Cucurbitacin I葫芦素 I,2222-07-3

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Cucurbitacin I

CAS No. : 2222-07-3

MCE 国际站：Cucurbitacin I

产品活性：Cucurbitacin I 是 JAK2/STAT3 的天然选择性抑制剂，并具有有效的抗肿瘤活性。

研究领域：JAK/STAT Signaling  |  Stem Cell/Wnt  |  Epigenetics  |  Protein Tyrosine Kinase/RTK

作用靶点：STAT  |  JAK

In Vitro: Exposure of the COLO205 cells to Cucurbitacin I significantly decreases cell viability. The anticancer activity of Cucurbitacin I is accomplished by downregulating p-STAT3 and MMP-9 expression. PE-induced cell enlargement and upregulation of ANF and β-MHC are significantly suppressed by pretreatment of the cardiomyocytes with Cucurbitacin I. Notably, Cucurbitacin I also impaires connective tissue growth factor (CTGF) and MAPK signaling, pro-hypertrophic factors, as well as TGF-β/Smad signaling, the important contributing factors to fibrosis. Incubation of the Seax cell line with the Jak/Stat3 inhibitor Cucurbitacin I result in a time- and concentration-dependent decrease of P-Stat3 and Stat3. In freshly isolated Sz cells (n=3), Cucurbitacin I induces a concentration-dependent decrease in Stat3 expression whereas P-Stat3 is undetectable. Finally, incubation of freshly isolated Sz cells (n=4) with 30 μM Cucurbitacin I for 6 hours induces apoptosis in the large majority (73-91%) of tumor cells.

In Vivo: No major side effects are noted throughout the study. It is shown that average tumor volumes at the end of the study are as follows: control, 616 mm³ (±130); CQ, 580 mm³ (±107); Cucurbitacin I, 346mm³ (±79); and combination, 220mm³ (±62). The differences in tumor volume between the Cucurbitacin I and control, combination and control, and combination and Cucurbitacin I arms are significant. Furthermore, combination-treated tumors exhibit a significantly lower average tumor weight at study termination than the control. Moreover, there was no effect on the body weights of mice.

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