參考價	￥ 440

天然產物

MedChemExpress (M

CAS	517-89-5	純度	99.80%
分子量	288.3	分子式	C??H??O?
供貨周期	現貨	規格	10 mM * 1 mL
貨號	HY-N0822	應用領域	醫療衛生,化工,生物產業,制藥

Shikonin 是中草藥紫草的主要成分。Shikonin 是一種有效的 TMEM16A 氯化物通道 (chloride channel) 抑制劑，IC50 為 6.5 μM。Shikonin 是一種特異的丙酮酸激酶 M2 (PKM2) 抑制劑，還可以抑制 TNF-α 和 NF-κB途徑。Shikonin 通過抑制糖酵解降低外泌體 (exosome) 的分泌。Shikonin 抑制 AIM2炎性體活化。

詳細介紹

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Shikonin

CAS No. : 517-89-5

MCE 國際站：Shikonin

產品活性：Shikonin 是中草藥紫草的主要成分。Shikonin 是一種有效的 TMEM16A 氯化物通道 (chloride channel) 抑制劑，IC₅₀ 為 6.5 μM。Shikonin 是一種特異的丙酮酸激酶 M2 (PKM2) 抑制劑，還可以抑制 TNF-α 和 NF-κB途徑。Shikonin 通過抑制糖酵解降低外泌體 (exosome) 的分泌。Shikonin 抑制 AIM2炎性體活化。

結構分類：醌類 | 萘醌類 | 結構分類

來源：植物 | 紫草科 | 紫草

In Vitro: Shikonin is an inhibitor of TMEM16A chloride channel with an IC₅₀ of 6.5 μM. Shikonin is also a specific inhibitor of PKM2 and can also inhibit tumor necrosis factor-α (TNF-α) and prevent activation of nuclear factor-κB (NF-κB) pathway. Shikonin at concentrations higher than 50 μM significantly inhibits ormal human keratinocytes (NHKs) viability, compare with that of control (P<0.05). Pretreatment with Shikonin for 2 h attenuates TNF-α-induced NF-κB p65 nuclear translocation. Treatments of Shikonin at 5 and 7.5 μM significantly inhibit the cell viability starting from 12 h and the inhibitory effects are presented in time-dependent patterns compare with the 0 h group in both cell lines. It is found that 5 μM Shikonin displays greater inhibition compare to 2.5 μM at the time points from 24 to 48 h. The invasiveness of U87 and U251 cells is significantly attenuated when treated with Shikonin at 2.5, 5, and 7.5 μM compare with the control group at 24 and 48 h (p<0.01).

In Vivo: Shikonin significantly inhibits the increase in IL-1β and TNF-α expression levels in the rat model of osteoarthritis, compare with those in the osteoarthritis group (P<0.01). The NF-κB protein expression level is significantly suppressed by Shikonin in the rat model of osteoarthritis, compare with that in the osteoarthritis group (P<0.01). The induction of the iNOS level is suppressed by treatment with Shikonin in the rat model of osteoarthritis, compare with that in the osteoarthritis group (P<0.01). The administration of Shikonin markedly weakens the up-regulation of COX-2 protein expression in the rat model of osteoarthritis, as compare with that in the osteoarthritis group (P<0.01). The elevation of caspase-3 activity is significantly reduced by Shikonin treatment in the rat model of osteoarthritis, compare with that in the osteoarthritis group (P<0.01). The downregulation of Akt phosphorylation is also significantly recovered by treatment with Shikonin in the rat model of osteoarthritis, compare with that in the osteoarthritis group (P<0.01).