2. Metabolic Enzyme/Protease Epigenetics Cell Cycle/DNA Damage Cytoskeleton Apoptosis Autophagy Protein Tyrosine Kinase/RTK NF-κB PI3K/Akt/mTOR
  3. NAMPT Sirtuin Microtubule/Tubulin Apoptosis Autophagy PDGFR NF-κB AMPK
  4. Myricanol

Myricanol 是一种具有多种生物活性的二芳基庚烷类化合物和 Nampt 激活剂。Myricanol 通过增加 Sirtuin 1 (SIRT1)、PRDX5 活性、调控炎症因子发挥抗炎作用并缓解糖皮质激素诱导的肌肉萎缩。Myricanol 对人肺腺癌 A549 细胞具有生长抑制和凋亡 (apoptosis) 诱导作用。Myricanol 可促进微管相关蛋白 tau 的自噬 (autophagy) 清除发挥神经保护作用。Myricanol 可抑制 PDGFRβ 和 NF-κB 信号通路发挥保护心血管功能。Myricanol 激活线粒体转录因子 A (TFAM) 表达发挥抗肾纤维化作用。Myricanol 可激活 AMPK 改善胰岛素抵抗。

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Myricanol

Myricanol Chemical Structure

CAS No. : 33606-81-4

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Myricanol 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

Myricanol is a diarylheptanoid and a Nampt activator. Myricanol exerts anti-inflammatory effects and alleviates glucocorticoid-induced muscle atrophy by increasing Sirtuin 1 (SIRT1) and PRDX5 activities while regulating inflammatory factors. Myricanol exhibits growth inhibition and induces apoptosis in human lung adenocarcinoma A549 cells. Myricanol promotes autophagy-mediated clearance of microtubule-associated protein tau to exert neuroprotective effects. Myricanol protects cardiovascular function by inhibiting PDGFRβ and NF-κB signaling pathways. Myricanol activates mitochondrial transcription factor A (TFAM) expression to exert anti-renal fibrosis effects. Myricanol improves insulin resistance through AMPK activation[1][2][3][4][5][6][7][8].

IC50 & Target[2][6][7]

SIRT1

 

NF-κB

 

AMPK

 

PDGFRβ

 

细胞效力
(Cellular Effect)
Cell Line Type Value Description References
RAW264.7 IC50
7.5 μM
Compound: 153
Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced NO production preincubated for 1 hrs followed by LPS stimulation and measured after 24 hrs by Griess reagent based spectrophotometrical method
Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced NO production preincubated for 1 hrs followed by LPS stimulation and measured after 24 hrs by Griess reagent based spectrophotometrical method
[PMID: 33422907]
体外研究
(In Vitro)

Myricanol (0.01-150 μM，1-72 小时) 可通过激活自噬有效降低 HEK293T 细胞 (IC50 约为 18.56 μM) 和小鼠急性离体脑组织 (100 和 150 μM) 中的 tau 水平[1]。
Myricanol (0-10 μM，24 小时) 显著逆转地塞米松 (DEX) (HY-14648) 引起的线粒体含量减少和功能障碍，并通过激活 sirtuin 1 促进自噬、抑制细胞凋亡，从而保护 C2C12 肌管[2]。
Myricanol (1.25-5 μmol/L，24 小时) 可减少经棕榈酸 (PA) (HY-N0830) 处理的 C2C12 肌管中的脂质积累，增强线粒体功能，保护 C2C12 肌管免受胰岛素抵抗的影响，并增加 C2C12 肌管中鸢尾素的产生和分泌，进而诱导脂肪细胞褐变[3]。
Myricanol (5-20 μM) 通过增强 TFAM 来抑制肾脏纤维化，改善 ZNRF1 和 LCN2 之间的相互作用，并加剧 TGF-β1 诱导的 HK2 细胞中的铁死亡[4]。
MY (2.5-10 μM) 可保护 C2C12 肌管免受叔丁基过氧化氢 (TBHP) 造成的氧化损伤，并通过靶向 PRDX5 来改善线粒体的生物合成和功能[5]。
Myricanol (3-30 μM, 24.5 小时) 通过抑制血小板衍生生长因子受体通路的激活和 NF-κB p65 易位来抑制血小板衍生生长因子-BB 诱导的血管平滑肌细胞增殖和迁移[6]。
Myricanol (5-40 μM, 24 小时) 靶向 C2C12 细胞中的 Nampt，后者参与胰岛素增敏作用[7]。
Myricanol (1.56-50 μg/mL，48 小时-10 天) 可抑制 A549 细胞增殖 (IC50 = 4.85 μg/mL) 和克隆形成并诱导细胞凋亡[8]。

