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    Isoliensinine
    Information
    CAS No. 6817-41-0 Price $208 / 20mg
    Catalog No.CFN99574Purity>=98%
    Molecular Weight610.75Type of CompoundAlkaloids
    FormulaC37H42N2O6Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Isoliensinine has anti-cancer, anti-fibrosis, anti-proliferative, antioxidant, and anti-inflammatory activities, it inhibited TNF-alpha and TGF-beta 1; decreased the overexpression of growth factors Platelet-derived growth factor (PDGF)-beta, basic fibroblast growth factor (bFGF), proto-oncogene c-fos, c-myc and hsp70; and activated ROS and p38 MAPK/JNK .
    Targets: TNF-α | TGF-β/Smad | ROS | p38MAPK | JNK | HSP (e.g. HSP90)
    In vitro:
    Sci Rep. 2015 Jul 29;5:12579.
    Isoliensinine induces apoptosis in triple-negative human breast cancer cells through ROS generation and p38 MAPK/JNK activation.[Pubmed: 26219228]
    Isoliensinine, liensinine and neferine are major bisbenzylisoquinoline alkaloids in the seed embryo of lotus (Nelumbo nucifera), and exhibit potential anti-cancer activity. Here, we explored the effects of these alkaloids on triple-negative breast cancer cells and found that among the three alkaloids Isoliensinine possesses the most potent cytotoxic effect, primarily by inducing apoptosis.
    METHODS AND RESULTS:
    Interestingly, Isoliensinine showed a much lower cytotoxicity against MCF-10A, a normal human breast epithelial cell line. Further studies showed that Isoliensinine could significantly increase the production of reactive oxygen species (ROS) in triple-negative breast cancer cells, but not in MCF-10A cells. The Isoliensinine-induced apoptosis could be attenuated by radical oxygen scavenger N-acetyl cysteine, suggesting that the cytotoxic effect of Isoliensinine on cancer cells is at least partially achieved by inducing oxidative stress. We found that both p38 MAPK and JNK signaling pathways were activated by Isoliensinine treatment and contributed to the induction of apoptosis. Furthermore, inhibitors or specific siRNAs of p38 MAPK and JNK could attenuate apoptosis induced by Isoliensinine. However, only the p38 inhibitor or p38-specific siRNA blocked the elevation of ROS in Isoliensinine-treated cells.
    CONCLUSIONS:
    Our findings thus revealed a novel antitumor effect of Isoliensinine on breast cancer cells and may have therapeutic implications.
    Yao Xue Xue Bao. 2005 Feb;40(2):105-10.
    Effects of isoliensinine on proliferation of porcine coronary arterial smooth muscle cells induced by phenylephrine.[Pubmed: 15875663]
    To investigate the inhibitory effects and mechanism of action of Isoliensinine (IL) on the proliferation of porcine coronary arterial smooth muscle cells (CASMCs) induced by phenylephrine (Phen) and its mechanisms of action.
    METHODS AND RESULTS:
    MTT assay, immunohistochemical method and Western blotting were adopted. IL (0.03 - 3 micromol x L(-1)) could inhibit the CASMCs proliferation induced by Phen (0.1 micromol x L(-1)) in a concentration-dependent manner. IL (0.1 micromol x L(-1)) antagonized Phen-induced overexpression of PDGF-beta and bFGF from 0.545 +/- 0.026 and 0.47 +/- 0.03 to 0.458 +/- 0.019 and 0.376 +/- 0.017 (P < 0.01 , P < 0.01). IL (0.1 micromol x L(-1)) also decreased c-fos, c-myc and hsp70 overexpression induced by Phen from 0.57 +/- 0.04, 0.44 +/- 0.04 and (173 +/- 36)% to 0.46 +/- 0.05, 0.372 +/- 0.021 and (115 +/- 35)% respectively (P < 0.01, P < 0.01, P < 0.01).
    CONCLUSIONS:
    IL exerted antiproliferative effect on CASMCs induced by phenylephrine, and its mechanisms were related to decrease the overexpression of growth factors (PDGF-beta, bFGF), protooncogene (c-fos, c-myc) and hsp70.
    In vivo:
    Planta Med. 2005 Mar;71(3):225-30.
