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Multi-endpoint assays reveal more severe toxicity induced by chloraminated effluent organic matter than chloraminated natural organic matter

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Journal of Environmental Sciences 2024年第1期135卷 310-317页

作者： Hai-Yan Wang De-xiu Wu ye Du Xiao-Tong Lv Qian-Yuan Wu State Key Laboratory of Environmental Criteria and Risk Assessment Chinese Research Academy of Environmental SciencesBeijing 100012China Environmental Protection Key Laboratory of Microorganism Application and Risk Control Guangdong Provincial Engineering Research Center for Urban Water Recycling and Environmental SafetyTsinghua Shenzhen International Graduate SchoolTsinghua UniversityShenzhen 518055China College of Architecture and Environment Sichuan UniversityChengdu 610000China

Disinfection by chloramination produces toxic byproducts and the difference in toxicity of reclaimed and drinking water treated by chloramination remains unclear.This study investigated cytotoxic effects at the same concentrations of dissolved organic matter and showed that chloraminated effluent organic matter(EfOM)induced 1.7 times higher cytotoxicity than chloraminated natural organic matter(NOM)applied to simulate drinking water.Chloraminated EfOM induced more reactive nitrogen species than chloraminated NOM,and chloraminated EfOM and NOM induced similar and higher levels of reactive oxygen species than the negative control,respectively.Consequently,intracellular macromolecule damage indicated by DNA/RNA damage marker 8–hydroxy-(deoxy)guanosine and the intracellular protein carbonyl concentration induced by chloraminated EfOM was higher and slightly more than that induced by chloraminated NOM,respectively.These data were consistent with the effects on cell physiological processes.Cell cycle arrest mainly occurred in G2 phase by chloraminated EfOM and NOM.Early apoptotic cells,which could return to normal,increased upon exposure to high concentrations of chloraminated EfOM and NOM.Moreover,necrotic cells were significantly increased from 0.5%to 2.5%when the concentration increased from 20-to 60-fold chloraminated EfOM,but were not obviously changed by chloraminated NOM.These results indicated that the comprehensive intracellular changes induced by toxic substances in chloraminated EfOM were more irreversible and induced more cell death than chloraminated NOM.

关键词： Cytotoxicity Intracellular active nitrogen/oxygen Intracellular oxidative damage Cell necrosis Reclaimed water

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Hypoglycemic effect and the mechanism of action of a polysaccharide from sweet corncob in a high-fat diet and streptozotocin-induced diabetic mice

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Food Science and Human Wellness 2024年第3期13卷 1543-1555页

作者： Xin Wang Weiye xiu ye Han Zhili Wang Yu Luo Yongqiang Ma Heilongjiang Provincial Key Laboratory of Cereals and Comprehensive Processing of Cereal Resources College of Food EngineeringHarbin University of CommerceHarbin 150028China

Type 2 diabetes mellitus(T2DM)is a metabolic disease caused by a glycolipid metabolism disorder and isletβ-cell dysfunction.SCP-80-I is a biologically active water-soluble polysaccharide isolated from sweet corncob,an agricultural byproduct.The hypoglycemic effects of SCP-80-I on T2DM mice and its mechanisms were investigated in this study.SCP-80-I was found to significantly reduce blood glucose and lipid deposition levels in T2DM mice,as well as decrease serum leptin and increase adiponectin secretion.Interestingly,real time-polymerase chain reaction(RT-PCR)and Western blotting results revealed that SCP-80-I could regulate the expression of several glycolipid metabolisms and insulin secretion genes and proteins,including 5'-AMP-activated protein kinase(AMPK),carnitine palmitoyltransferase I(CPTI),and acetyl coenzyme A carboxylase(ACC)in the liver and AMPK,sirtuin1(Sirtl),peroxisome proliferator-activated receptorycoactivator-1(PGC-1α),and uncoupling protein 2(UCP2)in the pancreas.To have a hypoglycemic effect,SCP-80-1 regulated glycolipid metabolism and islet cell function in the liver by regulating the AMPK/AC C/CPT1 signaling pathway and the AMPK/Sirt1/PGC-1αand AMPK/Sirtl/UCP2 signaling pathways.These findings improve our understanding of polysaccharides derived from sweet corncob and the use of SCP-80-I in the production of hypoglycemic foods.

