Cucurbitacin IIA
Cucurbitacin IIa has anti-cancer, anti-bacterial, and anti-inflammatory effects, it can induce apoptosis and enhance autophagy; it also can disrupt the actin cytoskeleton and direct the cell to undergo PARP-mediated apoptosis through the inhibition of survivin downstream of JAK2/STAT3.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Int Immunopharmacol. 2013 May;16(1):27-34.
Cucurbitacin IIa induces caspase-3-dependent apoptosis and enhances autophagy in lipopolysaccharide-stimulated RAW 264.7 macrophages.[Pubmed:
23541744]
Cucurbitacin IIA (CuIIa), a member of cucurbitacin family, is isolated from the root of Hemsleya amabilis which has been used as an ancient remedy for bacillary dysentery and gastroenteritis. The anti-inflammatory properties of Cucurbitacin IIA have long been recognized but the underlying mechanism is largely unknown.
METHODS AND RESULTS:
In this study, we investigated the anti-inflammatory effect of Cucurbitacin IIA on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. The results showed that Cucurbitacin IIA inhibited the proliferation and migration of RAW 264.7 cells in a dose-dependent manner. Whereas Cucurbitacin IIA did not cause apoptosis in unstimulated RAW 264.7 cells, it did induce a significant apoptosis in LPS-stimulated cells, which was caspase-3-dependent and associated with downregulation of survivin. Furthermore, LPS induced autophagy in RAW 264.7 cells and this effect was further enhanced by Cucurbitacin IIA as evidenced by increased levels of LC3-II conjugates and formation of LC3 puncta. In addition, Cucurbitacin IIA disrupted actin cytoskeleton via inducing actin aggregation. However, neither the synthesis of tumor necrosis factor-α, nor the activation of the mitogen-activated protein kinases and NF-κB pathways in LPS-stimulated cells was suppressed by Cucurbitacin IIA treatment.
CONCLUSIONS:
Collectively, these results suggested that induction of apoptosis and enhancement of autophagy contributed to the anti-inflammatory activity of Cucurbitacin IIA against inflammation-related diseases.
Br J Cancer. 2011 Mar 1;104(5):781-9.
Cucurbitacin IIa: a novel class of anti-cancer drug inducing non-reversible actin aggregation and inhibiting survivin independent of JAK2/STAT3 phosphorylation.[Pubmed:
21304528]
Cucurbitacin (Cuc) and triterpene-derived natural products exhibit anti-cancer potential in addition to their conspicuous anti-bacterial and anti-inflammatory activity. Recently, inhibition of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling was shown to underlie the effects of Cuc family on inducing cell death in cancer.
METHODS AND RESULTS:
We purified Cucurbitacin IIA, the active component from the medicinal plant Hemsleya amalils Diels, which shows different structural modifications from other Cuc derivatives. We investigated the mechanisms of its inhibitory effects on cancer cells in vitro and tumour growth in vivo. Cucurbitacin IIA induced the irreversible clustering of filamentous actin and arrested cell cycle by the increases in G2/M populations. Cucurbitacin IIA resulted in the reduced phospho-Histone H3 and markedly increased cleavage of poly-(ADP-ribose) polymerase or PARP, immediate upstream of DNA breakdown as the result of caspase activation, consistent with mitotic blockage-induced cell death. However, unlike other Cuc members, Cucurbitacin IIA did not suppress JAK2/STAT3 phosphorylation or alter phosphorylation of mitogen-activated protein kinases. Instead, the expression of the cell cycle-regulated Inhibitor of Apoptosis Protein (IAP) survivin was reduced. Introducing oncoprotein δ-catenin, which increased survivin expression and suppressed small GTPase RhoA, reduced efficacy of Cucurbitacin IIA to induce cell death. Supporting the effects of Cucurbitacin IIA on actin cytoskeletal signaling, RhoA phosphorylation was reduced suggesting its increased activity.
CONCLUSIONS:
Cucurbitacin IIA is a novel class of anti-cancer drug in suppression of cancer cell expansion by disrupting the actin cytoskeleton and directing the cell to undergo PARP-mediated apoptosis through the inhibition of survivin downstream of JAK2/STAT3.
