Juglanin

Research use only, not for human use.

Juglanin is a JNK activator. Juglanin with inflammation and anti-tumor activities. It can induce apoptosis and autophagy on human breast cancer cells.

Juglanin is a JNK activator. Juglanin with inflammation and anti-tumor activities. It can induce apoptosis and autophagy on human breast cancer cells.

Cell Viability Assay Cell Line:MCR-5 cell Concentration:0-40 μM Incubation Time:0-72 h Result:Reduced the cell viability of MCR-5 after 24 h exposure at 160 μM.Reduced the cell viability of MCR-5 after 72 h exposure at 40 μM.Western Blot Analysis Cell Line:MCF-7, SKBR3 Concentration:0-10 μM Incubation Time:24 hResult:Increased the expressions of phosphorylated Chk2, Chk2, phosphorylated Cdc25C, phosphorylated Cdc2, p27, cyclin D, Bad, Bax and decreased the levels of Cdc25C, Cdc2, Bcl-2.Activated caspases and led to Casapse-9, Casapse-8 and Caspase-3 cleavage.Increased the level of JNK phosphorylation.Western Blot Analysis Cell Line:Lipopolysaccharides (LPS, HY-D1056)-treated AST cells Concentration:40-160 μM Incubation Time:24 h Result:Decreased the expression of TLR4, MyD88, CD14, p-IKKα, p-IκBα, p-NF-κB, GFAP, BDNF, Aβ and p-Tau induced by LPS (HY-D1056).Increased the level of SYP, PSD-25 and SNAP-25.

Animal Model:Tumor-transplanted mouse model Dosage:10-20 mg/kg Administration:Intraperitoneal injection (i.p.), daily, 7 daysResult:Increased levels of cleaved Caspase-9 and Caspase-3, LC3BI, LC3BII and phosphorylated JNK.Increased dead cells and apoptosis proportion in juglanin-treated tumor tissues.Increase in mean areas that stained positively cleaved Caspase-3 in juglanin-treated tumor tissues.Animal Model:C57BL6 male miceDosage:10-30 mg/kg Administration:Intraperitoneal injection (i.p.), 5 times weekly Result:Increased number of platform crossings and expanded time in target quadrant.Decreased the expression level of α-synuclein, pro-inflammatory cytokines (IL-1β, TNF-α, IL-18 and COX-2), TLR-4, MyD88, CD14, Aβ, phosphorylation of Tau, Ibal and neurotrophic factor (BDNF).Reversed LPS-triggered effect on synaptic markers, up-regulating the expression of SYP, PSD-95 and SNAP-25.Restored TH levels in the hippocampus of mice in a dose-dependent manner.Decreased p-IKKα, p-IκBα and p-NF-κB levels combinated with LPS.Decreased the GFAP-positive cells.Animal Model:C57BL/6 male mice Dosage: 80 mg/kg Administration:i.g., daily, 1-21 days Result:Improved the survial rate of the BLM (HY-108345)-treated mice.Decreased the expression of BALF, CXCL1, IL-6, TNF-α, MPO activity, TGF-β1, and its down-streaming proteins (fibronectin/MMP-9/α-SMA/collagen I).Reduced the number of total cells, neutrophils and macrophages in BALF.

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Apoptosis

Apoptosis

Apoptosis|Autophagy|JNK

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5041-67-8

418.35

C20H16O10

>98% (HPLC)

Methanol:16 mg/mL (38.25 mM; Need ultrasonic)

O=C1C(O[C@H]2[C@@H]([C@H]([C@H](CO)O2)O)O)=C(C3=CC=C(O)C=C3)OC4=CC(O)=CC(O)=C14

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(-20℃)

With Ice Pack

≥ 2 years