关键词： Sweet corn cob polysaccharide Type 2 diabetes Signal pathway 5’-AMP-activated protein kinase(AMPK)

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Dynamic manipulation of multimodal emission in Er3+-activated non-core-shell structure for optical thermometry and information security

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Rare Metals 2024年第4期43卷 1702-1712页

作者： Xuan Liu zi-Xia Lin Yin-Biao Shi Xiao-Yan Wang Ming-ye Ding Xiao-Fei Yang College of Science Nanjing Forestry University Testing Center Yangzhou University

Regulating luminescent dynamics of lanthanide-based luminescent materials via external stimuli is of great significance in the fields of optical thermometry and high-level anti-counterfeiting.However,it is still a huge challenge to realize multimodal emissions with tunable color outputs from a single activator in simple structures via smart dynamic control of photon transition processes.Herein,we present a mechanistic strategy to achieve multimodal luminescence of Er3+activators with color-switchable outputs in a non-core-shell host.Under the control of excitation dynamics(λex=980,808,1532,377 nm),the population among the intermediate en ergy levels of Er3+and the interaction between Er3+and Yb3+could be precisely modulated through energy transfer and migration processes,leading to the generation of colortunable multimodal luminescence upon diverse excitation modes（non-steady-state,single-/dual-wavelength steady,thermal activation）.Inspired by its special luminescent performance,the as-obtained material exhibits great potential in noncontact thermometry,multimodal anticounterfeiting,and high-capacity information encryption by performing a series of proof-of-concept experiments.Our findings might provide a conceptual model to modulate the luminescent dynamics in a simple-structured system for the generation of color-adjustable multimodal emissions,which is convenient for the development of advanced luminescent materials toward versatile cuttingedge applications.

关键词： Lanthanide ions Multimodal emission Upconversion Downshifting Anti-counterfeiting Luminescent thermometry

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Ki-67 Change in Anthracyline-containing Neoadjuvant Chemotherapy Response in Breast Cancer

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Current Medical Science 2024年第1期44卷 156-167页

作者： zi-guo YANG Le-hao REN Feng WANG Pi-lin WANG Wen-yan WANG Shu-ye LIN Department of General Surgery Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070China Department of Critical Care Medicine Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China Cancer Research Center Beijing Chest HospitalCapital Medical University/Beijing Tuberculosis and Thoracic Tumor Research InstituteBeijing 101149China

Objective Anthracycline-containing regimens are irreplaceable in neoadjuvant chemotherapy(NAC)for breast cancer(BC)at present.However,30% of early breast cancer(EBC)patients are resistant to anthracycline-containing chemotherapy,leading to poor prognosis and higher mortality.Ki-67 is associated with the prognosis and response to therapy,and it changes after NAC.Methods A total of 105 BC patients who received anthracycline-containing NAC were enrolled.Then,the optimal model of Ki-67 was selected,and its predictive efficacy was analyzed.Immunohistochemistry(IHC)was used to determine the estrogen receptor(ER),progesterone receptor(PR),and human epidermal growth factor receptor 2(HER-2)status and Ki-67 level.Fluorescent in situ hybridization(FISH)was used to verify the HER-2 when the IHC score was 2+.Results The post-NAC Ki67 level after treatment with anthracycline drugs was lower than pre-NAC Ki-67(19.6%±23.3%vs.45.6%±23.1%,P<0.001).Furthermore,patients with the Ki-67 decrease had a border line higher pathological complete response(pCR)rate(17.2%vs.0.0%,P=0.068),and a higher overall response rate(ORR)(73.6%vs.27.8%,P<0.001),when compared to patients without the Ki-67 decrease.The ΔKi-67 and ΔKi-67%were valuable markers for the prediction of both the pCR rate and ORR.The area under the curve(AUC)for ΔKi-67 on pCR and ORR was 0.809(0.698-0.921)and 0.755(0.655-0.855),respectively,while the AUC for ΔKi-67% on pCR and ORR was 0.857(0.742-0.972)and 0.720(0.618-0.822),respectively.Multivariate logistic regression model 1 revealed thatΔKi-67 was an independent predictor for both pCR[odds ratio(OR)=61.030,95% confidence interval(CI)=4.709-790.965;P=0.002]and ORR(OR=10.001,95%CI:3.044-32.858;P<0.001).Multivariate logistic regression model 2 revealed thatΔKi-67%was also an independent predictor for both pCR(OR=408.922,95%CI=8.908-18771.224;P=0.002)and ORR(OR=5.419,95%CI=1.842-15.943;P=0.002).Conclusions The present study results suggest thatΔKi67 andΔKi67%are candidate predictors for anthracycline-containing NAC response,and

