2. PI3K/Akt/mTOR Stem Cell/Wnt NF-κB Apoptosis
  3. Akt GSK-3 Keap1-Nrf2 NF-κB Apoptosis
  4. Tovophyllin A

Tovophyllin A 是一种具有口服活性的呫吨酮类化合物。Tovophyllin A 可激活 Akt/GSK3β 信号通路实现对帕金森病的神经保护作用。Tovophyllin A 可通过激活 Nrf2 对肝损伤小鼠模型发挥保护作用。Tovophyllin A 对急性肺损伤小鼠有保护性抗炎活性。Tovophyllin A 可抑制 NF-κB 的活化及后续促炎细胞因子的释放。Tovophyllin A 可减少凋亡细胞凋亡 (Apoptosis)。Tovophyllin A 具有抗疟原虫活性。Tovophyllin A 对肺上皮癌细胞和乳腺癌细胞具有细胞毒性活性。Tovophyllin A 可用于帕金森病、肝损伤、急性肺损伤、肺上皮癌以及乳腺癌的相关研究。

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Tovophyllin A

Tovophyllin A Chemical Structure

CAS No. : 40738-44-1

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Tovophyllin A 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

Tovophyllin A is an orally active xanthonoid compound. Tovophyllin A exerts neuroprotective effects against Parkinson's disease by activating the Akt/GSK3β signaling pathway. Tovophyllin A protects mouse models of liver injury by activating Nrf2. Tovophyllin A exhibits protective anti-inflammatory activity in mouse models of acute lung injury. Tovophyllin A inhibits the activation of NF-κB and subsequent release of pro-inflammatory cytokines. Tovophyllin A reduces apoptotic cell death (Apoptosis). Tovophyllin A has antiplasmodial activity. Tovophyllin A shows cytotoxic activity against lung epithelial cancer cells and breast cancer cells. Tovophyllin A can be used in research related to Parkinson's disease, liver injury, acute lung injury, lung epithelial cancer, and breast cancer[1][2][3].

体外研究
(In Vitro)

Tovophyllin A (0.01-20 μM; 24 h) 可保护原代皮质神经元免受 MPP+ 和 paraquat (PQ) 诱导的神经细胞毒性，在联合处理 24 h 后，浓度≥0.1 μM 时对 MPP+ 模型、浓度≥1 μM 时对 PQ 模型的细胞活力均有显著提升[1]。
Tovophyllin A (serial twofold dilutions starting at 200 μM; 48 h) 抑制 A549 人肺腺癌细胞和 MCF7 乳腺癌细胞的增殖，其 IC50 分别为 2.2 μM 和 6.1 μM[3]。

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

Tovophyllin A 相关抗体:

Cell Cytotoxicity Assay[3]

Cell Line: A549 (epithelial lung carcinoma), MCF7 (breast carcinoma)
Concentration: Serial twofold dilutions starting at 200 μM
Incubation Time: 48 h
Result: Exhibited cytotoxic activity against A549 cells with an IC50 of 2.2 μM.
Exhibited cytotoxic activity against MCF7 cells with an IC50 of 6.1 μM.
体内研究
(In Vivo)

Tovophyllin A (5 mg/kg; single pre-treatment dose) 可通过恢复运动功能、保留黑质致密部 (SNc) 中的多巴胺能神经元以及激活 Akt/GSK3β 促存活信号通路，缓解雄性 C57BL/6 小鼠中 MPTP (HY-W114750) 诱导的帕金森病[1]。
Tovophyllin A (50-100 mg/kg; p.o.; once daily; 5 days) 可剂量依赖性地保护雄性 BALB/c 小鼠免受 Acetaminophen (HY-66005) 诱导的急性肝损伤，其中 100 mg/kg 剂量可几乎完全逆转肝坏死、氧化应激、炎症介质升高的情况，并可强效激活 Nrf2 细胞保护通路[2]。
Tovophyllin A (50-100 mg/kg; p.o.; daily; 5 days prior to LPS challenge) 可呈剂量依赖性改善雄性 BALB/c 小鼠中 LPS (HY-D1056) 诱导的急性肺损伤[3]。

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

Animal Model: C57BL/6 (male, 8-10 weeks old, 25-28 g, MPTP-induced Parkinson's disease)[1]
Dosage: 5 mg/kg
Administration: single pre-treatment dose
Result: Increased total distance traveled in the open field test to levels comparable to control mice.
Increased latency to fall in the rotarod test to levels comparable to control mice.
Alleviated MPTP-induced reductions in tyrosine hydroxylase (TH) protein levels in the midbrain, and striatum.
Increased the number of TH-positive dopaminergic neurons in the substantia nigra pars compacta (SNc).
Reversed MPTP-induced decreases in the ratio of phosphorylated Akt (Ser473) to total Akt in the midbrain, and striatum.
Reversed MPTP-induced decreases in phosphorylated GSK3β (Ser9) levels in the midbrain, and striatum.
Animal Model: BALB/c (male, 20-30 g, acetaminophen-induced acute liver injury)[2]
Dosage: 50 mg/kg; 100 mg/kg
Administration: p.o.; once daily; 5 days
Result: Reduced the elevated serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase levels induced by acetaminophen.
Reduced the elevated liver necrosis score and myeloperoxidase activity induced by acetaminophen.
Reduced the elevated liver malondialdehyde, 4-hydroxynonenal, and nitrite/nitrate levels induced by acetaminophen, while increasing the levels of superoxide dismutase, catalase, reduced glutathione, and total antioxidant capacity in the liver.
Increased the relative mRNA expression levels of Nrf2, NQO1, GCLm, GCLc, and HO-1 in the liver.
Increased the proportion of Nrf2-immunopositive and HO-1-immunopositive cells in the liver.
Reduced the elevated liver NF-κB levels induced by acetaminophen and decreases the proportion of NF-κB-immunopositive cells.
Reduced the elevated liver TNF-α, IL-1β, and IL-6 levels induced by acetaminophen.
Animal Model: BALB/c albino mice (male, 20-25 g, LPS-induced acute lung injury)[3]
Dosage: 50 mg/kg; 100 mg/kg
Administration: p.o.; daily; 5 days prior to LPS challenge
Result: Significantly reduced LPS-induced lung wet/dry ratio (W/D), total protein content in bronchoalveolar lavage fluid (BALF), and BALF lactate dehydrogenase (LDH) activity.
Inhibited LPS-induced total inflammatory cell count and differential inflammatory cell count (neutrophils, macrophages, lymphocytes) in BALF.
Decreased malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) levels in lung tissue, and increased superoxide dismutase (SOD) and reduced glutathione (GSH) levels in lung tissue.
Attenuated LPS-induced increases in lung tissue NF-κB levels and percentage of immunopositive cells, as well as decreases in lung tissue TNF-α and IL-6 levels and percentage of immunopositive cells, and decreases in lung tissue IL-1β levels.
Improved LPS-induced pathological damage in lung tissue.
分子量

462.53

Formula

C28H30O6
CAS 号
结构分类
初始来源
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

Tovophyllin A 相关分类

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Tovophyllin A40738-44-1AktGSK-3Keap1-Nrf2NF-κBApoptosisPKBProtein kinase BGlycogen synthase kinase-3Glycogen synthase kinase 3Nuclear factor-κBNuclear factor-kappaBxanthonoid compoundParkinson's diseaseliver injuryacute lung injurylung epithelial cancerbreast cancerprimary cortical neuronsC57BL/6 miceBALB/c mice
Inhibitorinhibitorinhibit

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