Propyl gallste and other gallic acid esters are used as antioxidants in lipsticks, lip balms and salves, cosmetic creams and lotions, bakery products, edible fats and other pharmaceutical and industrial products. Propyl gallate is used widely but allergic contact dermatits from propyl gallate is rare. A 44-year-old female patient had pruritic multiple tiny erythematous papules and vesicles on the margin of her lip for a week. We found that the causative material of the allergic contact cheilitis was propyl gallate. We proved it with a patch test, provocation use test and quantitative and qualitative analysis of the lipstick. To our knowledge, this is the first case report of lipstick allergic contact cheilitis from propyl gallate in Korean literature.
Adult ; Antioxidants ; Cheilitis* ; Esters ; Fats ; Female ; Gallic Acid ; Humans ; Lip ; Ointments ; Patch Tests ; Propyl Gallate*

To make a clear understanding of the in vivo metabolism of propyl gallate in rats and determine the original compounds of the metabolites of Paeoniae Radix Rubra (PRR), the urine and plasma of the rats administrated with propyl gallate were collected, and then the HPLC-DAD-ESI-IT-TOF-MS(n) technique was applied to screen and identify the metabolites of propyl gallate from these bio-samples. By comparing the collected LC-MS data, the origin of the metabolites of PRR were confirmed. Finally, 33 metabolites of propyl gallate were identified from urine sample, and 20 metabolites of propyl gallate were identified from the plasma sample. In total, 37 metabolites of propyl gallate were identified, and 17 of them were identical to the metabolites of PRR. They are mainly the phase II metabolites of propyl gallate, 3-hydroxypropyl 3,4,5-trihydroxybenzoate, gallic acid and pyrogallol. Phase I reactions (decarboxylation, hydroxylation) and phase II reactions (sulfation, glucuronidation and methylation) were observed as the main metabolic pathways of propyl gallate. In this research, the in vivo metabolism of proply gallate was reported for the first time and 37 metabolites were identified, among which 35 were new metabolites of propyl gallate, and 20 were new compounds. The results demonstrated that 17 metabolites of PRR can be formed from propyl gallate. This will enhance our understanding of the metabolism and Effective forms (the truly active structures) of propyl gallate and PRR.
Animals ; Chromatography, High Pressure Liquid ; methods ; Drugs, Chinese Herbal ; analysis ; metabolism ; Male ; Paeonia ; chemistry ; Propyl Gallate ; blood ; urine ; Rats ; Rats, Sprague-Dawley ; Spectrometry, Mass, Electrospray Ionization ; methods

The study was purposed to explore the suitable platelet activators to be used in slide platelet aggregation test. Experiments were as follows: (1) to detect the intensity and time in 15 healthy donors' platelet aggregation tests induced by cationic propyl gallate (c-PG) and the usual platelet activators: ADP, collagen, epinephrine, arachidonic acid and ristocentin, respectively; (2) to detect the time in platelet aggregation tests of 15 healthy donors induced by c-PG and the above usual platelet activators respectively after addition of PGI2, cAMP or EDTA; (3) to detect the time in 15 healthy donors' platelet aggregation tests induced by c-PG after addition of heparin; (4) to detect the intensity and time of platelet aggregation induced by c-PG at the platelet count of (240-15) x 10(9)/L, (5) to detect the time of platelet aggregation induced by c-PG in eight patients each of whom had taken 100 mg aspirin per day for five days. The results showed that (1) c-PG reduced the strongest intensity of platelet aggregation and the time taken was appropriate, (2) c-PG was the most effective activator to reveal the inhibitive effect on platelet by PGI2, cAMP or EDTA, (3) 0.5 - 3 U/ml heparin did not significantly change the platelet aggregation induced by c-PG, (4) 15 healthy donors' platelet aggregation induced by c-PG displayed clearly on the slide until the platelet count below 30 x 10(9)/L, (5) The platelet aggregation time induced by c-PG was significantly prolonged in eight patients who had taken aspirin. In conclusion, compared to the usual platelet activators, c-PG has remarkable potential advantages when used in slide platelet aggregation test.
Cyclic AMP ; pharmacology ; Edetic Acid ; pharmacology ; Epoprostenol ; pharmacology ; Heparin ; pharmacology ; Humans ; Male ; Platelet Activation ; drug effects ; Platelet Aggregation ; drug effects ; Propyl Gallate ; pharmacology

Animals ; Anti-Inflammatory Agents, Non-Steroidal ; pharmacology ; Antioxidants ; pharmacology ; Drugs, Chinese Herbal ; pharmacology ; Humans ; Paeonia ; chemistry ; Platelet Aggregation Inhibitors ; pharmacology ; Propyl Gallate ; isolation & purification ; pharmacology

OBJECTIVETo evaluate the protective effect of propyl gallate (PG), an alkyl ester of gallic acid which is an active ingredient of Radix Paeoniae, against oxidized low-density lipoprotein (ox-LDL)-induced apoptosis and death in endothelial cells (ECs) and to find out its preliminary mechanism.

METHODSThe cultured endothelial cells were divided into normal, model (ox-LDL), control (fetal bovine serum), PG high dose (20 μg/mL), PG middle dose (10 μg/mL), and PG low dose (5 μg/mL) groups, each derived from three different pools of umbilical cords. The model of injured human umbilical vein endothelial cells (HUVECs) was induced by ox-LDL. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, Hoechst 33258 staining, flow cytometry and measurement of nitrogen monoxidum (NO) release were used to evaluate the protective effect of PG against ox-LDL-induced apoptosis and death in HUVECs. To find out the mechanism of this protective effect, the expression of endothelial nitric oxide synthase (eNOS) mRNA, eNOS protein expression, immunofluorescence of intracellular reactive oxygen species (ROS) and activities of malondialdehyde (MDA), superoxidedismutase (SOD) and glutathione peroxidase (GPx) were observed.