关键词： breast cancer change in Ki-67 neoadjuvant chemotherapy anthracycline,response

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Ginsenoside Rg3 Promotes the Survival and Migration of Trophoblast Cells in a Rat Model of Gestational Hypertension by Regulating miR-100a/Insulin Growth Factor-2 Axis

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World Journal of Traditional Chinese Medicine 2024年第1期10卷 65-74页

作者： xiu-Mei Fan Li Yang Gang Zhao Sen-ye Huo Yan Gao Department of Obstetrics Xingtai Third HospitalXingtaiChina Department of Obstetrics Xingtai Maternal and Child Health Care HospitalXingtaiChina

Objective:Preeclampsia(PE)is a common complication during pregnancy.miR-100a is expressed in the placenta and regulates the survival and development of placental cells.Insulin growth factor-2(IGF-2)may serve as its downstream target.This study investigated the protective mechanisms of ginsenoside Rg3 against PE in rat model.Materials and Methods:LPS-induced rat PE models were suitable for intravenous administration of the highly expressed miR-100a ginsenoside Rg3 lentiviral vector.Human trophoblasts were cultured in vitro for JEG-3,and PE cell models were constructed.In vivo effects on tumor growth and apoptosis were observed.Ginsenoside Rg3 was treated with different concentrations of shRNA,miR-100a analogs,inhibitors,or IGF-2.Autophagy and the expression of autophagy-related proteins were examined.Trophoblast activity and migration were determined using Cell Counting Kit-8 and Transwell assays.Both drugs strongly inhibited trophoblasts under normal conditions with some synergy between them.Double-luciferase return assay confirmed the binding affinity of miR-100a for IGF-2.Results:In response to Rg3,autophagy and the expression of autophagy-related proteins LC3-I/II,Beclin1,and SQSTM1 were reduced in PE rat placental trophoblasts.Rg3 inhibited autophagy in JEG-3 cells and promoted JEG-3 survival and migration in a concentration-dependent manner.miR-100a upregulated PE expression.These results suggested that autophagy was a vital signaling system.Rg3 intervention inhibited miR-100a expression and miR-100a downregulated IGF-2 expression in placental tissues and promoted autophagy,thereby inhibiting JEG-3cell survival and migration.In rats,Rg3 inhibited PE development by regulating the activity of the miR-100a-IGF-2 signaling axis.Conclusion:Ginsenoside Rg3 positively regulates the miR-100a-IGF-2 axis and protects PE rats by inhibiting trophoblastic autophagy and promoting trophoblastic cell survival and migration.

