| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Cell lines | HepaRG cells |
Preparation Method | HepaRG cells at a concentration of 1.5 104 cells/mL were seeded on uncoated plastic tissue culture dishes and treated with sulforaphane at different concentrations (0 -40 uM) over a time course (12-48 h). The cells as well as the homogenates from liver tissues were solubilized, and the activity solution including a reporter dye were added to the supernatants. |
Reaction Conditions | 0 -40 uM sulforaphane for 12-48 h |
Applications | Sulforaphane amplifies ALDH2 activity in HepaRG cells and suppresses acetaldehyde-induced proliferation and activation in LX-2 cells. |
Animal models | Ten-week-old female C57BL/6J mice |
Preparation Method | Mice in the CD/ CCl4 group were fed the normal liquid diet and received 1 mL/kg body weight CCl4 dissolved in corn oil by intraperitoneal injection twice weekly. Mice in the ED/ CCl4 group were fed a 2.5% (v/v) ethanol-containing Lieber-DeCarli liquid diet (Research Diets) (ED) and received intraperitoneal CCl4 injection twice weekly (1 mL/kg body weight). Mice in the ED/ CCl4/SFN group were fed the ED with sulforaphane and received intraperitoneal CCl4 injection (1 mL/kg body weight) twice weekly; in this group, sulforaphane was administered peroral as a mixture of ED (5 µmoL/d/body weight). |
Dosage form | Sulforaphane was administered peroral as a mixture of ED (5 µmoL/d/body weight) twice weekly |
Applications | Sulforaphane exerts antioxidative effects with ALDH2 induction in liver fibrosis induced by ethanol exposure in CCl4-treated mice. |
| 文献引用 | |
| 产品描述 | Sulforaphane (SFN) known as [1-isothiocyanato-4-(methylsulfinyl)butane]. It is an isothiocyanate that is present naturally in widely consumed vegetables and has a particularly high concentration in broccoli[1,10]. Sulforaphane is a phytocompound with antioxidant, anti-inflammatory, and antiapoptotic effects[2]. Sulforaphane amplifies ALDH2 activity in HepaRG cells and suppresses acetaldehyde-induced proliferation and activation in LX-2 cells[3]. Sulforaphane reversed mesenchymal-like changes induced by TGF-β1 and restored cells to their epithelial-like morphology. The expression of the epithelial marker, E-cadherin, increased after Sulforaphane treatment, while expression of the mesenchymal markers, N-cadherin, vimentin, and α-SMA decreased in A549 cells after SFN treatment[4]. Sulforaphane inhibited cell growth and reduced collagen at the mRNA and protein levels in keloid fibroblasts. Moreover, sulforaphane markedly suppressed the expression of IL-6 and α-SMA and inhibited Stat3 and Smad3 signaling pathways in keloid fibroblast KF112 cells[8]. Sulforaphane inhibited XWLC-05 cell growth with inhibitory concentration (IC)50 of 4.04, 3.38, and 3.02 μg/mL at 24, 48, and 72 hours, respectively. Sulforaphane affected the XWLC-05 cell cycle as cells accumulated in the G2/M phase[9]. Sulforaphane exerts antioxidative effects with ALDH2 induction in liver fibrosis induced by ethanol exposure in CCl4-treated mice[3]. Nrf2 plays the indispensable role for Sulforaphane cardiac protection from T2DM with significant induction of MT and other antioxidants. MT expression induced by Sulforaphane is Nrf2 dependent, but is not indispensable for SFN-induced cardiac protection from T2DM[5]. Sulforaphane significantly reduced the incidence and size of 4NQO-induced tongue tumors in mice[6]. Sulforaphane suppresses skin cancer via blocking sulfatase-2 with subsequent elevation in HSPGs and reduction in glypican-3. Moreover, sulforaphane attenuated skin cancer-induced activation of inflammatory and apoptotic pathways[7]. References: |
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