI concentration on membrane morphologies and properties was systematically investigated. The membrane surface becomes more hydrophilic and transforms into positive charge after the PEI grafting. The optimized PES/Fe-TA-PEI membrane possesses high pure water flux (124.6 L·m−2·h−1) and excellent dye rejections (98.5%, 99.8%, 98.4%, and 86.4% for Congo red, Eriochrome black T, Alcian blue 8GX, and Bromophenol blue, respectively) under 2 bar operation pressure. Meanwhile, the LNM showed a high Alcian blue 8GX rejection (>98.4%) and low NaCl rejection (<5.3%) for the dye/salt mixed solutions separation. Moreover, the PES/Fe-TA-PEI LNM exhibited good antifouling performance and long-term performance stability. These results reveal that such LNM shows great potential for effective fractionation of dyes and salts and recycling of textile wastewater.Keywords:loose nanofiltration;dye desalination;polyphenol;polyethyleneimine;grafting
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Nutrients
·
2024
·Vol. 16
·期 4
·514
·
IF 4.8
Xiao Wang,Yongjie Liang,Bohan Zhang,Lixin He,Wenxuan Li,Wenwen Zhang,Chengzong Li,Lihong Luo,Talha Umar,Huili Feng,Changwei Qiu
2’-Hydroxychalcone is a hydroxyl derivative of chalcones, which are biosynthetic precursors of flavonoids and rich in the human diet. The anticancer activity of 2’-hydroxychalcone has been reported in several cancers but remains to be investigated in breast cancer. In the current study, 2’-hydroxychalcone showed significant cytotoxicity against breast cancer cell lines MCF-7 and CMT-1211. It could inhibit breast cancer cell proliferation, migration, and invasion in vitro and suppress tumor growth and metastasis in vivo. Mechanistic investigation revealed that the NF-κB pathway was significantly inhibited by 2’-hydroxychalcone treatment accompanied by an excessive intracellular accumulation of reactive oxygen species, induction of endoplasmic reticulum stress, and activation of JNK/MAPK. In addition, 2’-hydroxychalcone elevated the autophagic levels in breast cancer cells equipped with increasing numbers of autophagy vesicles and complete autophagic flux. Finally, autophagy-dependent apoptosis was observed in 2’-hydroxychalcone-induced cell death. In conclusion, 2’-hydroxychalcone enhances the autophagic levels and induces apoptosis in breast cancer cells, which could be contributed to the inhibition of the pro-survival NF-κB signaling, indicating a promising potential for 2’-hydroxychalcone in future anticancer drug development.
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PHYTOMEDICINE
·
2025
·
IF 8.3
Bao-xin Zheng,Yan Yi,Xing-wen Wang,Chun-ying Li,Yong Zhao,Jing-zhuo Tian,Lian-mei Wang,Jia-yin Han,Chen Pan,Su-yan Liu,Chen-yue Liu,Sha-sha Qin,Xuan Tang,Mei-ting Liu,Ai-hua Liang
Background Geniposide (GE) has potential efficacy in treating ulcerative colitis (UC). However, its reactivity can be affected by rapid degradation after oral administration. Furthermore, increasing oral doses may lead to hepatotoxicity. Thus, We used enema administration, characterized by smaller dose and higher localized concentration in the lesion, to improve the above situation. Purpose We aimed to confirm that enema administration is a better modality than oral administration for GE against UC and to explore its mechanism. Study design/Method We established UC mouse model, monitoring Disease Activity Index (DAI), inflammatory cytokines levels, and histopathology. Macrogenomics and bile acid (BAs) metabolomics analysed the major intestinal flora and BAs. Simultaneouslly, we conducted quantitative proteomics analysis and screened core proteins and pathway. In vitro validation was taken by qPCR, immunofluorescence and immunoblotting experiments. Results GE via enema alleviate UC by inhibiting inflammatory factor production through downregulating S100A8/S100A9/NF-κB pathway. Analysis of the intestinal flora and BAs revealed that the enhanced abundance of Lachnospiraceae , which improves the ratio of primary to secondary BAs, and the reduced abundance of Provocaceae , which increases intestinal permeability and promotes inflammation, favored the restoration of the intestinal barrier. In addition, in vitro experiments confirmed that the key BA metabolites (mainly UDCA, DCA, and LCA) stimulated TGR5 signal to inhibit the assembly of the NLRP3 inflammasome and alleviated inflammation. Conclusion We firstly confirmed that GE alleviates UC via the enema route in a better manner than the oral route, through enhancing the intestinal barrier, restoring intestinal flora and BAs homeostasis, and inhibiting inflammatory injury. This study initially revealed that GE can alleviate UC through elevating UDCA, DCA, and LCA levels at the colonic site to activate TGR5 receptor for inhibiting the NLRP3 inflammasome, in addition to downregulating the S100A8/S100A9/-TLR4-NF-κB pathway related inflammatory response directly. The evidences offer a promising strategy and profround meaning for UC treatment.
