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β-Elemene induces apoptosis and autophagy in colorectal cancer cells through regulating the ros/amPK/mTOR pathway

Chinese Journal of Natural Medicines 2022年第1期20卷 9-21页

作者： WANG Guo-Yu ZHANG Lei GENG ya-Di WANG Bin FENG Xiao-Jun CHEN Zhao-Lin WEI Wei JIANG Ling Department of Pharmacy the First Affiliated Hospital of USTCDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiAnhui230001China Institute of Clinical Pharmacology Anhui Medical UniversityHefei 230001China Department of Pharmacy Hefei Cancer HospitalChinese Academy of SciencesHefei 230031China

β-Elemene is an effective anti-cancer ingredient extracted from the genus Curcuma(Zingiberaceae familiy).In the present study,we demonstrated thatβ-elemene inhibited the proliferation of colorectal cancer cells and induced cell cycle arrest in the G2/M *** addition,β-elemene induced nuclear chromatin condensation and cell membrane phosphatidylserine eversion,decreased cell mitochondrial membrane potential,and promoted the cleavage of caspase-3,caspase-9 and PARP proteins,indicating apoptosis in colorectal cancer *** the same time,β-elemene induced autophagy response,and the treated cells showed autophagic vesicle bilayer membrane structure,which was accompanied by up-regulation of the expression of LC3B and ***,β-elemene increased ros levels in colorectal cancer cells,promoted phosphorylation of amPK protein,and inhibited mTOR protein *** the experiments in vivo,β-elemene inhibited the tumor size and induced apoptosis and autophagy in nude *** summary,β-elemene inhibited the occurrence and development of colon cancer xenografts in nude mice,and significantly induced apoptosis and autophagy in colorectal cancer cells in *** effects were associated with regulation of the ros/amPK/mTOR *** offered a molecular basis for the development ofβ-elemene as a promising anti-tumor drug candidate for colorectal cancer.

关键词： β-Elemene Colorectal cancer Apoptosis Autophagy amPK mTOR

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从肝治心组方调控铁自噬保护缺血/再灌注损伤心肌细胞机制研究

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中国中西医结合杂志 2024年第2期44卷 183-192页

作者：何飘朴美虹谢丽华曾阳王瑾茜汪辛强张程程胡国恒陈亚湖南中医药大学第一附属医院老年病科长沙410007 湖南中医药大学第一中医临床学院长沙410007

目的探讨从肝治心组方改善心肌缺血/再灌注损伤的机制。方法将50只SD大鼠随机分为假手术组、模型组、从肝治心组方组、麝香保心丸组、地尔硫䓬组,每组10只,制备心肌缺血/再灌注损伤大鼠模型,干预组分别给予从肝治心组方[5.32 g/(kg·d)]... 详细信息

目的探讨从肝治心组方改善心肌缺血/再灌注损伤的机制。方法将50只SD大鼠随机分为假手术组、模型组、从肝治心组方组、麝香保心丸组、地尔硫䓬组,每组10只,制备心肌缺血/再灌注损伤大鼠模型,干预组分别给予从肝治心组方[5.32 g/(kg·d)]、麝香保心丸[10.27 mg/(kg·d)]、地尔硫䓬[6.86 mg/(kg·d)]灌胃给药,假手术组和模型组给予等量生理盐水灌胃,干预14天后取材,HE染色观察心肌组织形态,透射电子显微镜观察心肌细胞线粒体形态,RT-PCR及Western Blot检测核受体共激活因子4(NCOA4)、铁蛋白重链1(FTH1)、前列腺素G/H合酶2(PTGS2)mRNA和蛋白表达情况。H9c2大鼠心肌细胞分为正常组、模型组、空白血清组、中药组、铁死亡抑制剂组(Ferrostatin-1)、铁死亡诱导剂组(Erastin)、中药诱导剂组,缺氧12 h复氧2 h造模,检测各组细胞存活率、活性氧(ros)含量、线粒体膜电位水平、Fe^(2+)水平,RT-PCR及Western Blot检测NCOA4、FTH1、PTGS2 mRNA和蛋白表达情况。结果动物实验显示,模型组大鼠心肌纤维断裂或稀疏,可见心肌局灶性坏死,细胞间质浸润炎性细胞,心肌细胞内线粒体肿胀变大,纤维瘢痕组织增生;干预组病理改变减轻。与假手术组比较,模型组NCOA4、PTGS2 mRNA及蛋白表达升高,FTH1 mRNA及蛋白表达降低(Pros、Fe^(2+)水平、NCOA4、PTGS2 mRNA和蛋白表达升高(Pros、Fe^(2+)水平、NCOA4、PTGS2 mRNA和蛋白表达降低(Pros、Fe^(2+)水平、NCOA4、PTGS2 mRNA和蛋白表达升高(Pros、Fe^(2+)水平、NCOA4、PTGS2 mRNA和蛋白表达降低(P<0.05,P<0.01)。结论从肝治心组方可能通过调控NCOA4/FTH1信号通路抑制铁自噬,从而减轻心肌细胞铁死亡,起到保护缺血/再灌注损伤心肌细胞的作用。

