||Caffeic acid has antidiabetic, antioxidant, anticarcinogenic, and anti-inflammatory activities, it can suppress ultraviolet B(UVB)-induced COX-2 expression by blocking Fyn kinase activity, inhibits HBV-DNA replication as well as HBsAg production, also reduces serum DHBV level in DHBV-infected duckling model. Caffeic acid may be used as designed novel therapeutic drugs for Parkinson's disease by inhibiting α-synuclein fibrillation.
|Antiviral Res. 2009 Aug;83(2):186-90. |
|Anti-hepatitis B virus activity of chlorogenic acid, quinic acid and caffeic acid in vivo and in vitro.[Pubmed: 19463857 ]|
|Chlorogenic acid and its related compounds are abundant plant polyphenols that have a diverse antiviral activity.
METHODS AND RESULTS:
In this study, HepG2.2.15 cells and duck hepatitis B virus infection model were used as in vitro and in vivo models to evaluate their anti-HBV activity. In the cell model, all the three compounds inhibited HBV-DNA replication as well as HBsAg production. Chlorogenic acid and Caffeic acid also reduced serum DHBV level in DHBV-infected duckling model. Moreover, the anti-HBV activity of crude extracts of coffee beans, which have a high content of chlorogenic acid, was studied.
Both the extracts of regular coffee and that of decaffeinated coffee showed inhibitory effect on HBV replication.
|J Pharmacol Exp Ther. 2006 Aug;318(2):476-83 |
|Antihyperglycemic and antioxidant properties of caffeic acid in db/db mice.[Pubmed: 16644902 ]|
|This study investigated the blood glucose-lowering effect and antioxidant capacity of Caffeic acid in C57BL/KsJ-db/db mice.
METHODS AND RESULTS:
Caffeic acid induced a significant reduction of the blood glucose and glycosylated hemoglobin levels than the control group. The plasma insulin, C-peptide, and leptin levels in Caffeic acid group were significantly higher than those of the control group, whereas the plasma glucagon level was lower. Increased plasma insulin by Caffeic acid was attributable to an antidegenerative effect on the islets. Caffeic acid also markedly increased glucokinase activity and its mRNA expression and glycogen content and simultaneously lowered glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities and their respective mRNA expressions, accompanied by a reduction in the glucose transporter 2 expression in the liver. In contrast to the hepatic glucose transporter 2, adipocyte glucose transporter 4 expression was greater than the control group. In addition, Caffeic acid significantly increased superoxide dismutase, catalase, and glutathione peroxidase activities and their respective mRNA levels, while lowering the hydrogen peroxide and thiobarbituric acid reactive substances levels in the erythrocyte and liver of db/db mice.
These results indicate that Caffeic acid exhibits a significant potential as an antidiabetic agent by suppressing a progression of type 2 diabetic states that is suggested by an attenuation of hepatic glucose output and enhancement of adipocyte glucose uptake, insulin secretion, and antioxidant capacity.
|Free Radic Res. 2004 Nov;38(11):1241-53. |
|Caffeic acid derivatives: in vitro and in vivo anti-inflammatory properties.[Pubmed: 15621702]|
|Caffeic acid and some of its derivatives such as Caffeic acid phenetyl ester (CAPE) and octyl caffeate are potent antioxidants which present important anti-inflammatory actions. |
METHODS AND RESULTS:
The present study assessed the in vitro and in vivo effects of five Caffeic acid derivatives (Caffeic acid methyl, ethyl, butyl, octyl and benzyl esters) and compared their actions to those of CAPE. In the model of LPS-induced nitric oxide (NO) production in RAW 264.7 macrophages, the pre-incubation of all derivatives inhibited nitrite accumulation on the supernatant of stimulated cells, with mean IC50 (microM) values of 21.0, 12.0, 8.4, 2.4, 10.7 and 4.80 for methyl, ethyl, butyl, octyl, benzyl and CAPE, respectively. The effects of Caffeic acid derivatives seem to be related to the scavenging of NO, as the compounds prevented SNAP-derived nitrite accumulation and decreased iNOS expression. In addition, butyl, octyl and CAPE derivatives significantly inhibited LPS-induced iNOS expression in RAW 264.7 macrophages. Extending the in vitro results, we showed that the pre-treatment of mice with butyl, octyl and CAPE derivatives inhibited carrageenan-induced paw edema and prevented the increase in IL-1beta levels in the mouse paw by 30, 24 and 36%, respectively. Butyl, octyl and CAPE derivatives also prevented carrageenan-induced neutrophil influx in the mouse paw by 28, 49 and 31%, respectively.
Present results confirm and extend literature data, showing that Caffeic acid derivatives exert in vitro and in vivo anti-inflammatory actions, being their actions mediated, at least in part by the scavenging of NO and their ability to modulate iNOS expression and probably that of other inflammatory mediators.