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Gnetol is a phenolic compound isolated from the root of Gnetum ula Brongn. Gnetol potently inhibits COX-1 (IC₅₀ of 0.78 μM) and HDAC. Gnetol is a potent tyrosinase inhibitor with an IC₅₀ of 4.5 μM for murine tyrosinase and suppresses melanin biosynthesis. Gnetol has antioxidant, antiproliferative, anticancer and hepatoprotective activity. Gnetol also possesses concentration-dependent α-Amylase, α-glucosidase, and adipogenesis activities.

The antiproliferative activities of Gnetol are tested in HCT-116, Hep-G2, MDA-MB-231, and PC-3 cell lines by measuring cell viability after treatment with 4.1 μM, 40.9 μM, 204.7 μM, 409.4 μM, and 1023.6 μM. Gnetol shows concentration-dependent reductions in cell viability in cancer cell lines with greatest activity in colorectal cancer.
Gnetol at 200 µg/mL significantly offers the highest protection of 54.3% against the toxicant. A lower dose of Gnetol (50 µg/mL) also shields the cell line from the toxic effects of CCl4.
The ligand molecule TGF-β and PPARα protein show that Gnetol has the binding affinity of 7.0 and 8.4, respectively.

Male Sprague-Dawley rats were cannulated and dosed either intravenously with Gnetol (10 μg/kg) or orally (100 mg/kg). After oral and intravenous administration, Gnetol is detected in both serum and urine as the parent compound and as a glucuronidated metabolite. The bioavailability of Gnetol is determined to be 6%. Gnetol is rapidly glucuronidated and is excreted in urine and via nonrenal routes.
Pretreatment of Male NIH Swiss mice (20-35 g) with Gnetol (50mg/kg, SC) is able to increase the latency period to response in analgesia models.

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