关键词：从肝治心组方缺血再灌注损伤核受体共激活因子4 铁蛋白重链1 铁自噬铁死亡中药复方

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Carbon quantum dots/Bi_(4)O_(5)Br_(2) photocatalyst with enhanced photodynamic therapy:killing of lung cancer(A549)cells in vitro

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Rare Metals 2022年第1期41卷 132-143页

作者： Bing He Hai-yan Jin ya-Wen Wang Cai-Mei Fan Yun-Fang Wang Xiao-Chao Zhang Jian-Xin Liu Rui Li Jue-Wen Liu College of Chemistry and Chemical Engineering Taiyuan University of TechnologyTaiyuan 030024China Department of Chemistry University of WaterlooWaterlooON N2L 3G1Canada

Inorganic photocatalysts have been regarded as a promising candidate in the domain of tumor photodynamic therapy(PDT)due to their inspirational photocatalytic *** this study,a Bi_(4)O_(5)Br_(2)photocatalyst was synthesized and it exhibited effective photo-killing activity of A549 cells(a human lung carcinoma epithelial cell line)in *** this basis,we modified Bi_(4)O_(5)Br_(2)with carbon quantum dots(CQDs)via a hydrolysis method at room temperature,which resulted in an improved photo-killing effect of Bi_(4)O_(5)Br_(2)to A549 *** samples and the interaction between samples and cells were fully *** has been found that the loading of CQDs on Bi_(4)O_(5)Br_(2)can reduce the hydration ratio,increase the cellular uptake and improve the photogenerated reactive oxygen species(ros)as compared with pristine Bi_(4)O_(5)Br_(2).Electron spin resonance(ESR)analysis and radical-trapping experiments manifested that the ros contributed to PDT may be·O^(2-)and ·*** study may provide a useful strategy to ameliorate the penetrability,cell compatibility and PDT effect upon cancer cells of other inorganic photocatalysts.

关键词： CQDs/Bi_(4)O_(5)Br_(2) Photocatalyst PDT A549 cell Reactive oxygen species

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低剂量电离辐射对人淋巴细胞氧化应激及DNA损伤的影响

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癌变．畸变．突变 2024年第2期36卷 94-99页

作者：孙鑫李爽陆雪蔡恬静刘雅刘青杰张伟中国疾病预防控制中心辐射防护与核安全医学所辐射防护与核应急中国疾病预防控制中心重点实验室北京100088

目的:探讨低剂量^(137)Cs γ射线照射后正常人淋巴细胞(AHH-1)是否产生氧化应激及DNA损伤,并引发DNA修复。方法:以剂量率为8.32 mGy/min的^(137)Cs γ射线照射AHH-1细胞,剂量分别为0(未照射)、0.01、0.02、0.05、0.075、0.1和0.2 Gy,照... 详细信息

目的:探讨低剂量^(137)Cs γ射线照射后正常人淋巴细胞(AHH-1)是否产生氧化应激及DNA损伤,并引发DNA修复。方法:以剂量率为8.32 mGy/min的^(137)Cs γ射线照射AHH-1细胞,剂量分别为0(未照射)、0.01、0.02、0.05、0.075、0.1和0.2 Gy,照射后分别培养1、24、48和72 h。采用CCK-8试剂盒检测细胞存活率变化;丙二醛(MDA)、超氧化物歧化酶(SOD)和活性氧(ros)试剂盒检测细胞氧化损伤水平;免疫荧光方法分析γH2AX和53BP1焦点形成情况;实时荧光定量PCR方法检测DNA损伤修复相关基因CDKN1A、DDB2和POLH的mRNA表达水平变化。结果:与未照射组相比,照射后24和48 h,各剂量组细胞存活率显著增强(Pros相对荧光强度显著升高(P<0.05);0~0.2 Gy γ射线照后1 h,γH2AX和53BP1焦点数量随剂量增加而增加,且具有明显的剂量-效应关系(P<0.01);与未照射组相比,照射后48 h,DDB2和POLH mRNA相对表达水平显著升高,差异具有统计学意义(P<0.05)。结论:低剂量电离辐射引起人淋巴细胞产生氧化应激和DNA损伤,并促进DNA损伤修复相关基因在转录水平发生改变。