关键词： Ginsenoside Rg3 inflammatory response miR-100a/insulin growth factor-2 axis preeclampsia pregnancy-induced hypertension

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Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/m TOR Signaling Pathway

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Chinese Journal of Integrative Medicine 2024年第3期30卷 251-259页

作者： YAO Jun-peng FENG xiu-mei WANG Lu LI Yan-qiu ZHU zi-yue YAN Xiang-yun YANG Yu-qing LI Ying ZHANG Wei Acupuncture and Tuina School Chengdu University of Traditional Chinese MedicineChengdu611137China Department of Rehabilitation Medicine Guanghan People’s HospitalGuanghanSichuan Province618399China Academic Affairs Office Chengdu University of Traditional Chinese MedicineChengdu611137China

Objective:To explore the mechanism of electroacupuncture(EA) in promoting recovery of the facial function with the involvement of autophagy,glial cell line-derived neurotrophic factor(GDNF),and phosphatidylinositol-3-kinase(PI3K)/mammalian target of rapamycin(mTOR) signaling pathway.Methods:Seventy-two male Sprague-Dawley rats were randomly allocated into the control,sham-operated,facial nerve injury(FNI),EA,EA+3-methyladenine(3-MA),and EA+GDNF antagonist groups using a random number table,with 12 rats in each group.An FNI rat model was established with facial nerve crushing method.EA intervention was conducted at Dicang(ST 4),Jiache(ST 6),Yifeng(SJ 17),and Hegu(LI 4) acupoints for 2 weeks.The Simone’s 10-Point Scale was utilized to monitor the recovery of facial function.The histopathological evaluation of facial nerves was performed using hematoxylin-eosin(HE) staining.The levels of Beclin-1,light chain 3(LC3),and P62 were detected by immunohistochemistry(IHC),immunofluorescence,and reverse transcriptionpolymerase chain reaction,respectively.Additionally,IHC was also used to detect the levels of GDNF,Rai,PI3K,and mTOR.Results:The facial functional scores were significantly increased in the EA group than the FNI group(Pyelin sheaths,which were destroyed immediately after the injury,were recovered with EA treatment.The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats(P<0.01);however,EA treatment reversed these abnormal changes(P<0.01).Meanwhile,EA stimulation significantly increased the levels of GDNF,Rai,PI3K,and mTOR(P<0.01).After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist,the repair effect of EA on facial function was attenuated(P<0.05 or P<0.01).Conclusions:EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI.EA may exert this neuroreparative effect through mediating the release of GDNF,activating the PI3

关键词： electroacupuncture facial nerve injury autophagy glial cell line-derived neurotrophic factor phosphatidylinositol-3-kinase/mammalian target of rapamycin Chinese medicine

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Semaphorin 7A impairs barrier function in cultured human corneal epithelial cells in a manner dependent on nuclear factor-kappa B

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International Journal of Ophthalmology(English edition) 2024年第3期17卷 444-453页

作者： Cheng-Cheng Yang xiu-Xia Yang Xiao-Jing Zhao Heng Wang zi-Han Guo Kai Jin Yang Liu Bin-Hui Li Department of Ophthalmology the Fifth Affiliated HospitalSun Yat-sen UniversityZhuhai 519000Guangdong ProvinceChina Department of Ophthalmology Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical UniversityHangzhou 310006Zhejiang ProvinceChina Eye Institute of Xiamen University Fujian Provincial Key Laboratory of Ophthalmology and Visual ScienceSchool of MedicineXiamen UniversityXiamen 361005Fujian ProvinceChina

●AIM:To evaluate the role of semaphorin 7A(Sema7A)and its associated regulatory mechanisms in modulating the barrier function of cultured human corneal epithelial cells(HCEs).●METHODS:Barrier models of HCEs were treated with recombinant human Sema7A at concentrations of 0,125,250,or 500 ng/mL for 24,48,or 72h in vitro.Transepithelial electrical resistance(TEER)as well as Dextran-fluorescein isothiocyanate(FITC)permeability assays were conducted to assess barrier function.To quantify tight junctions(TJs)such as occludin and zonula occludens-1(ZO-1)at the mRNA level,reverse transcriptionpolymerase chain reaction(RT-PCR)analysis was performed.Immunoblotting was used to examine the activity of the nuclear factor-kappa B(NF-κB)signaling pathway and the production of TJs proteins.Immunofluorescence analyses were employed to localize the TJs.Enzyme-linked immunosorbent assay(ELISA)and RT-PCR were utilized to observe changes in interleukin(IL)-1βlevels.To investigate the role of NF-κB signaling activation and IL^(-1)βin Sema7A’s anti-barrier mechanism,we employed 0.1μmol/L IκB kinase 2(IKK2)inhibitor IV or 500 ng/mL IL^(-1)receptor(IL-1R)antagonist.●RESULTS:Treatment with Sema7A resulted in decreased TEER and increased permeability of Dextran-FITC in HCEs through down-regulating mRNA and protein levels of TJs in a time-and dose-dependent manner,as well as altering the localization of TJs.Furthermore,Sema7A stimulated the activation of inhibitor of kappa B alpha(IκBα)and expression of IL-1β.The anti-barrier function of Sema7A was significantly suppressed by treatment with IKK2 inhibitor IV or IL-1R antagonists.●CONCLUSION:Sema7A disrupts barrier function through its influence on NF-κB-mediated expression of TJ proteins,as well as the expression of IL-1β.These findings suggest that Sema7A could be a potential therapeutic target for the diseases in corneal epithelium.