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BIOLOGICAL & PHARMACEUTICAL BULLETIN
·
2023
·Vol. 46
·期 2
·209-218
·
IF 2
Chenhao Li,Cuizhi Geng
Triple-negative breast cancer (TNBC) puts a great threat to women’s health. GLIS family zinc finger 3 (GLIS3) belongs to the GLI transcription factor family and acts as a critical factor in cancer progression. Nevertheless, the part of GLIS3 played in TNBC is not known. Immunohistochemical (IHC) staining analysis displayed that GLIS3 was highly expressed in TNBC tissues. The effect of GLIS3 on the malignant phenotype of TNBC was tested in two different cell lines according to GLIS3 regulation. Upregulation of GLIS3 promoted the proliferation, migration, and invasion of TNBC cell lines, whereas the knockdown of GLIS3 suppressed these tumor activities. Inhibition of GLIS3 induced TNBC cell apoptosis. Furthermore, study as immunofluorescence and electrophoretic mobility shift assay confirmed that the nuclear factor-κB (NF-κB) signaling pathway activated by GLIS3 played an important role in TNBC cells’ malignant phenotype. In conclusion, the present work demonstrated that GLIS3 acts as a crucial element in TNBC progression via activating the NF-κB signaling pathway. Accordingly, above mentioned findings indicated that modulation of GLIS3 expression is a potential tactic to interfere with the progression of TNBC.
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PHYTOMEDICINE
·
2022
·
IF 6.656
Zhenhao Li,Haitao Pan,Jihong Yang,Dongjie Chen,Yu Wang,Han Zhang,Yiyu Cheng
Background Xuanfei Baidu Formula (XBF) is an effective traditional Chinese medicine (TCM) remedy for treating coronavirus disease 2019 (COVID-19) in China. This herbal medicine has shown effects in reducing clinical symptoms and shortening the average length of hospital stay for COVID-19 patients. Previous studies have demonstrated that XBF alleviates acute lung injury (ALI) by regulating macrophage-mediated immune inflammation, but the mechanisms of action remain elusive. Purpose This study aimed to evaluate the lung-protective and anti-inflammatory effects of XBF and its underlying mechanisms. Methods Here, XBF's effects were investigated in an ALI mouse model induced by inhalation of atomized lipopolysaccharide (LPS). Besides, the LPS-induced inflammation model in RAW264.7 cells was used to clarify the underlying mechanisms of XBF against ALI. Results Our results showed that XBF treatment alleviated LPS-induced lung injury, as evidenced by reduced histopathological changes, pulmonary alveoli permeability, fibrosis, and apoptosis in the lung tissues. In addition, inflammation was alleviated as shown by decreased levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β in serum and bronchoalveolar lavage fluid (BALF), and reduced white blood cell (WBC) count in BALF. Furthermore, consistent with the in vivo assay, XBF inhibited LPS-induced inflammatory cytokines release and pro-inflammatory polarization in RAW264.7 cells. Mechanistically, XBF increased mitochondrial fusion by upregulating Mfn1 and attenuated NLRP3 inflammasome activation by repressing Casp11, respectively, to inhibit NF-κB and MAPK pathways, thus repressing pro-inflammatory macrophage polarization. Conclusion In this study, we demonstrate that XBF exerts anti-ALI and -inflammatory effects by recovering mitochondrial dynamics and reducing inflammasome activation, providing a biological illustration of the clinical efficacy of XBF in treating COVID-19 patients.