关键词：电离辐射 γ射线人淋巴细胞氧化应激 DNA损伤细胞增殖

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罗伊氏黏液乳杆菌通过抑制ros依赖性NLRP3炎性通路缓解大鼠肠缺血/再灌注损伤

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畜牧兽医学报 2024年第9期55卷 4186-4195页

作者：李亚楠马天文杨晓钰吴佳鑫吕晓萍任昊阮红日刘滢张建涛魏成威东北农业大学动物医学学院黑龙江省动物疾病致病机制与比较医学重点实验室哈尔滨150030

本研究旨在以ros/NLRP3炎性小体为切入点,探讨罗伊氏黏液乳杆菌(Limosilactobacillus reuteri,LR)改善肠缺血性再灌注损伤(intestinal ischemia-reperfusion injury,IR)的作用机制。通过缺氧/复氧方法来构建IR细胞模型,以及微动脉夹夹闭/灌注方法来构建大鼠IR模型。细胞试验分为4组,对照组、缺血再灌注细胞模型组、罗伊氏黏液乳杆菌预处理组、罗伊氏黏液乳杆菌组。动物试验分为3组(每组10只大鼠),假手术组、缺血再灌注损伤组、罗伊氏黏液乳杆菌灌胃处理组。检测各组ros水平,NLRP3炎性小体相关蛋白(NLRP3、ASC、Caspase p10、GSDMD)表达情况,炎性相关指标(TNF-α、IL-1β、IL-6、IL-10)水平,氧化应激相关指标(ros、SOD、GSH-Px、MDA)含量,并进行病理组织学评价。结果显示,1)罗伊氏黏液乳杆菌可以减弱IR导致的氧化应激以及NLRP3炎性小体的激活。2)罗伊氏黏液乳杆菌通过减弱ros的表达来缓解NLRP3炎性小体的激活。3)罗伊氏黏液乳杆菌能够缓解IR对肠道组织的损伤,以及炎性因子的表达。综上所述,LR可缓解大鼠肠IR和氧化应激,其作用机制与抑制ros依赖性NLRP3炎性小体有关,为LR在肠道相关疾病的兽医临床治疗提供试验依据。

关键词：罗伊氏黏液乳杆菌肠缺血再灌注损伤活性氧 NLRP3炎性小体

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New progress in roles of nitric oxide during hepatic ischemia reperfusion injury

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World Journal of Gastroenterology 2017年第14期23卷 2505-2510页

作者： ya-Qi Zhang Ning Ding Yong-Fen Zeng Yuan-Yuan Xiang Mei-Wen yang Fen-Fang Hong Shu-Long yang Department of Physiology Basic Medical CollegeNanchang University Medical Experimental Teaching Center Jiangxi Medical CollegeNanchang University

Hepatic ischemia reperfusion injury (HIRI) is a clinical condition which may lead to cellular injury and organ dysfunction. The role of nitric oxide (NO) in HIRI is complicated and inconclusive. NO produced by endothelial nitric oxide synthase (eNOS) activation plays a protective role during early HIRI. But eNOS overexpression and the resulting excessive NO bioavailability can aggravate liver injury. NO induced by inducible nitric oxide synthase (iNOS) may have either a protective or a deleterious effect during the early phase of HIRI, but it may protect the liver during late HIRI. Here, we reviewed the latest findings on the role of NO during HIRI: (1) NO exerts a protective effect against HIRI by increasing NO bioavailability, downregulating p53 gene expression, decreasing inflammatory chemokines, reducing ros via inhibiting the mitochondrial respiratory chain, activating sGC-GTP-cGMP signal pathway to reduce liver cell apoptosis, and regulating hepatic immune functions; (2) eNOS protects against HIRI by increasing NO levels, several eNOS/NO signal pathways (such as Akt-eNOS/NO, amPK-eNOS/NO and HIF-1 alpha-eNOS/NO) participating in the anti-HIRI process, and inhibiting over-expression of eNOS also protects against HIRI; and (3) the inhibition of iNOS prevents HIRI. Thus, the adverse effects of NO should be avoided, but its positive effect in the clinical treatment of diseases associated with HIRI should be recognized.