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

Myricanol 相关抗体:

Western Blot Analysis[1]

Cell Line: HEK293T cells
Concentration: 18 μM
Incubation Time: 1, 6, 24, 48, 72 h
Result: Completely be blocked the tau-lowering effect by 3-MA (HY-19312).
Increased the LC3β-II/I ratio.

Western Blot Analysis[2]

Cell Line: C2C12 myotubes stimulated by with DEX
Concentration: 0, 0.25, 5, 10 μM
Incubation Time: 24 h
Result: Restored the expression of myosin heavy chain (MyHC), muscle atrophy F-box protein (atrogin-1), and muscle ring-finger protein 1 (MuRF1).
Dose-dependent upregulated SIRT1 expression.
Restored the phosphorylation of Akt and FoxO3a that is inhibited by DEX.
Increased the expression levels of Cox2, Tom20, UCP3, and PGC-1α.
Reversed DEX-induced increases of total and acetylated FoxO3a levels, which were abolished by co-treatment of EX-527 (HY-15452).
Inhibited expression of apoptosis-associated proteins Bax, cleaved caspase-3 and Increased Bcl-2.

Western Blot Analysis[3]

Cell Line: C2C12 myotubes stimulated by with PA
Concentration: 1.25, 2.5, and 5 μmol/L
Incubation Time: 24 h
Result: Activated the AMPK/ACC signaling pathway and upregulated the expression of PGC-1α.
Activated of the insulin signaling pathway (IRS-1/Akt/GSK-3β).
Promoted the production and secretion of FNDC5/irisin.
Decreased the lipid accumulation in 3T3‐L1 adipocytes in a dose-dependent manner.
Increased the browning markers, PGC‐1α and UCP1, and the mitochondrial marker, COX2, and Suppressed the adipogenic marker, PPARγ, in 3T3‐L1 adipocytes, dose-dependently.

Cell Migration Assay [6]

Cell Line: Primary VSMCs
Concentration: 3, 10 and 30 μM
Incubation Time: Pretreated 30 min and treated with PDGF-BB for 24 h
Result: Partially suppressed the migration at 10 and 30 μM.

Western Blot Analysis[6]

Cell Line: Primary VSMCs
Concentration: 3, 10 and 30 μM
Incubation Time: Pretreated 30 min and treated with PDGF-BB for 24 h
Result: Reduced PCNA, E2F1 and p-Rb.
Reduced Cyclin D1, Cyclin E1 and recovered p53.
Inhibited MM2 and MM9.
Inhibited PDGFRβ pathway and MAPK pathway.
Significantly inhibited p65 nuclear accumulation.

Cell Proliferation Assay[8]

Cell Line: A549 cells
Concentration: 1.56, 3.125, 6.25, 12.5, 25 and 50 μg/mL
Incubation Time: 48 h
Result: Inhibited cell proliferation in a concentration-dependent manner.

Apoptosis Analysis[8]

Cell Line: A549 cells
Concentration: 5 μg/mL
Incubation Time: 48 h
Result: Increased the apoptosis rate from 4.13% to 34.3%, and the proportion of early apoptosis increased significantly.
Upregulated Caspase-3, Caspase-9, Bax and p21, downregulated Bcl-2.
体内研究
(In Vivo)

