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Construction of antibacterial layer on polyvinylchloride three-channel hollow fiber membranes
Mei-Sheng Li,Ming-Xing Wang,Fei-Yue Wu,Xiao-Zhong Chu 한국공업화학회 2016 Journal of Industrial and Engineering Chemistry Vol.39 No.-
The inner surfaces of polyvinylchloride (PVC) three-channel hollow fiber membranes were successfullymodified with poly(methacryloxylethyl benzyl dimethyl ammonium chloride) (PDMAE-BC) in a modulescale via remote plasma-induced surface graft polymerization method. After grafting a PDMAE-BC layer,the PVC surface hydrophilicity was improved greatly due to the introduction of large amounts of oxygenand nitrogen containing polar groups onto polymer backbone. This hydrophilicity improvement directlyleaded to a high pure water flux and a good antifouling property for the obtained PVC-PDMAE-BCmembrane module. Meanwhile, the inner surface morphologies of modified PVC membranes changedslightly and the surface structures were maintained well. The tensile strength, though deceased slightlyat the remote plasma-treated stage, showed no significant change during overall grafting process. Theobtained PVC-PDMAE-BC membrane module exhibited highly effective and stable antibacterialactivities against Escherichia coli. The antibacterial efficacy of PVC-PDMAE-BC membrane module withonly 6 fibers can achieve about 96.3% and could be further enhanced by increasing the packing density. The antibacterial membrane module may have great potential applications in actual wastewatertreatment and membrane bioreactor (MBR).
Jun-Nan Hu,Xing-Yue Xu,Wei Li,Yi-Ming Wang,Ying Liu,Zi Wang,Ying-Ping Wang 고려인삼학회 2019 Journal of Ginseng Research Vol.43 No.1
Background: Frequent overdose of paracetamol (APAP) has become the major cause of acute liver injury. The present study was designed to evaluate the potential protective effects of ginsenoside Rk1 on APAPinduced hepatotoxicity and investigate the underlying mechanisms for the first time. Methods: Micewere treated with Rk1 (10 mg/kg or 20 mg/kg) by oral gavage once per d for 7 d. On the 7th d, all mice treatedwith250mg/kgAPAPexhibitedsevere liver injuryafter24h, andhepatotoxicitywas assessed. Results: Our results showed that pretreatment with Rk1 significantly decreased the levels of serum alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor, and interleukin-1b compared with the APAPgroup.Meanwhile, hepatic antioxidants, including superoxide dismutase andglutathione,were elevated compared with the APAP group. In contrast, a significant decrease in levels of the lipid peroxidation product malondialdehyde was observed in the ginsenoside Rk1-treated group compared with the APAP group. These effectswere associatedwith a significant increase of cytochromeP450 E1 and 4-hydroxynonenal levels in liver tissues. Moreover, ginsenoside Rk1 supplementation suppressed activation of apoptotic pathways by increasing Bcl-2 and decreasing Bax protein expression levels, which was shown using western blotting analysis.Histopathological observation also revealed that ginsenoside Rk1 pretreatment significantly reversed APAP-induced necrosis and inflammatory infiltration in liver tissues. Biological indicators of nitrative stress, such as 3-nitrotyrosine, were also inhibited after pretreatment with Rk1 compared with the APAP group. Conclusion: The results clearly suggest that the underlying molecular mechanisms in the hepatoprotection of ginsenoside Rk1 in APAP-induced hepatotoxicity may be due to its antioxidation, antiapoptosis, anti-inflammation, and antinitrative effects.
Hu, Jun-Nan,Xu, Xing-Yue,Li, Wei,Wang, Yi-Ming,Liu, Ying,Wang, Zi,Wang, Ying-Ping The Korean Society of Ginseng 2019 Journal of Ginseng Research Vol.43 No.1
Background: Frequent overdose of paracetamol (APAP) has become the major cause of acute liver injury. The present study was designed to evaluate the potential protective effects of ginsenoside Rk1 on APAP-induced hepatotoxicity and investigate the underlying mechanisms for the first time. Methods: Mice were treated with Rk1 (10 mg/kg or 20 mg/kg) by oral gavage once per d for 7 d. On the 7th d, allmice treated with 250mg/kg APAP exhibited severeliverinjury after 24 h, and hepatotoxicitywas assessed. Results: Our results showed that pretreatment with Rk1 significantly decreased the levels of serum alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor, and interleukin-$1{\beta}$ compared with the APAP group. Meanwhile, hepatic antioxidants, including superoxide dismutase and glutathione, were elevated compared with the APAP group. In contrast, a significant decrease in levels of the lipid peroxidation product malondialdehyde was observed in the ginsenoside Rk1-treated group compared with the APAP group. These effects were associated with a significant increase of cytochrome P450 E1 and 4-hydroxynonenal levels in liver tissues. Moreover, ginsenoside Rk1 supplementation suppressed activation of apoptotic pathways by increasing Bcl-2 and decreasing Bax protein expression levels, which was shown using western blotting analysis. Histopathological observation also revealed that ginsenoside Rk1 pretreatment significantly reversed APAP-induced necrosis and inflammatory infiltration in liver tissues. Biological indicators of nitrative stress, such as 3-nitrotyrosine, were also inhibited after pretreatment with Rk1 compared with the APAP group. Conclusion: The results clearly suggest that the underlying molecular mechanisms in the hepatoprotection of ginsenoside Rk1 in APAP-induced hepatotoxicity may be due to its antioxidation, antiapoptosis, anti-inflammation, and antinitrative effects.