关键词： Liver Hepatic ischemia reperfusion injury Nitric oxide Nitric oxide synthase

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一种新型香豆素衍生物P492B的抗神经炎症效应分析

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华夏医学 2024年第4期37卷 34-40页

作者：蒋艳林向文静牙东姗陈鑫邓俊刚廖儒佳桂林医学院附属医院药学部桂林541001 桂林医学院附属医院神经科学实验室桂林541002 桂林市人民医院神经内科桂林541001

目的研究新型香豆素衍生物P492B对小胶质细胞介导的神经炎症的作用。方法以香豆素为母核,合成新型香豆素衍生物P95B、P613B和P492B。通过MTT法评估P95B、P613B和P492B对SH-SY5Y神经元细胞系细胞活力的影响,筛选最优化合物P492B。构建脂... 详细信息

目的研究新型香豆素衍生物P492B对小胶质细胞介导的神经炎症的作用。方法以香豆素为母核,合成新型香豆素衍生物P95B、P613B和P492B。通过MTT法评估P95B、P613B和P492B对SH-SY5Y神经元细胞系细胞活力的影响,筛选最优化合物P492B。构建脂多糖(LPS)诱导的BV-2小胶质细胞神经炎症模型,给予P492B处理后,形态学观察P492B对小胶质细胞活化的影响。Western blot法检测P492B对小胶质细胞释放一氧化氮合成酶(iNOS)蛋白水平的影响。ELISA法检测P492B对小胶质细胞释放的炎症因子TNF-α和IL-6水平的影响,DCFH-DA荧光探针检测P492B对小胶质细胞ros水平的影响。结果香豆素、P95B和P613B均可剂量依赖性降低神经细胞活力,而P492B对神经细胞活力无显著影响。P492B可显著改善小胶质细胞的活化,并剂量依赖性的显著降低活化的小胶质细胞iNOS蛋白水平、剂量依赖性的显著减少炎症因子TNF-α和IL-6的表达水平、剂量依赖性的显著降低活化的小胶质细胞活性氧水平。结论新型香豆素衍生物P492B可显著抑制小胶质细胞介导的神经炎症,为神经炎症相关疾病的治疗提供新的潜在治疗药物。

关键词：香豆素衍生物神经炎症小胶质细胞神经保护

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ZYZ451 Protects cardiomyocytes from hypoxia-induced apoptosis by enhancing MnSOD and STAT3 interaction

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中国药理学与毒理学杂志 2015年第S1期29卷 27-28页

作者： Shan-shan LUO ya-qi SHEN Li-ming MA Xian-feng GU Yi-zhun ZHU Department of Pharmacology School of Pharmacy Fudan University Shanghai 201203 China Department of Medicinal Chemistry School of Pharmacy Fudan University Shanghai 201203 China Department of Pharmacology Loo Yong Lin School of Medicine National University of Singapore Singapore

OBJECTIVE 3,5-Dimethoxy-4-(2-amino-3-prop-2-ynylsulfanyl-propionyl)-benzoic acid 4-guanidino-butyl ester(ZYZ451)showed excellent cardio-protective effects in our previous ***,its therapeutic potential in vivo and the mechanism remained to be ***,we evaluated cardiac protective role of ZYZ451 in post-myocardial infarction(post-MI)rats,and elucidated the underlying *** Neonatal rat ventricular cardiomyoctys(NRVCs)were separated and subjected to pre-deoxidized(1%O2,5%CO2),and serum-free medium for 4h to obtain ischemic *** ros,MnSOD activity and cell apoptosis were tested to verify the cardiac protective effects of *** and siRNA for Stat3 were used to determine role of Stat3 played in cardio-protective effectes of *** were isolated from NRVCs to determine expression of Stat3 and *** and coimmunoprecipitation were conducted to determine the interaction between MnSOD and *** apply post-MI model in rats,the rats were subjected to ligation of LAD except for control *** vehicle or ZYZ451(1,2or 5mg·kg-1)or mixture of Leonurine and SPRC(15mg·kg-1)was administered 7dbefore and 3more days after the *** at risk(AAR),apoptosis in AAR,LDH and MDA levels,and MnSOD activity and expression were detected to evaluate the cardiac *** mitochondria were isolated to determine MnSOD and Stat3 expression in ischemia,and coimmunoprecipitaion was performed to verify the interaction between MnSOD and Stat3 in *** ZYZ451 prevented hypoxia induced NRVCs apoptosis via increasing MnSOD activity and inhibiting mitochondrial ros ***,5,15-DPP(STAT3phosphorylation inhibitor)failed to inhibit MnSOD activity,while knockout of STAT3 resulted in significant reduction of MnSOD activity,followed by increased mitochondrial ros production and cardiomyocytes apoptosis in ***,protective effects of ZYZ451 were blunted in Stat3 deficient

