2. Apoptosis Autophagy Metabolic Enzyme/Protease Immunology/Inflammation PI3K/Akt/mTOR Protein Tyrosine Kinase/RTK Epigenetics NF-κB JAK/STAT Signaling Stem Cell/Wnt
  3. Apoptosis Autophagy DGK Mitochondrial Metabolism NO Synthase PI3K Akt Interleukin Related Src AMPK mTOR NF-κB c-Met/HGFR STAT Keap1-Nrf2 Reactive Oxygen Species (ROS) Oxidative Phosphorylation Endogenous Metabolite
  4. Momordicine I

Momordicine I 是一种葫芦烷型三萜类化合物。Momordicine I 通过促进细胞凋亡 (apoptosis) 和损害线粒体氧化磷酸化抑制胶质瘤生长。Momordicine I 抑制糖酵解、脂质代谢，诱导 HNC 细胞自噬 (autophagy)，从而抑制头颈癌的生长。Momordicine I 通过抑制 PLA2G6 和 DGK-ζ 减轻异丙肾上腺素诱导的心肌细胞肥大。Momordicine I 通过上调 NO、抑制血管紧张素转换酶 (ACE) 活性、激活 PI3K/Akt 通路、减少氧化应激和炎症发挥其心血管益处。Momordicine I 可抑制 AKT1、IL-6 和 SRC，暗示其应用于 2 型糖尿病的潜力。

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Momordicine I

Momordicine I Chemical Structure

CAS No. : 91590-76-0

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Momordicine I 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

Momordicine I is a cucurbitane-type triterpenoids. Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation. Momordicine I inhibits glycolysis, lipid metabolism, induces autophagy in HNC cells to suppress head and neck cancer growth. Momordicine I alleviates isoproterenol-induced cardiomyocyte hypertrophy through suppression of PLA2G6 and DGK-ζ. Momordicine I exerts its cardiovascular benefits by upregulating nitric oxide, inhibiting the activity of angiotensin-converting enzyme (ACE), activating the PI3K/Akt pathway, reducing oxidative stress and inflammation. Momordicine I inhibits AKT1, IL-6, and SRC, suggesting its potential application in type 2 diabetes[1][2][3][4][5].

IC50 & Target[3][4][5]

PI3K

 

mTOR

 

IL-6

 

Akt1

 

NF-κB

 

STAT3

 

体外研究
(In Vitro)

Momordicine I (1.625-25 μg/mL, 24-25 h) 在 1.625-12.5 μg/mL 的浓度下对 H9c2 细胞活性无显著影响，可抑制 Isoproterenol (ISO) (HY-B0468) 诱导的 PLA2G6 和 DGK-ζ mRNA 水平和蛋白表达上调[1]。
Momordicine I 对 LN229 细胞、GBM 8401 细胞和 SVGp12 细胞表现出选择性细胞毒性，IC50 分别为 9.2、9.6 和 14.4 μM[2]。
Momordicine I (0-10 μM, 16-48 h) 可改变上皮-间质转化 (EMT) 标志物的表达，阻碍 LN229 和 GBM8401 细胞的迁移和侵袭[2]。
Momordicine I (0-10 μM，48 h) 可通过调节 LN229 和 GBM8401 细胞周期诱导细胞凋亡并抑制胶质瘤细胞存活[2]。
Momordicine I (0-90 μM) 可增加细胞内 ROS 生成和衰老，并降低 LN229 和 GBM8401 细胞的氧化磷酸化 (OXPHOS) 能力[2]。
Momordicine I (0-8 μM) 可克服 Temozolomide (TMZ) (HY-17364) 耐药 GBM 细胞的致瘤性[2]。
Momordicine I (10-15 μg/mL) 可显著降低在 Cal27 和 JHU22 细胞中，关键糖酵解分子 (SLC2A1 (GLUT-1)、HK1、PFKP、PDK3、PKM 和 LDHA) 以及参与从头脂肪生成的关键酶 (包括 ACLY、ACC1、FASN、SREBP1 和 SCD1) 的表达[3]。
Momordicine I (10-15 μg/mL) 可在 Cal27 和 JHU22 细胞中诱导自噬，激活 AMPK 并抑制 mTOR 和 Akt 信号通路，从而导致细胞凋亡[3]。
Momordicine I 可稳定地与 AKT1、IL6 和 SRC 靶点结合[4]。
Momordicine I 可能通过以下机制减轻炎症：抑制促炎细胞因子、降低粘附分子表达、抑制 NF-κB 活化、调节 Nrf2 通路并抑制 c-Met/STAT3 通路[5]。

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

Momordicine I 相关抗体:

RT-PCR[1]

Cell Line: H9c2 cells
Concentration: 12.5 μg/mL
Incubation Time: Pretreated for 1 h, and then exposed to Isoproterenol (10 µM) for 24 h
Result: Significantly down-regulated the mRNA expressions of myocardial hypertrophy marker genes (ANP, β-MHC, α-SKA) and PLA2G6, DGK-ζ.

Western Blot Analysis[1]

Cell Line: H9c2 cells
Concentration: 12.5 μg/mL
Incubation Time: Pretreated for 1 h, and then exposed to Isoproterenol (10 µM) for 24 h
Result: Significantly inhibited the upregulation of PLA2G6 and DGK-ζ proteins.

Cell Migration Assay [2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 10 μM
Incubation Time: 16 h
Result: Significantly inhibited wound healing.

Cell Invasion Assay[2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 10 μM
Incubation Time: 16 h
Result: Significantly inhibited transwell invasion.

Apoptosis Analysis[2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 8, 10 μM
Incubation Time: 48 h
Result: Increased the rate of cell apoptosis.

Cell Cycle Analysis[2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 8, 10 μM
Incubation Time: 48 h
Result: Significantly increased the proportion of G1 phase cells.

Western Blot Analysis[2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 8, 10 μM
Incubation Time: 1, 2, 3, 4, 48 h
Result: Reduced the expression of interstitial markers N-cadherin and Twist.
Downregulated Ki-67 and survivin expression.
体内研究
(In Vivo)

Momordicine I (30 mg/kg，腹腔注射，每日一次，连续 21 天) 可诱导小鼠头颈癌 (HNC) 细胞自噬，并减小肿瘤体积[3]。

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

Animal Model: MOC2 induced xenograft model established in C57BL/6 mice (6-7 weeks)[3]
Dosage: 30 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 21 days
Result: Reduced the volume and weight of the tumor.
Reduced Hk1, Pdk3, Fasn, and Acly expression.
分子量

472.70

Formula

C30H48O4
CAS 号
性状

固体

颜色

White to off-white

结构分类
初始来源
运输条件

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

-20°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

纯度 & 产品资料

纯度: ≥97.0%

COA (290 KB)

产品使用指南 (1538 KB)
参考文献

Momordicine I 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:

Momordicine I91590-76-0ApoptosisAutophagyDGKMitochondrial MetabolismNO SynthasePI3KAktInterleukin RelatedSrcAMPKmTORNF-κBc-Met/HGFRSTATKeap1-Nrf2Reactive Oxygen Species (ROS)Oxidative PhosphorylationEndogenous MetaboliteDiacylglycerol kinaseNitric oxide synthasesNOSPhosphoinositide 3-kinasePKBProtein kinase BILAMP-activated protein kinaseMammalian target of RapamycinNuclear factor-κBNuclear factor-kappaBCardiomegalyGlycerophospholipidsRNA sequencingHead and neck cancerGlycolysisLipid metabolismMetabolitesInhibitorinhibitorinhibit

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