Myricanol (5-50 mg/kg，腹腔注射，每日一次，连续 10 天) 可通过激活 SIRT1 来预防地塞米松引起的小鼠肌肉萎缩和无力[2]。
Myricanol (0.5-2.5 mg/mL，溶于PEG 400 (HY-Y0873A) 溶液中，腹腔注射，每日一次，连续 18 周) 可延缓高脂饮食 (HFD) 小鼠的脂肪质量增长、改善血脂状况并提高其胰岛素敏感性[3]。
Myricanol (0.5-2 mg/mL，腹腔注射，每日一次，连续 1 周) 可有效改善慢性肾病 (CKD) 小鼠的肾功能并抑制纤维化[4]。
Myricanol (10-50 mg/kg，腹腔注射，每日一次，连续 20 天) 可通过减轻线粒体的氧化损伤来保护老年小鼠免于肌肉萎缩，并确定直接的蛋白质靶点及其潜在机制[5]。
Myricanol (5 mg/kg，腹腔注射，每日一次，连续 14 天) 可显著减少颈动脉结扎引起的内膜增生[6]。

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

Animal Model: DEX-induced muscle dysfunction established in male C57BL/6 mice (8-10 weeks old)[2]
Dosage: 5 and 50 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 10 days
Result: Reduced the loss of muscle mass.
Rescued dexamethasone-induced muscle weakness, indicated by improved grip strength.
Upregulated SIRT1 and PGC-1α, reduced atrogin-1/MuRF1.
Animal Model: HFD model established in male C57BL/6 mice (8-10 weeks old)[3]
Dosage: 0.5 and 2.5 mg/mL, dissolved in PEG 400 (HY-Y0873A) solution
Administration: Intraperitoneal injection (i.p.), once daily for 18 weeks
Result: Inhibited weight gain induced by high-fat diet and reduces fat tissue accumulation.
Improved the glucose tolerance and insulin sensitivity of HFD mice (reduce the HOMA-IR index).
Reduced serum triglycerides, total cholesterol and LDL cholesterol, and increased HDL cholesterol).
Increased energy consumption (oxygen consumption).
Reduced lipid deposition in skeletal muscles and improved muscle function (as measured by grip strength test).
Activated the AMPK/PGC-1α signaling pathway in skeletal muscle.
Increased the expression of FNDC5 in skeletal muscle and the serum level of irisin.
Induced the browning of white adipose tissue in the groin region.
Animal Model: CKD model induced by unilateral ureteral obstruction (UUO) established in male C57BL/6 mice (6-8 weeks old)[4]
Dosage: 0.5 and 2 mg/mL along with an equal volume of normal saline
Administration: Intraperitoneal injection (i.p.), once daily for one weeks
Result: Significantly reduced serum creatinine and urea nitrogen levels.
Showed a 40-60% reduction in collagen deposition.
Downregulated fibrosis markers (FN, α-SMA).
Significantly upregulated TFAM and GPX4 expressions and decreased 4-HNE.
Animal Model: Sarcopenia phenotypes model established in 18-month-old male C57BL/6J mice[5]
Dosage: 10 and 50 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 10 days
Result: Improved grip strength in aging mice.
Significantly improved Quad, Gast and TA muscle index.
Reduced mitochondrial vacuolization and cristae structure disruption.
Animal Model: Carotid artery wire ligation injury model established in eight-week-old male C57BL/6 mice[6]
Dosage: 5 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 14 days
Result: Showed significantly reduced intima, both the ratio of intima to media (I/M ratio) and intimal area.
Had significantly inhibited Ki67 expression and F4/80 expression.
分子量

358.43

Formula

C21H26O5
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

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

纯度 & 产品资料

纯度: ≥98.0%

COA (296 KB)

产品使用指南 (1538 KB)
参考文献

Myricanol 相关分类

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Keywords:

Myricanol33606-81-4NAMPTSirtuinMicrotubule/TubulinApoptosisAutophagyPDGFRNF-κBAMPKNicotinamide phosphoribosyl transferasePBEFVisfatinpre-B cell-enhancing factorPre-B cell colony enhancing factorPlatelet-derived growth factor receptorNuclear factor-κBNuclear factor-kappaBAMP-activated protein kinaseSIRT1DexamethasoneMuscle atrophyPGC-1αAnti-cancer activityCell growth inhibitionInhibitorinhibitorinhibit

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