关键词： hypoxia acute myocardial infarction ros MnSOD apop

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Dicoumarol Alters Cellular Redox State and Inhibits Nuclear Factor Kappa B to Enhance Arsenic Trioxide-Induced Apoptosis

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Acta Biochimica et Biophysica Sinica 2004年第3期36卷 235-242页

作者： ya-Wu JING, Jing YI, Yu-Ying CHEN, Qing-Shen HU, Gui-Ying SHI, Hue LI, and Xue-Ming TANG* Department of Cell Biology, Shanghai Second Medical University, Shanghai 200025, China Department of Cell Biology Shanghai Second Medical University

The effects of a number of cytotoxic drugs are influenced by cellular reduction/oxidation (redox) state. In the present study, we attempt to explore if dicoumarol, an inhibitor of NADPH: quinone oxidoreductase (NQO1), alters the cellular redox state and how this alteration affects the redox-related apoptosis. Flow cytometry was used to assess the reactive oxygen species (ros) level and apoptotic rates of HeLa cells treated with arsenic trioxide (As2O3) alone or in combination with natural anthraquinone emodin and dicoumarol or plus N-acetyl-cysteine. Western blot, immunofluorescence, electrophoretic mobility shift assay and luciferase assay were used to detect Nuclear Factor kappa B (NF-κB) activation. The results showed that dicoumarol synergized with emodin to sensitize HeLa cells to As2O3-induced apoptosis through raising the ros level. More notably, this enhanced susceptibility was associated with a ros-mediated inhi- bition of NF-κB activation in which the combinative treatment with dicoumarol prevented NF-κB from binding to target DNA. It was suggested that dicoumarol in combination with anthraquinones might be a novel strategy to expand the chemotherapeutic spectrum of As2O3 by means of interfering the cellular redox state.

关键词： dicoumarol arsenic trioxide reduction/ oxidation state apoptosis NF-κB

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Thioredoxin-Interacting Protein(TXNIP) Regulates Parkin/PINK1-mediated Mitophagy in Dopaminergic Neurons Under High-glucose Conditions: Implications for Molecular Links Between Parkinson’s Disease and Diabetes

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Neuroscience Bulletin 2020年第4期36卷 346-358页

作者： Cun-Jin Su Zhu Shen Ru-Xiao Cui ya Huang De-Lai Xu Feng-Lun Zhao Jie Pan Ai-Ming Shi Tong Liu Yun-Li Yu Department of Pharmacy The Second Affiliated Hospital of Soochow UniversitySuzhou 215004China Institute of Neuroscience Soochow UniversitySuzhou 215004China Department of Clinical Pharmacology The Second Affiliated Hospital of Soochow UniversitySuzhou 215004China

Patients with diabetes mellitus have a higher risk of developing Parkinson’s disease(PD). However, the molecular links between PD and diabetes remain *** this study, we investigated the roles of thioredoxininteracting protein(TXNIP) in Parkin/PINK1-mediated mitophagy in dopaminergic(DA) cells under high-glucose(HG) conditions. In streptozotocin-induced diabetic mice,TXNIP was upregulated and autophagy was inhibited in the midbrain, while the loss of DA neurons was accelerated by hyperglycemia. In cultured PC12 cells under HG, TXNIP expression was upregulated and the intracellular reactive oxygen species(ros) levels increased, leading to cell death. Autophagic flux was further blocked and PINK1 expression was decreased under HG conditions. Parkin expression in the mitochondrial fraction and carbonyl cyanide 3-chlorophenylhydrazone(CCCP)-induced co-localization of COX IV(marker for mitochondria) and LamP1(marker for lysosomes) were also significantly decreased by HG. Overexpression of TXNIP was sufficient to decrease the expression of both PINK1 and Parkin in PC12 cells, while knockdown of the expression of TXNIP by si RNA decreased intracellular ros and attenuated cellular injury under HG. Moreover, inhibition of TXNIP improved the CCCP-induced co-localization of COX IV and LamP1 in PC12 cells under HG. Together, these results suggest that TXNIP regulates Parkin/PINK1-mediated mitophagy under HG conditions, and targeting TXNIP may be a promising therapeutic strategy for reducing the risk of PD under hyperglycemic conditions.

关键词： Diabetes mellitus Parkinson’s disease High glucose TXNIP Mitophagy PC12 cells

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