| Description: |
Procyanidin A2 is a potential precursor of 5-(3',4'-dihydroxyphenyl)-γ-valerolactone, exhibits antioxidant, anti-inflammary, anti-hyperglycemia, and anti-type 2 diabetes activities. Procyanidin A2 demonstrates liver cell regenerative activity in scratch wound healing assays and alcohol-induced liver cell injury in vitro. |
| Targets: |
GLUT | IFN-γ | IL Receptor | TNF-α | NF-kB | IkB | IKK |
| In vitro: |
| Int J Mol Sci. 2016 Nov 12;17(11). pii: E1888. | | Procyanidin A2 Modulates IL-4-Induced CCL26 Production in Human Alveolar Epithelial Cells.[Pubmed: 27845745 ] | Allergic asthma is an inflammatory lung disease that is partly sustained by the chemokine eotaxin-3 (CCL26), which extends eosinophil migration into tissues long after allergen exposure. Modulation of CCL26 could represent a means to mitigate airway inflammation.
METHODS AND RESULTS:
Here we evaluated Procyanidin A2 as a means of modulating CCL26 production and investigated interactions with the known inflammation modulator, Interferon γ (IFNγ). We used the human lung epithelial cell line A549 and optimized the conditions for inducing CCL26. Cells were exposed to a range of Procyanidin A2 or IFNγ concentrations for varied lengths of time prior to an inflammatory insult of interleukin-4 (IL-4) for 24 h. An enzyme-linked immunosorbent assay was used to measure CCL26 production. Exposing cells to 5 μM Procyanidin A2 (prior to IL-4) reduced CCL26 production by 35% compared with control. Greatest inhibition by Procyanidin A2 was seen with a 2 h exposure prior to IL-4, whereas IFNγ inhibition was greatest at 24 h. Concomitant incubation of Procyanidin A2 and IFNγ did not extend the inhibitory efficacy of Procyanidin A2.
CONCLUSIONS:
These data provide evidence that Procyanidin A2 can modulate IL-4-induced CCL26 production by A549 lung epithelial cells and that it does so in a manner that is different from IFNγ. | | Food Chemistry, 2010, 119(2):753-7. | | Antioxidant activities and contents of polyphenol oxidase substrates from pericarp tissues of litchi fruit[Reference: WebLink] | The experiments were performed to extract and purify substrates for polyphenol oxidase (PPO) from pericarp tissue of postharvest litchi fruit. Two purified PPO substrates were identified as (−)-epicatechin and Procyanidin A2. The antioxidant properties of two PPO substrates were further evaluated in the present study.
METHODS AND RESULTS:
Variation in the content of the major substrate (−)-epicatechin of litchi fruit during storage at 25 °C was analysed using the HPLC-UV method. The results showed that (−)-epicatechin exhibited stronger antioxidant capability than Procyanidin A2, in terms of reducing power and scavenging activities of DPPH radical, hydroxyl radical and superoxide radical. Furthermore, (−)-epicatechin content in pericarp tissue tended to decrease with increasing skin browning index of litchi fruit during storage at 25 °C.
CONCLUSIONS:
Thus, these two compounds can be used as potential antioxidants in litchi waste and the fresh pericarp tissue of litchi fruit exhibited a better utilisation value. |
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| In vivo: |
| J Physiol Pharmacol. 2016 Apr;67(2):243-52. | | Preventive effects of procyanidin A2 on glucose homeostasis, pancreatic and duodenal homebox 1, and glucose transporter 2 gene expression disturbance induced by bisphenol A in male mice.[Pubmed: 27226184] | Procyanidins (PCs) as oligomeric compounds with antidiabetic properties formed from catechin and epicatechin molecules. Bisphenol A(BPA) is a common chemical material use in food and beverage packaging.
METHODS AND RESULTS:
The aim of this study was to explore the protective effects of procyanidin A2 (PCA2) against glucose homeostasis disturbance and gene expression of pancreatic and duodenal homebox 1 (Pdx1) as well as glucose transporter 2 (Glut2) induced by BPA in male mice. First tested these five concentrations of PCA2 (3 - 300 μM) alone and in combination with BPA(100 μg/L), on insulin secretion from isolated islets at in vitro condition. Next, examined the influence of BPA and PCA2 on islet apoptosis using flowcytometry. At in vivo condition, the BPA (100 μg/kg) and PCA2 (10 μmol/kg) administered for 20 days then, blood glucose and insulin, Pdx1 and, Glut2 genes expression, and oxidative stress markers examined.
CONCLUSIONS:
The results indicated that PCA2 strongly prevents islet cells apoptosis induced by BPA and, co-administration of PCA2 and BPA modified hyperglycemia. BPA reduced Pdx1 and Glut2 mRNA expression and antioxidant level in pancreas tissue, whereas PCA2 prevented from these effects. The findings from these studies suggest that use of PCA2 rich plants have preventive effects on hyperglycemia, and type 2 diabetes. |
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