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Antioxidants
·
2023
·Vol. 12
·期 1
·194
·
IF 7
Chongshan Dai,Xueyong Zhang,Jiahao Lin,Jianzhong Shen
Acute liver injury is a type of liver diseases, and it has raised concerns worldwide due to the lack of effective therapies. The aim of this study is to investigate the protective effects of nootkatone (NOOT) on carbon tetrachloride (CCl4)-caused acute liver injury in mice. Mice were randomly divided into control, CCl4model, NOOT, and NOOT (5, 10, and 20 mg/kg/day) plus CCl4groups, respectively. Mice in the CCl4plus NOOT groups were orally administrated with NOOT at 5, 10, and 20 mg/kg/days for seven days prior to 0.3% CCl4injection at 10 mL/kg body weight, respectively. Our results showed that NOOT supplementation significantly ameliorated CCl4-induced increases of serum AST and ALT levels, hepatocyte necrosis, inflammatory response, oxidative stress, and caspases-9 and -3 activities in the livers of mice. Moreover, NOOT supplementation significantly upregulated the expression of Nrf2 and HO-1 mRNAs but downregulated the expression of NF-κB mRNAs and the levels of IL-1β, IL-6, and TNF-α proteins in the liver tissues, compared to those in the CCl4model group. In conclusion, for the first time, our results reveal that NOOT could offer protective effects against CCl4-caused oxidative stress and inflammatory response via the opposite regulation of Nrf2/HO-1 pathway and NF-κB pathway.Keywords:nootkatone;oxidative stress;acute liver injury;Nrf2/HO-1 pathway;NF-κB pathway
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CELL CYCLE
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2022
·
IF 5.173
Tianjiao Lai,Haifeng Qiu,Lulu Si,Yu Zhen,Danxia Chu,Ruixia Guo
Endometrial carcinoma (EC) originates from the endometrium and is one of the most common tumors in female patients, and its incidence has continued to increase in recent decades. LncRNAs are involved in the pathogenesis and metastasis of a variety of malignant tumors, which indicates that lncRNAs can be used as tumor diagnostic markers and potential therapeutic targets. In this study, we analyzed the RNA transcripts of EC cells from The Cancer Genome Atlas (TCGA) and first reported a novel lncRNA, BMPR1B-AS1, that was more highly expressed in endometrial cancer tissues than in adjacent tissues, and BMPR1B-AS1 could promote endometrial cancer cell proliferation and metastasis. Bioinformatics prediction and experimental results both suggested that BMPR1B-AS1 could modulate the malignant behaviors of endometrial cancer cell lines by sponging miR-7-2-3p to modulate DCLK1, and a DCLK1 inhibitor blocked the activation of the PI3K/Akt/NF-κB signaling pathway. Collectively, this study suggests that the BMPR1B-AS1/miR-7-2-3p/DCLK1 axis contributes to the proliferation and metastasis of endometrial cancer cells via the PI3K/Akt/NF-κB pathway.
