Neohesperidin CAS NO.13241-33-3

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
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Chemical Properties of Neohesperidin

Source of Neohesperidin

The peel of Citrus aurantium L.

Biological Activity of Neohesperidin

Protocol of Neohesperidin

Preparing Stock Solutions of Neohesperidin

References on Neohesperidin

Inhibition of beta-amyloid Aggregation By Albiflorin, Aloeemodin And Neohesperidin And Their Neuroprotective Effect On Primary Hippocampal Cells Against beta-amyloid Induced Toxicity.[Pubmed:25938872]

Curr Alzheimer Res. 2015;12(5):424-33.

Being one of the hallmarks of Alzheimer's disease, beta-amyloid (Abeta) aggregates induce complicated neurotoxicity. Evidences show that the underlying mechanism of neurotoxicity involves a glutamate receptor subtype, N-methyl-D-aspartate (NMDA) receptor, an increase in intracellular calcium(II) ion loading as well as an elevation in oxidation stress. In this work, among the 35 chemical components of Chinese herbal medicines (CHMs) being screened for inhibitors of Abeta aggregation, four of them, namely albiflorin, aloeemodin, Neohesperidin and physcion, were found for the first time to exhibit a potent inhibitory effect on Abeta(1-40) and Abeta(1-42) aggregation. Their neuroprotective capability on primary hippocampal neuronal cells was also investigated by MTT assay, ROS assay and intracellular calcium(II) ion concentration measurement. It was interesting to find that physcion was rather toxic to neuronal cells while albiflorin, aloeemodin and Neohesperidin reduced the toxicity and ROS induced by both monomeric and oligomeric Abeta species. In addition, albiflorin was particularly powerful in maintaining the intracellular Ca(2+) concentration.

Effect of hesperidin and neohesperidin from bittersweet orange (Citrus aurantium var. bigaradia) peel on indomethacin-induced peptic ulcers in rats.[Pubmed:24691249]

Environ Toxicol Pharmacol. 2014 May;37(3):907-15.

Hesperidin and Neohesperidin are the major flavanones isolated from bittersweet orange. It was recently reported that they have potent anti-inflammatory effects in various inflammatory models. In the present study, the effects of hesperidin and Neohesperidin on indomethacin-induced ulcers in rats and the underlying mechanisms were investigated. Gastric ulcers were induced in rats with a single dose of indomethacin. The effects of pretreatment with hesperidin and Neohesperidin were assessed in comparison with omeprazole as reference standard. Ulcer index, gene expression of gastric cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-alpha), lipid peroxidation product, malondialdhyde (MDA), and reduced glutathione (GSH) content in stomach were measured. Furthermore, gross and histopathological examination was performed. Our results indicated that both hesperidin and Neohesperidin significantly aggravated gastric damage caused by indomethacin administration as evidenced by increased ulcer index and histopathological changes of stomach.

Protective effects of neohesperidin and poncirin isolated from the fruits of Poncirus trifoliata on potential gastric disease.[Pubmed:19367677]

Phytother Res. 2009 Dec;23(12):1748-53.

The effects of Poncirus trifoliata (P. trifoliata) (Ponciri Fructus, PF) extract and its constituents such as Neohesperidin and poncirin on gastritis in rats and human gastric cancer cells were investigated. The PF 70% ethanol extracts (1 g) showed approximately 11.38% of acid-neutralizing capacities and cytotoxicity (IC50=85.39 microg/mL) against human AGS gastric cancer cells. In addition, Neohesperidin exhibited antioxidant activity (IC50=22.31 microg/mL) in the 1,1-diphenyl-2-picryldydrazyl (DPPH) radical-scavenging assay. Neohesperidin (50 mg/kg) and poncirin (100 mg/kg) significantly inhibited 55.0% and 60.0% of HCl/ethanol-induced gastric lesions, respectively, and increased the mucus content. In pylorus ligated rats, Neohesperidin (50 mg/kg) significantly decreased the volume of gastric secretion and gastric acid output, and increased the pH. From these results, it could be suggested that Neohesperidin and poncirin isolated from PF may be useful for the treatment and/or protection of gastritis.

Neohesperidin attenuates cerebral ischemia-reperfusion injury via inhibiting the apoptotic pathway and activating the Akt/Nrf2/HO-1 pathway.[Pubmed:23952707]

J Asian Nat Prod Res. 2013 Sep;15(9):1023-37.

Oxidative stress is well known to play a pivotal role in cerebral ischemia-reperfusion injury. On the basis of this fact, antioxidative agents have been demonstrated to be neuroprotective. Neohesperidin (NH) is abundant in citrus flavonoids and possesses reactive oxygen species scavenging activity and neuroprotective effects in vitro. However, little is known about its effects on cerebral ischemia-reperfusion injury and the underlying mechanisms. In this study, we use a rat model of middle cerebral artery occlusion (MCAO) to investigate the neuroprotective effects of NH. NH significantly improved neurological functions and attenuated MCAO-induced infarct volume, pathological changes, and neuronal loss. Moreover, it enhanced antioxidant capacity and suppressed oxidative stress in the brain. NH inhibited the MCAO-induced upregulation of Bax, cytochrome c, and cleaved caspase-9 and -3, as well as the downregulation of Bcl-2. Interestingly, NH treatment upregulated heme oxygenase-1 (HO-1) in a concentration-dependent manner, which was due to the NH-mediated activation of the protein kinase B (Akt)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. NH also abolished the MCAO-induced inhibition of the Akt/Nrf2 pathway. In conclusion, NH attenuates cerebral ischemia-reperfusion injury via the inhibition of neuronal apoptosis and oxidative stress through the regulation of the apoptotic pathway and the Akt/Nrf2/HO-1 pathway. NH might be a promising preventive agent for ischemic stroke.

Neohesperidin induces cellular apoptosis in human breast adenocarcinoma MDA-MB-231 cells via activating the Bcl-2/Bax-mediated signaling pathway.[Pubmed:23285810]

Nat Prod Commun. 2012 Nov;7(11):1475-8.

Neohesperidin, a flavonoid compound found in high amounts in Poncirus trifoliata, has free radical scavenging activity. For the first time, our study indicated that Neohesperidin also induces cell apoptosis in human breast adenocarcinoma MDA-MB-231 cells, which was possibly mediated by regulating the P53/Bcl-2/Bax pathway. MDA-MB-231 cells were subjected to treatment with Neohesperidin. MTT and Trypan blue exclusion assays were applied to assess the cell viability. The morphological changes of cells were observed using an inverted microscope, and cell apoptosis was detected by flow cytometric analysis. Immunoblot analysis was conducted to evaluate the protein expressions of apoptosis-related genes, including P53, Bcl-2 and Bax. Our results indicated that the proliferation of MDA-MB-231 cells was inhibited by the treatment with Neohesperidin in a time- and dose-dependent manner. The IC50 values of Neohesperidin at 24 and 48 h were 47.4 +/- 2.6 microM and 32.5 +/- 1.8 microM, respectively. The expressions of P53 and Bax in the Neohesperidin-treated cells were significantly up-regulated, while that of Bcl-2 was down-regulated. Our study suggested that Neohesperidin could induce apoptosis of MDA-MB-231 cells, a process which was associated with the activation of the Bcl-2/Bax-mediated signaling pathway.

Description

Neohesperidin is a flavonoid compound found in high amounts in Poncirus trifoliata with anti-oxidant and anti-inflammatory effects.

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