关键词： human corneal epithelial barrier function transepithelial electrical resistance zonula occludens-1 occludin nuclear factor-kappa B

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SIRT1 inhibits apoptosis of human lens epithelial cells through suppressing endoplasmic reticulum stress in vitro and in vivo

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International Journal of Ophthalmology(English edition) 2024年第7期17卷 1205-1216页

作者： Hui Cui Di Sun Sheng Meng Tian-Ju Ma zi ye Zhao-Hui Li Medical School of Chinese PLA Beijing 100089China Senior Department of Ophthalmology the Third Medical Center of PLA General HospitalBeijing 100853China

AIM:To explore the effect of silent information regulator factor 2-related enzyme 1(SIRT1)on modulating apoptosis of human lens epithelial cells(HLECs)and alleviating lens opacification of rats through suppressing endoplasmic reticulum(ER)stress.METHODS:HLECs(SRA01/04)were treated with varying concentrations of tunicamycin(TM)for 24h,and the expression of SIRT1 and C/EBP homologous protein(CHOP)was assessed using real-time quantitative polymerase chain reaction(RT-PCR),Western blotting,and immunofluorescence.Cell morphology and proliferation was evaluated using an inverted microscope and cell counting kit-8(CCK-8)assay,respectively.In the SRA01/04 cell apoptosis model,which underwent siRNA transfection for SIRT1 knockdown and SRT1720 treatment for its activation,the expression levels of SIRT1,CHOP,glucose regulated protein 78(GRP78),and activating transcription factor 4(ATF4)were examined.The potential reversal of SIRT1 knockdown effects by 4-phenyl butyric acid(4-PBA;an ER stress inhibitor)was investigated.In vivo,age-related cataract(ARC)rat models were induced by sodium selenite injection,and the protective role of SIRT1,activated by SRT1720 intraperitoneal injections,was evaluated through morphology observation,hematoxylin and eosin(H&E)staining,Western blotting,and RT-PCR.RESULTS:SIRT1 expression was downregulated in TMinduced SRA01/04 cells.Besides,in SRA01/04 cells,both cell apoptosis and CHOP expression increased with the rising doses of TM.ER stress was stimulated by TM,as evidenced by the increased GRP78 and ATF4 in the SRA01/04 cell apoptosis model.Inhibition of SIRT1 by siRNA knockdown increased ER stress activation,whereas SRT1720 treatment had opposite results.4-PBA partly reverse the adverse effect of SIRT1 knockdown on apoptosis.In vivo,SRT1720 attenuated the lens opacification and weakened the ER stress activation in ARC rat models.CONCLUSION:SIRT1 plays a protective role against TM-induced apoptosis in HLECs and slows the progression of cataract in rats by inhibiting ER stress.These findings sug

关键词： silent information regulator factor 2-related enzyme 1 endoplasmic reticulum stress apoptosis human lens epithelial cells cataract

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Liu-Jun-zi decoction alleviates chemotherapy-induced anorexia by regulating gut microbiota and TLR4/MyD88/NF-κB p65 signaling pathway