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JOURNAL OF ETHNOPHARMACOLOGY
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2021
·
IF 4.36
Feng-mao An,Zheng Liu,Xin-ran Xuan,Qing-shan Liu,Cheng-xi Wei
Ethnopharmacological relevance The traditional Chinese medicine Sanweidoukou decoction (DK-3) was a classical formula for the treatment of nervous system diseases , recorded in the Chinese medical classic Sibu Yidian . Aim of the study The present study is aim to investigate the neuroprotective effects of DK-3 on β-amyloid (Aβ) protein -induced AD-like pathologies and underlying molecular mechanisms both in vitro and in vivo studies. Materials and methods Hydrolysates of DK-3 were analyzed by LC-ESI-MS/MS. In vitro , MTT was utilized to examine effects of DK-3 on Aβ 25-35 -induced cytotoxicity in PC12 cells. In vivo , male Sprague-Dawley rats were administered with Aβ 25-35 to induce AD-like pathologies and behavioral evaluations were conducted via Morris water maze (MWM) test. Histopathological changes were observed by Hematoxylin-eosin (HE) straining. Immunohistochemistry (IHC) was used to detect the tau hyperphosphorylation at Thr181 site. The expression levels of tau hyperphosphorylation, inflammation-related cytokines such as COX-2, iNOS , TNF-α, IL-1β, IL-6, the phosphorylated state of various mitogen-activated protein kinase (MAPK) signaling molecules (p38 MAPK, ERK, and JNK) and activation of nuclear factor κB (NF-κB) in vitro and in vivo were assessed via Western blot . Results In vitro , DK-3 dose-dependently increased cell viability of PC12 cells induced by Aβ 25-35 . In vivo , DK-3 improved learning and memory abilities of Aβ 25-35 -induced AD-like rats. Moreover, DK-3 reversed hyperphosphorylation of tau and reduced the production of inflammation-related cytokines through significantly inhibited MAPK and NF-κB signaling pathways both in vitro and in vivo studies. Conclusion The present study suggested that the traditional Chinese medicine DK-3 may play a role in preventing and treating AD by reducing the hyperphosphorylation of tau protein and the expressions of inflammation-related cytokines via modulating the MAPK/NF-κB signaling pathways.
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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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2019
·
IF 2.705
Jinyue Zhu,Weiqing Wang,Xia Wu
Hyperplasia of airway smooth muscle cells (ASMCs) is key to the progression of asthma. Isorhynchophylline (IRN) derived from Uncaria rhynchophylla can inhibit the proliferation of AMSCs. The major purpose of the current study was to assess the effect of IRN on the asthma symptoms was assessed both in vitro and in vivo, and the associated mechanism of the effect was also explored by focusing on the function of miR-200a. Asthma model was induced using ovalbumin (OVA) method and AMSC hyperplasia model was induced using TGF-β1. The effect of IRN on allergic asthma mice and the effect of IRN on the proliferation of ASMCs were investigated as well, and the changes in miR-200a level and FOXC1/NF-κB pathway were detected. The administration of IRN attenuated the eosinophils recruitment in BALF, reduced collagen deposition in lung tissues, and suppressed production of IgE and pro-inflammation cytokines. IRN also inhibited the proliferation and induced the apoptosis of ASMCs. Moreover, the administration of IRN increased the level of miR-200a while inhibited the activation of FOXC1/NF-κB pathway. However, after the inhibition of miR-200a level, the function of IRN on ASMCs was impaired. Collectively, it was demonstrated that the effect of IRN on asthma relied on the up-regulation of miR-200a, which then deactivated FOXC1/NF-κB pathway.
