2. Metabolic Enzyme/Protease Cytoskeleton Cell Cycle/DNA Damage Apoptosis PI3K/Akt/mTOR Autophagy NF-κB Immunology/Inflammation MAPK/ERK Pathway
  3. Herbicide Microtubule/Tubulin Paraptosis PI3K Akt Apoptosis Autophagy Reactive Oxygen Species (ROS) NF-κB p38 MAPK
  4. Ethalfluralin

Ethalfluralin 是一种二硝基苯胺类除草剂和微管 (microtubule) 抑制剂。Ethalfluralin 通过抑制核内纺锤体形成，阻断寄生虫的核分裂和胞质分裂。Ethalfluralin 可激活 NF-κB 和 P38 MAPK 的磷酸化水平，并抑制 PI3K/AKT 信号通路，抑制线粒体功能，诱导细胞凋亡 (apoptosis)、内质网应激、自噬 (autophagy) 及 ROS 生成。Ethalfluralin 可用于弓形虫病的相关研究。

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Ethalfluralin

Ethalfluralin Chemical Structure

CAS No. : 55283-68-6

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Ethalfluralin 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Ethalfluralin is a dinitroaniline herbicide and microtubule inhibitor. Ethalfluralin blocks nuclear division and cytokinesis of parasites by inhibiting intranuclear spindle formation. Ethalfluralin activates the phosphorylation levels of NF-κB and P38 MAPK, inhibits the PI3K/AKT signaling pathway, impairs mitochondrial function, and induces apoptosis, endoplasmic reticulum stress, autophagy, and ROS production. Ethalfluralin is applicable to research related to toxoplasmosis[1][2][3].

体外研究
(In Vitro)

Ethalfluralin (2-20 μM; 48 h) 可降低 pLE 和 pTr 细胞的活力[1]。
Ethalfluralin (20 μM; 48 h) 可抑制 pLE 和 pTr 细胞中增殖标志物 PCNA 的表达[1]。
Ethalfluralin (20 μM; 4 h) 会损伤 pLE 和 pTr 细胞的迁移能力[1]。
Ethalfluralin (5-20 μM; 48 h) 可诱导 pLE 和 pTr 细胞发生细胞周期阻滞，使亚 G1 期细胞群增加、S 期细胞群减少[1]。
Ethalfluralin (5-20 μM; 48 h) 可诱导 pLE 和 pTr 细胞发生凋亡性细胞死亡，增加两种细胞系的晚期凋亡细胞群以及 pTr 细胞的早期凋亡细胞群[1]。
Ethalfluralin (5-20 μM; 48 h) 可降低 pLE 和 pTr 细胞中的胞质钙水平[1]。
Ethalfluralin (5-20 μM; 48 h) 可降低 pLE 和 pTr 细胞的线粒体基质钙水平[1]。
Ethalfluralin (5-20 μM; 48 h) 会破坏 pLE 和 pTr 细胞的线粒体膜电位[1]。
Ethalfluralin (20 μM; 20 h) 会损伤 pLE 和 pTr 细胞的线粒体呼吸功能，降低 pLE 细胞的基础呼吸、最大呼吸、备用呼吸容量及 ATP 生成，同时降低 pTr 细胞的最大呼吸、备用呼吸容量及 ATP 生成[1]。
Ethalfluralin (20 μM; 24 h) 可下调 pLE 和 pTr 细胞中线粒体呼吸复合物 I-V 亚基基因的 mRNA 表达[1]。
Ethalfluralin (5-20 μM; 48 h) 可激活 pLE 和 pTr 细胞中的内质网应激及自噬通路，上调 GRP78、磷酸化 eIF2α、GADD153、磷酸化 ULK1、磷酸化 P62 的表达水平，并促进 LC3B II/I 转换[1]。
Ethalfluralin (5-20 μM; 48 h) 可激活 P38 MAPK 和 NF-κB 信号通路，并抑制 pLE 和 pTr 细胞中的 PI3K/AKT 信号通路[1]。
Ethalfluralin (20 μM; 48 h) 会损伤 pLE 和 pTr 细胞中的自噬流并降低线粒体质量[1]。
Ethalfluralin 可强效抑制刚地弓形虫 RH 株速殖子在人原代包皮成纤维细胞内的复制，其 IC50 为 100 nM[3]。
Ethalfluralin (0.5 μM; 36 h) 对刚地弓形虫 RH 株速殖子侵袭原代人包皮成纤维细胞无显著抑制作用，但会导致细胞内寄生虫出现严重的形态异常[3]。
Ethalfluralin (1 μM; 0-24 h) 可在 8-12 h 内消除人原代包皮成纤维细胞内刚地弓形虫 RH 株速殖子的噬斑形成能力，但对处理 12 h 的胞外速殖子活力无影响[3]。
Ethalfluralin (1 μM; 0-24 h) 作用时长可达 24 h，却不会抑制人原代包皮成纤维细胞内刚地弓形虫 RH 株速殖子的核酸合成，尽管它能完全清除寄生虫的活性[3]。
Ethalfluralin (1 μM; 20 h) 可通过抑制核内纺锤体形成来阻断人原代包皮成纤维细胞内刚地弓形虫 RH 株速殖子的核分裂，同时保留其亚膜微管并导致内膜区室扩张[3]。
Ethalfluralin (1 μM) 可抑制钙离子载体诱导的人原代包皮成纤维细胞内刚地弓形虫 RH 株速殖子释放，同时会在载体处理后导致空泡间隙缩小及经处理寄生虫的折光性增强[3]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Ethalfluralin 相关抗体:

Cell Viability Assay[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 2, 5, 10, 20 μM
Incubation Time: 48 h
Result: Suppressed pLE cell viability to 42% and pTr cell viability to 43% relative to vehicle-treated cells at 20 μM.

