|Arch Pharm Res. 2005 Feb;28(2):195-202. |
|The isolation and antioxidative effects of vitexin from Acer palmatum.[Pubmed: 15789751]|
|Free radicals and reactive oxygen species (ROS) caused by UV exposure or other environmental factors are critical players in cellular damage and aging. |
METHODS AND RESULTS:
In order to develop a new anti-photoaging agent, this work focused on the antioxidant effects of the extract of tinged autumnal leaves of Acer palmatum. One compound was isolated from an ethyl acetate soluble fraction of the A. palmatum extract using silica gel column chromatography. The chemical structure was identified as apigenin-8-C-beta-D-glucopyranoside, more commonly known as Vitexin, by spectral analysis including LC-MS, FT-IR, UV, 1H-, and 13C-NMR. The biological activities of Vitexin were investigated for the potential application of its anti-aging effects in the cosmetic field. Vitexin inhibited superoxide radicals by about 70% at a concentration of 100 microg/mL and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals by about 60% at a concentration of 100 microg/mL. Intracellular ROS scavenging activity was indicated by increases in dichlorofluorescein (DCF) fluorescence upon exposure to UVB 20 mJ/cm2 in cultured human dermal fibroblasts (HDFs) after the treatment of Vitexin. The results show that oxidation of 5-(6-)chloromethyl-2',7'-dichlorodihydrofluorescein diacetate (CM-H2DCFDA) is inhibited by Vitexin effectively and that Vitexin has a potent free radical scavenging activity in UVB-irradiated HDFs. In ROS imaging using a confocal microscope we visualized DCF fluorescence in HDFs directly.
In conclusion, our findings suggest that Vitexin can be effectively used for the prevention of UV-induced adverse skin reactions such as free radical production and skin cell damage.
|Eur J Pharmacol. 2013 Jan 15;699(1-3):250-7. |
|Anti-depressant-like effect of vitexin in BALB/c mice and evidence for the involvement of monoaminergic mechanisms.[Pubmed: 23099258 ]|
|The present study was designed to investigate the putative effect of Vitexin, a flavone C-glucoside present in some drugs, medicinal plants and nutraceuticals, on the central nervous system. |
METHODS AND RESULTS:
Vitexin (10-30 mg/kg) did not show significant alterations in the behaviour of mice tested in hole-board, plus-maze or activity cage tests. However, immobility time of the mice significantly reduced by Vitexin administrations in both the tail-suspension and modified forced swimming tests. The anti-immobility effect of Vitexin in the tail-suspension test was reversed with α-methyl-para-tyrosine methyl ester (AMPT, an inhibitor of catecholamine synthesis, 100mg/kg, i.p.), yohimbine (an α(2)-adrenoceptor antagonist, 1mg/kg, i.p.), NAN 190 (a 5-HT(1A) antagonist, 0.5mg/kg, i.p.), SCH 23390 (a dopamine D(1) antagonist, 0.05 mg/kg, s.c.) and sulpiride (a dopamine D(2)/D(3) antagonist, 50mg/kg, i.p.). The same effect was not reversed, however, by p-chlorophenylalanine methyl ester (PCPA; an inhibitor of serotonin synthesis 100mg/kg, i.p., administered for 4 consecutive days), ketanserin (a 5-HT(2A/2C) antagonist, 1-4 mg/kg, i.p.), ondansetron (a 5-HT(3) antagonist, 0.1-0.4 mg/kg, i.p.), prazosin (an α(1)-adrenoceptor antagonist, 1-4 mg/kg, i.p.), or propranolol (a non-selective β-adrenoceptor antagonist, 5-20mg/kg, i.p.).
