Icariside I (GH01) 是一种具有口服活性的 Icarlin 代谢产物。Icariside I 通过同时调节成骨细胞和破骨细胞分化改善雌激素缺乏引起的骨质疏松症。Icariside I 促进 ATP (HY-B2176) 或 Nigericin (HY-127019) 诱导的 mtROS 产生以及 NLRP3 炎症小体激活并引起特异质肝毒性。Icariside I 不会改变 NLRC4 和 AIM2 炎性小体的激活。Icariside I 通过靶向 IL-6/STAT3 通路抑制乳腺癌的增殖、凋亡 (apoptosis)、侵袭和转移。Icariside I 是犬尿氨酸-AhR 通路抑制剂，通过阻断肿瘤免疫逃逸来缓解癌症。
Icariside I (GH01) is an orally active metabolite of icalin. Icariside I improves estrogen deficiency-induced osteoporosis by simultaneously regulating osteoblast and osteoclast differentiation. Icariside I promotes ATP (HY-B2176) or Nigericin (HY-127019)-induced mtROS production and NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity. Icariside I does not alter the activation of NLRC4 and AIM2 inflammasomes. Icariside I inhibits breast cancer proliferation, apoptosis, invasion, and metastasis by targeting the IL-6/STAT3 pathway. Icariside I is a kynurenine-AhR pathway inhibitor that alleviates cancer by blocking tumor immune escape[1][2][3][4].
Promoted caspase-1 activation and IL-1β production, was not affected the expression of NLRP3, ASC, pro-IL-1β, and pro-caspase-1 (p45) induced by ATP in LPS-primed.
Had no effect on caspase-1 cleavage, IL-1β secretion and LDH release triggered by SiO2 and poly.
Did not alter caspase-1 cleavage, IL-1β secretion, and LDH release in Pam3CSK4 (HY-P1180)-primed BMDMs transfected with LPS, did not affect the expression of pro-IL-1β, ASC, NLRP3 and pro-caspase-1.
Did not alter the release of caspase-1 cleavage, IL-1β secretion, LDH and ASC oligomerization release in response to Salmonella typhimurium infection and triggered by Poly (dA:dT) (HY-138646) transfection, was not affected the expression of NLRP3, ASC, pro-IL-1β and pro-caspase-1 (p45) in cell lysate.
Promoted ATP-induced ASC oligomerization and the production of caspase-1 and IL-1β induced by Nigericin but not SiO2, poly(I:C) and intracellular LPS in LPS-primed.
Reduced the phosphorylation of STAT3 induced by IL-6, decreased p-STAT3 (Tyr705) exposed to IL-6 (50 ng/mL) after 12 h.
Decreased the protein level of vimentin in the presence of IL-6.
Entered a viable G1 arrest state, decreased IL-6-induced the proliferative phase of the cell cycle (S+G2/M), prevented cells from entering the S phase.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
LPS-mediated susceptible C57BL/6 mice (Female 6-8-week-old) model of IDILI[1]
Dosage:
25 mg/kg, 50 mg/kg, 100 mg/kg
Administration:
i.p., once
Result:
Induced the elevation of ALT and AST serum levels, increased the production of IL-1β and TNF-α production.
Did not alter liver tissue structure Icariside I and LPS alone treatment, led to a trend of hepatocyte focal necrosis and inflammatory cell infiltration in the liver tissue used in combination with LPS.
Facilitated the number of macrophages, leucocytes, macrophages and neutrophils used in combination with LPS.
Reduced tumor weight and tumor volume, reduced phosphorylated STAT3 levels and IL-6.
Decreased the expressions of vimentin, bcl-2, Cyclin D1, and CDK4, increased the expressions of pro-apoptotic proteins bax and cleaved caspase 3.
Reduced lung metastasis and damage, decreased mRNA expression of the invasive proteins MMP9 and vimentin.
Reduced tumor volume and tumor weight without body weight changes, inhibited tumor cell proliferation and promoted cell shrinkage, nuclear condensation and necrosis of mouse tumor cells.
Restored the size and weight of immune organs (thymus and spleen), alleviated thymus atrophy and splenomegaly in tumor-bearing mice, and improved the total T cells, CD4+T cells, and CD8+T cells and their ratios in the peripheral blood of the tumor group, enhanced the proportion of TILs and CD8+ T cells and up-regulated the CD8+/CD4+ ratio in tumor tissues.
Upregulated mRNAs levels of CCL4 and CCL8 and CXCL9 and CXCL10, as well as IFN-γ and GZMB and CD69 and Klrk1.
Rescued the levels of intermediate metabolites including Trp, Kyn, kynurenic acid, xanthurenic acid, 3 H-KYN, 3-HAA, quinolinic acid and picolinic acid involved in Trp-Kyn pathway in plasma, reduced the levels of Kyn, kynurenic acid and xanthurenic acid and ratio of Kyn to Trp, downregulated mRNA levels of multiple genes including Ido1, Kat1, Kat3, Kmo, Kynu and Ahr involved in Kyn-AhR pathway.
Down-regulated the mRNA level of SLC7A8, PAT4 transporters of Kyn, kynurenic acid and xanthurenic acid, inhibited AhR, down-regulated the mRNA level of PD-1, p27.
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可选溶剂
浓度溶剂体积质量
1 mg
5 mg
10 mg
25 mg
DMSO
1 mM
1.8849 mL
9.4247 mL
18.8494 mL
47.1236 mL
5 mM
0.3770 mL
1.8849 mL
3.7699 mL
9.4247 mL
10 mM
0.1885 mL
0.9425 mL
1.8849 mL
4.7124 mL
15 mM
0.1257 mL
0.6283 mL
1.2566 mL
3.1416 mL
20 mM
0.0942 mL
0.4712 mL
0.9425 mL
2.3562 mL
25 mM
0.0754 mL
0.3770 mL
0.7540 mL
1.8849 mL
30 mM
0.0628 mL
0.3142 mL
0.6283 mL
1.5708 mL
40 mM
0.0471 mL
0.2356 mL
0.4712 mL
1.1781 mL
50 mM
0.0377 mL
0.1885 mL
0.3770 mL
0.9425 mL
60 mM
0.0314 mL
0.1571 mL
0.3142 mL
0.7854 mL
80 mM
0.0236 mL
0.1178 mL
0.2356 mL
0.5890 mL
100 mM
0.0188 mL
0.0942 mL
0.1885 mL
0.4712 mL
Help & FAQs
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.
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