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Traditional Medicine Research 2024年第8期9卷 47-58页

作者： Yu-Jie Gao Xi-Pei Wu Bin-Bin ye Yong-Zhao Dai Yao-Zhong Zhao xiu-xiu Liao Ke Nie School of Chinese Materia Medica Guangdong Pharmaceutical UniversityGuangzhou 510006China

Background:Liu-Jun-zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-induced anorexia was discussed from the aspects of regulating gut microbiota,repairing intestinal barrier injury and inhibiting inflammatory pathways.Methods:A rat model of chemotherapy-induced anorexia was established using cisplatin.The study evaluated the therapeutic effects of LJZD by observing the weight,food intake,and intestinal pathology of rats.The impact of LJZD on gut microbiota and metabolites,specifically short-chain fatty acids,was investigated through gut microbiota analysis and targeted metabolomics.The anti-inflammatory and intestinal protective effects of LJZD were assessed by examining the expression of intestinal tight junction proteins associated with the inflammatory pathway.Results:LJZD alleviated cisplatin-induced inflammation and intestinal barrier disruption,as evidenced by upregulated expression of tight junction protein 1(TJ-1)and occludin,along with reduced serum levels of interleukin 6(IL-6),interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and lipopolysaccharide.Additionally,LJZD alleviated microbiota imbalance and regulated the levels of short-chain fatty acids,especially increased the relative abundance of Coriobacteriales Incertae Sedis,Lactabacillus johnsonii F19785,Parasutterella,and reduced the Tyzzerella.In the hypothalamus,LJZD exerts suppressive effects on the toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)p65 signaling pathway,leading to a downregulation in the transcriptional activity of IL-6 and IL-1β,as well as Interleukin 6 receptors(IL-6R)and Interleukin-1βreceptors(IL-1R1)mRNA expression levels.Conclusion:In summary,LJZD alleviate chemotherapy-induced anorexia by modulating the gut microbiota,repairing the intestinal mechanical barriers,and suppressing the TLR4/MyD88/NF-κB p65 signaling pathway.

关键词： Liu-Jun-zi decoction chemotherapy-induced anorexia cisplatin TLR4/MyD818/NF-κB p65 gut microbiota rat

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Regulation and function of endoplasmic reticulum autophagy in neurodegenerative diseases

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Neural Regeneration Research 2025年第1期20卷 6-20页

作者： xiu-Yun Zhao De-En Xu Ming-Lei Wu Ji-Chuan Liu zi-Ling Shi Quan-Hong Ma Department of Neurology and Clinical Research Center of Neurological Disease the Second Affiliated Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina Institute of Neuroscience&Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases Soochow UniversitySuzhouJiangsu ProvinceChina Department of Neurology Jiangnan University Medical CenterWuxiJiangsu ProvinceChina

The endoplasmic reticulum,a key cellular organelle,regulates a wide variety of cellular activities.Endoplasmic reticulum autophagy,one of the quality control systems of the endoplasmic reticulum,plays a pivotal role in maintaining endoplasmic reticulum homeostasis by controlling endoplasmic reticulum turnover,remodeling,and proteostasis.In this review,we briefly describe the endoplasmic reticulum quality control system,and subsequently focus on the role of endoplasmic reticulum autophagy,emphasizing the spatial and temporal mechanisms underlying the regulation of endoplasmic reticulum autophagy according to cellular requirements.We also summarize the evidence relating to how defective or abnormal endoplasmic reticulum autophagy contributes to the pathogenesis of neurodegenerative diseases.In summary,this review highlights the mechanisms associated with the regulation of endoplasmic reticulum autophagy and how they influence the pathophysiology of degenerative nerve disorders.This review would help researchers to understand the roles and regulatory mechanisms of endoplasmic reticulum-phagy in neurodegenerative disorders.

关键词： autophagy endoplasmic reticulum endoplasmic reticulum autophagy endoplasmic reticulum quality control system endoplasmic reticulum receptors endoplasmic reticulum-associated degradation neurodegeneration neurodegenerative disease selective autophagy unfolded protein response

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