These results suggest that the anti-depressant-like effect of Vitexin is mediated through an increase in catecholamine levels in the synaptic cleft as well as through interactions with the serotonergic 5-HT(1A), noradrenergic α(2), and dopaminergic D(1), D(2), and D(3) receptors. To our knowledge, this is the first study to show findings that indicate an anti-depressant-like effect of Vitexin and its underlying mechanisms.
|J Nat Prod. 2013 Jun 28;76(6):1141-9. |
|Vitexin inhibits inflammatory pain in mice by targeting TRPV1, oxidative stress, and cytokines.[Pubmed: 23742617]|
|The flavonoid Vitexin (1) is a flavone C-glycoside (apigenin-8-C-β-D-glucopyranoside) present in several medicinal and other plants. Plant extracts containing 1 are reported to possess antinociceptive, anti-inflammatory, and antioxidant activities. However, the only evidence that 1 exhibits antinociceptive activity was demonstrated in the acetic acid-induced writhing model. Therefore, the analgesic effects and mechanisms of 1 were evaluated. |
METHODS AND RESULTS:
In the present investigation, intraperitoneal treatment with 1 dose-dependently inhibited acetic acid-induced writhing. Furthermore, treatment with 1 also inhibited pain-like behavior induced by phenyl-p-benzoquinone, complete Freund's adjuvant (CFA), capsaicin (an agonist of transient receptor potential vanilloid 1, TRPV1), and both phases of the formalin test. It was also observed that inhibition of carrageenan-, capsaicin-, and chronic CFA-induced mechanical and thermal hyperalgesia occurred. Regarding the antinociceptive mechanisms of 1, it prevented the decrease of reduced glutathione levels, ferric-reducing ability potential, and free-radical scavenger ability, inhibited the production of hyperalgesic cytokines such as TNF-α, IL-1β, IL-6, and IL-33, and up-regulated the levels of the anti-hyperalgesic cytokine IL-10.
These results demonstrate that 1 exhibits an analgesic effect in a variety of inflammatory pain models by targeting TRPV1 and oxidative stress and by modulating cytokine production.
|J Ethnopharmacol. 2007 Sep 5;113(2):258-66. |
|The spasmolytic effect of Aloysia citriodora, Palau (South American cedrón) is partially due to its vitexin but not isovitexin on rat duodenums.[Pubmed: 17640836 ]|
|The spasmolytic effects of an acqueous extract of cedrón (AEC) were studied on rat isolated duodenums. This plant (Aloysia citriodora Palau, Verbenaceae) is widely used for gastrointestinal disorders and as eupeptic in South America. |
METHODS AND RESULTS:
AEC non-competitively inhibited the dose-response curve (DRC) of Ach (IC50 of 1.34 +/- 0.49 mg lyophilized/mL) and the DRC of Ca(2+) in high-[K(2-)](o) (IC50 of 2.64 +/- 0.23 mg/mL). AEC potentiated the non-competitive inhibition of either 30 micromol/L W-7 (a calmodulin blocker) and 5-15 micromol/L papaverine on the Ca(2+)-DRC. Also, AEC relaxed the contracture produced by high-[K(+)](o) (IC50 of 2.6 +/- 0.2 mg/mL) until 81.0 +/- 3.2% of the maximal effect of papaverine and 78.1+/- 5.0% of the quercetin, the most selective inhibitor of PDE. The AEC relaxation was non-competitively inhibited by 10-30 micromol/L methylene blue and competitively antagonized by 40 mmol/L TEA. The relaxation of 1mg/mL AEC was inhibited by hypoxia, but not that of 2mg/mL. Two flavonoids were identified by HPLC in the AEC: Vitexin and isoVitexin. Vitexin non-competitively inhibited the Ach-DRC (pD(2') of 5.7 +/- 0.4) but significantly run leftward the DRC of Ca(2+). IsoVitexin did not significantly inhibit the DRC of Ach nor Ca(2+).
The results suggest that the spasmolytic effect of AEC could be mostly associated to the increase in cGMP (target shared with the PDE inhibitors) and the activation of K(+)-channels. At low concentrations, AEC also inhibits the aerobic metabolism. The flavonoid Vitexin is partially responsible for the effect, since it non-competitively inhibits Ach but not the Ca(2+) influx. IsoVitexin was devoid of activity on duodenums.