( Jia-yi Dou ),( Yu-chen Jiang ),( Zhong-he Hu ),( Kun-chen Yao ),( Ming-hui Yuan ),( Xiao-xue Bao ),( Mei-jie Zhou ),( Yue Liu ),( Zhao-xu Li ),( Li-hua Lian ),( Ji-xing Nan ),( Yan-ling Wu ) 한국응용약물학회 2022 Biomolecules & Therapeutics(구 응용약물학회지) Vol.30 No.3
The present study focused on the potential mechanism of betulin (BT), a pentacyclic triterpenoid isolated from the bark of white birch (Betula pubescens), against chronic alcohol-induced lipid accumulation and metaflammation. AML-12 and RAW 264.7 cells were administered ethanol (EtOH), lipopolysaccharide (LPS) or BT. Male C57BL/6 mice were fed Lieber-DeCarli liquid diets containing 5% EtOH for 4 weeks, followed by single EtOH gavage on the last day and simultaneous treatment with BT (20 or 50 mg/kg) by oral gavage once per day. In vitro, MTT showed that 0-25 mM EtOH and 0-25 μM BT had no toxic effect on AML-12 cells. BT could regulate sterolregulatory-element-binding protein 1 (SREBP1), lipin1/2, P2X7 receptor (P2X7r) and NOD-like receptor family, pyrin domains-containing protein 3 (NLRP3) expressions again EtOH-stimulation. Oil Red O staining also indicated that BT significantly reduced lipid accumulation in EtOH-stimulated AML-12 cells. Lipin1/2 deficiency indicated that BT might mediate lipin1/2 to regulate SREBP1 and P2X7r expression and further alleviate lipid accumulation and inflammation. In vivo, BT significantly alleviated histopathological changes, reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and triglyceride (TG) levels, and regulated lipin1/2, SREBP1, peroxisome proliferator activated receptor α/γ (PPARα/γ) and PGC-1α expression compared with the EtOH group. BT reduced the secretion of inflammatory factors and blocked the P2X7r-NLRP3 signaling pathway. Collectively, BT attenuated lipid accumulation and metaflammation by regulating the lipin1/2-mediated P2X7r signaling pathway.
Yang, Xiao-Li,Zhang, Cheng-Dong,Wu, Hua-Yu,Wu, Yong-Hu,Zhang, Yue-Ning,Qin, Meng-Bin,Wu, Hua,Liu, Xiao-Chun,Lina, Xing,Lu, Shao-Ming Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.11
Trichostatin A (TSA) is a histone deacetylase (HDAC) inhibitor. We here investigated its effects on proliferation and apoptosis of the CNE2 carcinoma cell line, and attempted to establish genome-wide DNA methylation alteration due to differentially histone acetylation status. After cells were treated by TSA, the inhibitory rate of cell proliferation was examined with a CCK8 kit, and cell apoptosis was determined by flow cytometry. Compared to control, TSA inhibited CNE2 cell growth and induced apoptosis. Furthermore, TSA was found to induce genome-wide methylation alteration as assessed by genome-wide methylation array. Overall DNA methylation level of cells treated with TSA was higher than in controls. Function and pathway analysis revealed that many genes with methylation alteration were involved in key biological roles, such as apoptosis and cell proliferation. Three genes (DAP3, HSPB1 and CLDN) were independently confirmed by quantitative real-time PCR. Finally, we conclude that TSA inhibits CNE2 cell growth and induces apoptosis in vitro involving genome-wide DNA methylation alteration, so that it has promising application prospects in treatment of NPC in vivo. Although many unreported hypermethylated/hypomethylated genes should be further analyzed and validated, the pointers to new biomarkers and therapeutic strategies in the treatment of NPC should be stressed.