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PHYTOMEDICINE
·
2023
·
IF 7.9
Mei-Qi Wang,Kai-Hui Zhang,Fang-Le Liu,Rui Zhou,Yun Zeng,A-Li Chen,Yang Yu,Quan Xia,Chen-Chen Zhu,Chao-Zhan Lin
Background : Cholestatic liver diseases (CLD) comprise a variety of disorders of bile formation, which causes chronic exposure to bile acid (BA) in the liver generally and results in hepatotoxicity and progressive hepatobiliary injury. Wedelolactone (7-methoxy-5, 11, 12-trihydroxy-coumestan, WED), the natural active compound derived from Ecliptae Herba, has been reported with valuable bioactivity for liver protection. Nevertheless, the effect of WED on cholestatic liver injury (CLI) remains unexplored. Purpose : The present study aims to elucidate the protective effect of WED on Alpha-naphthylisothiocyanate (ANIT)-induced CLI mice, and to investigate its potential pharmacological mechanism. Methods : The anti-cholestasis and hepatoprotective effects of WED were evaluated in ANIT-induced CLI mice. Non-targeted metabolomics study combined with ingenuity pathway analysis (IPA) was used to explore the key mechanism of WED. The BA metabolic profile in enterohepatic circulation was analyzed to evaluate the effect of WED in regulating BA metabolism. Further, molecular dynamics (MD) simulation and cellular thermal shift assay (CETSA) were used to simulate and verify the targeting activation of WED on the Farnesoid X receptor (FXR). The core role of FXR in WED promoting BA transportation, and alleviating BA accumulation-induced hepatotoxicity was further evaluated in WT and FXR knockout mice or hepatocytes. Results : WED dose-dependently alleviated ANIT-induced cholestasis and liver injury in mice, and simultaneously suppressed the nuclear signaling pathway of factor-kappa B/nuclear factor-erythroid 2-related factor 2 (NF-κB/NRF2) to relieve inflammation and oxidative stress. At the metabolite level, WED improved the metabolic disorder in CLI mice focusing on the metabolism of BA, arachidonic acid, and glycerophospholipid, closely related to the process of BA regulation, inflammation, and oxidative damage. WED targeting activated FXR, which then transcribed its target genes, including the bile salt export pump (BSEP) and the BA transporter, which subsequently increased BA transportation to restore the damaged enterohepatic circulation of BA. Meanwhile, WED alleviated hepatic BA accumulation and protected the liver from BA-induced damage via NF-κB/NRF2 signaling pathway. Furthermore, FXR deficiency suppressed the protective effect of WED in vitro and in vivo . Conclusion : WED regulated BA metabolism and alleviated hepatic damage in cholestasis. It protected the liver according to adjusted BA transportation and relieved BA accumulation-related hepatotoxicity via FXR-bile acid-NF-κB/NRF2 axis. Our study provides novel insights that WED might be a promising strategy for cholestatic liver disease.
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Food & Function
·
2023
·
IF 6.1
Zhongcai Wu,Xuezhi Zuo,Xiuru Wang,Mengxia Shi,Han Zhu,Chujin Cao,Xiaoqin Liu,Wangqun Liang,Ying Yao,Le Wang
Peritoneal fibrosis is a complication of long-term peritoneal dialysis (PD) that restricts its clinical application for the treatment of end-stage renal disease. Lactobacillus casei Zhang (LCZ), a probiotic strain isolated from traditional fermented koumiss, exhibits health benefits such as anti-inflammatory and antioxidative effects, improvement of insulin resistance and mitigation of renal injury. However, whether LCZ can prevent peritoneal fibrosis remains unknown. Here, we assessed the effects of LCZ in a mouse model of PD-induced peritoneal fibrosis. Our results showed that the administration of LCZ significantly ameliorated peritoneal fibrosis in experimental mice. Macrophage infiltration, inflammatory M1 polarization and inflammatory cytokines in peritoneal dialysis effluents were effectively reduced by LCZ. Meanwhile, LCZ corrected gut dysbiosis and enriched beneficial bacteria that produce short-chain fatty acids, specifically Dubosiella, Lachnospiraceae, Parvibacter, and Butyricicoccus. Correspondingly, the local butyrate level in peritoneal dialysis effluents was significantly elevated by LCZ. Mechanistically, we found activation of PPARγ and inhibition of the NF-κB pathway in LCZ-treated mice, an observation that was replicated in a butyrate-treated macrophage cell line. In conclusion, our study suggests that LCZ is beneficial for preventing PD-induced peritoneal fibrosis through modulating the gut microbiota, enhancing butyrate production, activating PPARγ, and suppressing NF-κB-mediated inflammation.
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