Background
Naringin dihydrochalcone is an artificial sweetener and flavonoid that has been isolated from various plants and has antioxidant activity.1,2 It scavenges ABTS , oxygen, and 2,2-diphenyl-1-picrylhydrazyl radicals in cell free assays (IC50s = 24, 322.8, and 318.9 μM, respectively).2
1.Gentili, B., and Horowtiz, R.M.Chromatography of dihydrochalcone sweeteners and related compounds: A reagent for detecting dihydrochalconesJ. Chromatogr.63(5730)467-469(1971)
2.Li, X., Chen, B., Xie, H., et al.Antioxidant structure-activity relationship analysis of five dihydrochalconesMolecules23(5)E1162(2018)
Protocol
Cell experiment: | HBZY-1 cells are plated into 96-well plates and pretreated with various concentrations(1, 5, 10, 25, 50, 100 μM) of naringin for 2 h. Then cells are treated with 30 mM glucose for 24 h. The control group is added sterile normal saline in the same volume. After treatment, all the wells are incubated with 20 μl of 5 mg/ml MTT for 4 h at 37°C. Subsequently, 100 μl of DMSO are used to dissolve the formed formazan crystals after removal of the supernatant. The result is recorded at 490 nm on a microplate reader[1]. |
Animal experiment: | Rats: The rats are randomly divided into six groups: control, naringin (80 mg/kg), STZ, STZ+naringin (20 mg/kg), STZ+naringin (40 mg/kg), STZ+naringin(80 mg/kg). The rats in the STZ and STZ+naringin groups are intraperitoneally injected with STZ (65 mg/kg). The control and naringin groups are intraperitoneally injected with 0.1 M citrate buffer of same volume. After injection of STZ for 3 and 5 days, blood glucose levels are measured by tail vein puncture blood sampling[1]. Mice: Sixty 4-week-old male mice are randomized into four groups and fed for 20 weeks with either control diet or high-fat diet chow. Mice are dosed with 100 mg/kg of naringin daily. Mice body weight and food intake are weekly measured. Following behavioral assessment, animals are deeply anesthetized with isoflurane and sacrificed by decapitation after fasting for at least 5 h. Their plasma is collected for further analysis[4]. |
参考文献: [1]. Chen F, et al. Naringin Alleviates Diabetic Kidney Disease through Inhibiting Oxidative Stress and Inflammatory Reaction. PLoS One. 2015 Nov 30;10(11):e0143868.
[2]. Raha S, et al. Naringin induces autophagy-mediated growth inhibition by downregulating the PI3K/Akt/mTOR cascade via activation of MAPK pathways in AGS cancer cells. Int J Oncol. 2015 Sep;47(3):1061-9.
[3]. Kulasekaran G, et al. Neuroprotective efficacy of naringin on 3-nitropropionic acid-induced mitochondrial dysfunction through the modulation of Nrf2 signaling pathway in PC12 cells. Mol Cell Biochem. 2015 Nov;409(1-2):199-211.
[4]. Wang D, et al. Naringin Improves Neuronal Insulin Signaling, Brain Mitochondrial Function, and Cognitive Function in High-Fat Diet-Induced Obese Mice. Cell Mol Neurobiol. 2015 Oct;35(7):1061-71. |
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