    Inhibitory effects of isoliensinine on bleomycin-induced pulmonary fibrosis in mice.[Pubmed: 15770542 ]
    The effects of Isoliensinine (IL), a bisbenzylisoquinoline alkaloid extracted from the Chinese traditional medicine seed embryo of Nelumbo nucifera Gaertn., on bleomycin (BLM)-induced pulmonary fibrosis in mice were investigated.
    METHODS AND RESULTS:
    Seventy-two male Kungming mice were divided randomly into eight groups as BLM-IL10, BLM-IL20, BLM-IL40, BLM-Sal, Sal-IL10, Sal-IL20, Sal-IL40 and Sal-Sal groups. BLM (0.1 mg in 0.05 ml saline per animal, once) or saline (0.05 ml per animal, once) was applied intratracheally, and IL (10, 20, 40 mg/kg) or saline was administered orally 3 times per day in the appropriate groups. Animals were sacrificed 14 days after intratracheal treatment. Lung tissue and serum superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels, tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta 1 (TGF-beta (1)) were determined by biochemical measurements and immunohistochemistry. BLM treatment resulted in a significant increase of the hydroxyproline content and an obvious lung histological injury as compared to the Sal-Sal group. Administration of IL remarkably suppressed the increase in hydroxyproline content and abated the lung histological injury induced by BLM. There was a decrease in SOD activity and an increase in MDA level in lung tissue and serum in the BLM-Sal group (p < 0.01 , p < 0.01, vs. Sal-Sal group, respectively). And IL could obviously enhance the SOD activity and decrease the MDA level in a concentration-dependent manner. Moreover, IL also significantly inhibited the overexpression of TNF-alpha and TGF-beta (1) induced by BLM.
    CONCLUSIONS:
    These results indicated that IL possessed a significant inhibitory effect on BLM-induced pulmonary fibrosis, probably due to its antioxidant and/or anti-inflammatory activities and inhibitory overexpressing TNF-alpha and TGF-beta (1) induced by BLM.
    Isoliensinine Description
    Source: The plantule of Nelumbo nucifera Gaertn.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: 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.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: 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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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.6373 mL 8.1867 mL 16.3733 mL 32.7466 mL 40.9333 mL
    5 mM 0.3275 mL 1.6373 mL 3.2747 mL 6.5493 mL 8.1867 mL
    10 mM 0.1637 mL 0.8187 mL 1.6373 mL 3.2747 mL 4.0933 mL
    50 mM 0.0327 mL 0.1637 mL 0.3275 mL 0.6549 mL 0.8187 mL
    100 mM 0.0164 mL 0.0819 mL 0.1637 mL 0.3275 mL 0.4093 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Cell Research:
    J Asian Nat Prod Res. 2006 Apr-May;8(3):209-16.
    Effects of isoliensinine on angiotensin II-induced proliferation of porcine coronary arterial smooth muscle cells.[Pubmed: 16864426]
    The inhibitory effects of Isoliensinine (IL), a bisbenzylisoquinoline alkaloid extracted from the seed embryo of the traditional chinese medicinal herb Nelumbo nucifera Gaertn, on the proliferation of porcine coronary arterial smooth muscle cells (CASMCs) induced by angiotensin II(Ang II) and its mechanisms of action were investigated.
    METHODS AND RESULTS:
    Counting cultured cell number, MTT assay, immunohistochemical method and Western blot were adopted. Ang II 0.1 micromol l (-1) significantly evoked CASMC proliferation by 42%, which could be dose-dependently inhibited by IL 0.01-3 micromol l (-1) and the percentage of inhibition of IL 0.1 micromol l (-1) was 25%. Irbesartan (Irb) 0.1 micromol l (-1) inhibited CASMC proliferation by 22%. IL or Irb 0.1 micromol l (-1) decreased Ang II-induced overexpression of Platelet-derived growth factor (PDGF)-beta and basic fibroblast growth factor (bFGF), respectively. Both of them also declined c-fos, c-myc and hsp70 overexpression, respectively. At the same concentration, the inhibitory effects of IL on PDGF-beta were even stronger than those of Irb (P < 0.05).
    CONCLUSIONS:
    In summary, the data showed that IL possesses an anti-proliferative effect, which is related to the decrease of the overexpression of growth factors PDGF-beta, bFGF, proto-oncogene c-fos, c-myc and hsp70.