Naringin dihydrochalcone

Research use only, not for human use.

Naringin Dihydrochalcone(Naringin DC) is an inhibitor of CYP enzymes, used as an artificial sweetener.

Naringin Dihydrochalcone(Naringin DC) is an inhibitor of CYP enzymes, used as an artificial sweetener.(In Vitro):Naringin suppresses NF-κ B signaling pathway activation. Naringenin inhibits high glucose-induced proliferation, inflammatory reaction and oxidative stress injury in HBZY-1 cells. Naringin inhibits AGS cancer cell proliferation in a dose- and time-dependent manner. Phosphorylation of PI3K and its activated downstream targets p-Akt and p-mTOR are significantly decreased at 2 mM in Naringin-treated AGS cells. Naringin induces autophagic cell death in AGS cells. Naringin activated the autophagy related protein in AGS cells. Naringin protects PC12 cells from 3-NP neurotoxicity. The lactate dehydrogenase release is decreased upon naringin treatment in 3-NP-induced PC12 cells. Naringin treatment enhances the antioxidant defense by increasing the activities of enzymatic antioxidants and the level of reduced glutathione.(In Vivo):Treatment with naringin significantly alleviates renal injury in diabetic rats and increases diabetic rats body weight significantly. Administration of naringin effectively alleviates the collagen deposition and renal interstitial fibrosis in diabetic rats. Treatment with naringin could result in decreased levels of ROS and MDA and increased activities of SOD and GSH-Px. Oral administration of naringin significantly improves the learning and memory abilities. Naringin significantly enhances insulin signaling pathway.

Naringin suppresses NF-κ B signaling pathway activation. Naringenin inhibits high glucose-induced proliferation, inflammatory reaction and oxidative stress injury in HBZY-1 cells. Naringin inhibits AGS cancer cell proliferation in a dose- and time-dependent manner. Phosphorylation of PI3K and its activated downstream targets p-Akt and p-mTOR are significantly decreased at 2 mM in Naringin-treated AGS cells. Naringin induces autophagic cell death in AGS cells. Naringin activated the autophagy related protein in AGS cells. Naringin protects PC12 cells from 3-NP neurotoxicity. The lactate dehydrogenase release is decreased upon naringin treatment in 3-NP-induced PC12 cells. Naringin treatment enhances the antioxidant defense by increasing the activities of enzymatic antioxidants and the level of reduced glutathione.

Treatment with naringin significantly alleviates renal injury in diabetic rats and increases diabetic rats body weight significantly. Administration of naringin effectively alleviates the collagen deposition and renal interstitial fibrosis in diabetic rats. Treatment with naringin could result in decreased levels of ROS and MDA and increased activities of SOD and GSH-Px. Oral administration of naringin significantly improves the learning and memory abilities. Naringin significantly enhances insulin signaling pathway.

Naringin DC

Others

Other Targets

Others

Others-Field

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18916-17-1

582.55

C27H34O14

>98% (HPLC)

DMSO : ≥ 32 mg/mL; 54.93 mM

C[C@H]1[C@@H]([C@H]([C@H]([C@@H](O1)O[C@@H]1[C@H]([C@@H]([C@H](O[C@H]1Oc1cc(c(c(c1)O)C(=O)CCc1ccc(cc1)O)O)CO)O)O)O)O)O

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(-20℃)

With Ice Pack

≥ 2 years