Immunofluorescence[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 20 μM
Incubation Time: 48 h
Result: Markedly reduced relative green fluorescence (PCNA expression) in both pLE and pTr cells compared to vehicle-treated cells.

Cell Migration Assay[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 20 μM
Incubation Time: 4 h
Result: Reduced wounded area closure to 9.1% in pLE cells and 10.9% in pTr cells, compared to 27.4% and 30% in vehicle-treated cells, respectively.

Cell Cycle Analysis[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 5, 10 and 20 μM
Incubation Time: 48 h
Result: Increased the sub-G1 population up to 3.3-fold in pLE cells and 2.2-fold in pTr cells.
Decreased the S phase population by 46% in pLE cells and 63% in pTr cells relative to vehicle-treated cells.

Apoptosis Analysis[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 5, 10 and 20 μM
Incubation Time: 48 h
Result: Increased the late apoptotic cell population up to 2.7-fold in pLE cells at 20 μM.
Increased the early apoptotic population to 198% at 10 μM and 321% at 20 μM, and increased the late apoptotic population by over 2-fold in pTr cells.

Real Time qPCR[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 20 μM
Incubation Time: 24 h
Result: Downregulated mRNA expression of all tested mitochondrial respiratory complex I-V subunit genes (including NDUFS3, SDHB, UQCRC2, MT-CO1, and MT-ATP6) in both pLE and pTr cells.

Western Blot Analysis[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 5, 10 and 20 μM
Incubation Time: 48 h
Result: Increased GRP78 protein levels by 2.9-fold in pLE cells and 2.8-fold in pTr cells at 20 μM.
Increased phosphorylated eIF2α by 1.7-1.8-fold in pLE cells and up to 2-fold in pTr cells at 20 μM.
Increased GADD153 by 2.4-fold in pLE cells and up to 2-fold in pTr cells at 20 μM.
Increased phosphorylated ULK1, phosphorylated P62, and LC3B I to LC3B II conversion ratio by 2-4-fold in both cell lines at 20 μM.\nIncreased phosphorylated p38 MAPK by over 4-fold in pLE cells and 2.2-fold in pTr cells at 20 μM.
Increased phosphorylated NF-κB by over 2-fold in both cell lines at 20 μM.
Reduced phosphorylated AKT by almost half in both cell lines at 20 μM.
Reduced phosphorylated S6 in both cell lines at 20 μM.

Cell Autophagy Assay[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 20 μM (with 10 μM chloroquine pretreatment for 3 h)
Incubation Time: 48 h
Result: Markedly increased p-p62 levels in both cell lines, did not further increase LC3B II/I conversion ratio compared to chloroquine alone, and reduced mitochondrial mass significantly in pLE cells (with a similar trend in pTr cells).
体内研究
(In Vivo)

Ethalfluralin (6-12 mg/L；水体浸泡；每日持续；96 小时) 对斑马鱼胚胎具有剂量依赖性发育毒性，包括存活率降低、形态发育受损、细胞凋亡和 ROS 生成增加、血管生成受抑以及炎症反应增强，其 LC50 为 18.49 mg/L[2]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: wild-type, fli1a:eGFP and flk1:eGFP transgenic lines[2]
Dosage: 6 mg/L, 9 mg/L, 12 mg/L
Administration: aqueous immersion; daily continuous; 96 hours
Result: Reduced survival rate, hatching rate and heart rate.
Led to edema of the heart and yolk sac, shortened body length, and spinal cord deformity.
Induced cell apoptosis, oxidative stress and verification.
Inhibited of angiogenesis.
分子量

333.26

Formula

C13H14F3N3O4
CAS 号
中文名称

乙丁烯氟灵； 丁氟消草
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Ethalfluralin 相关分类

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Keywords:

Ethalfluralin55283-68-6乙丁烯氟灵 丁氟消草HerbicideMicrotubule/TubulinParaptosisPI3KAktApoptosisAutophagyReactive Oxygen Species (ROS)NF-κBp38 MAPKPhosphoinositide 3-kinasePKBProtein kinase BNuclear factor-κBNuclear factor-kappaBzebrafishpLE cellsP38 MAPKprimary human foreskin fibroblastsautophagyToxoplasma gondiiapoptosispTr cellsPI3K/AKT signaling pathwayInhibitorinhibitorinhibit

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