RESULTSPG significantly reduced ox-LDL-induced apoptosis and cell death. The percentage of cells death and apoptosis was significantly higher in the ox-LDL group than that in the control group (P<0.05). Compared with the control group, the cells death and apoptosis of PG group was no different (P>0.05). As compared with the ox-LDL group, results of the PG high dose group showed that cell viability was significantly increased (P<0.05), the level of NO release, expression of eNOS mRNA, densitometric value of eNOS protein expression, as well as the activities of SOD and GPx were all significantly higher (all P<0.05).

CONCLUSIONPG could potentially serve as a novel endothelial protective agent against ox-LDL-induced injury of endothelial cell.

Apoptosis ; drug effects ; Cell Survival ; drug effects ; Cells, Cultured ; Cytoprotection ; drug effects ; Human Umbilical Vein Endothelial Cells ; drug effects ; metabolism ; Humans ; Lipoproteins, LDL ; toxicity ; Oxidative Stress ; drug effects ; Propyl Gallate ; pharmacology ; Reactive Oxygen Species ; metabolism

OBJECTIVETo investigate the therapeutic effects of propyl gallate (PrG) in combination with standard medication on patients with non-ST-elevation acute coronary syndrome (NST-ACS), including unstable angina and acute non-ST-elevation myocardial infarction, and its influences on serum inflammatory marker and platelet activation.

METHODSFifty-five patients with NST-ACS were randomly assigned to two groups. Accessory to the standard Western medicine, the 27 patients in the tested group treated with PrG and the 28 in the control group with salvia composite (SC), all being medicated for 14 days. Effects on angina pectoris and electrocardiogram were observed. The positive rate and mean fluorescence density (MFI) of GP IIb-IIIa and CD62p expression on platelet surface were detected using flow cytometer; the serum concentration of high sensitive C-reactive protein (Hs-CRP) was determined using ELISA before and after treatment respectively.

RESULTSThe therapeutic effects on angina and electrocardiogram between the two groups showed no significant difference. Serum level of Hs-CRP, GP IIb-IIIa MFI and CD62p positive rate were significantly lowered after treatment in both groups (P < 0.05), no significant difference was found between groups, though the lowering of Hs-CRP and GP IIb-IIIa MFI in the tested group displayed a further decreasing trend.

CONCLUSIONIn combination with standard medication of Western medicine, PrG and SC showed no obvious difference in the therapeutic effect and influences on angina pectoris and electrocardiogram in patients with non-ST-elevation acute coronary syndrome.

Acute Coronary Syndrome ; drug therapy ; genetics ; metabolism ; Adult ; Aged ; C-Reactive Protein ; metabolism ; Female ; Gene Expression ; drug effects ; Humans ; Male ; Middle Aged ; P-Selectin ; genetics ; metabolism ; Propyl Gallate ; therapeutic use

OBJECTIVETo investigate the effects of Propyl Gallate (PrG) on cellular adhesion between human To investigate the effects of Propyl Gallate (PrG) on cellular adhesion between human umbilical vein endothelial cells (HUVEC) and polymorphonuclear leukocytes (PMN) as well as the expression umbilical vein endothelial cells (HUVEC) and polymorphonuclear leukocytes (PMN) as well as the expression of intercellular adhesion molecule-1 (ICAM-1, CD54) and E-selectin (CD62E) on the VEC surface. of intercellular adhesion molecule-1 (ICAM-1, CD54) and E-selectin (CD62E) on the VEC surface.

METHODSA human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-alpha). VECs were pre- A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-alpha). VECs were preincubated with varying concentrations of PrG (0.001-5 mmol/L) or 1 per thousand DMSO (v:v) or 10 mmol/L acetylsalicylic incubated with varying concentrations of PrG (0.001-5 mmol/L) or 1 per thousand DMSO (v:v) or 10 mmol/L acetylsalicylic acid (ASA) for 1 h, and then were stimulated with 10 ng/mL TNF-alpha for 6 h. Rose bengal vital staining method acid (ASA) for 1 h, and then were stimulated with 10 ng/mL TNF-alpha for 6 h. Rose bengal vital staining method was used to measure the adherence rate of PMN to VEC, while flow cytometry was used to determine the was used to measure the adherence rate of PMN to VEC, while flow cytometry was used to determine the expression of CD54 and CD62E on the VEC surface. expression of CD54 and CD62E on the VEC surface.

RESULTSAfter 6 h of incubation with TNF-alpha, the adherence After 6 h of incubation with TNF-alpha, the adherence of PMN to HUVECs as well as the percentage of fluorescence-positive cells and mean fluorescence intensity of PMN to HUVECs as well as the percentage of fluorescence-positive cells and mean fluorescence intensity (MFI) of surface CD54 and CD62E in HUVECs increased significantly ( (MFI) of surface CD54 and CD62E in HUVECs increased significantly (P<0.01). Pre-treatment of HUVECs with <0.01). Pre-treatment of HUVECs with PrG (0.1-5 mmol/L) significantly suppressed the adherence of PMN to VECs induced by TNF-alpha (PrG (0.1-5 mmol/L) significantly suppressed the adherence of PMN to VECs induced by TNF-alpha (P<0.05). PrG <0.05). PrG (1-5 mmol/L) inhibited the VEC surface expression of CD62E and CD54 in a dose-dependent way ( (1-5 mmol/L) inhibited the VEC surface expression of CD62E and CD54 in a dose-dependent way (P<0.05). PrG <0.05). PrG at lower concentrations (0.001-0.1 mmol/L) showed no effect on CD54 expression, while it showed a slightly at lower concentrations (0.001-0.1 mmol/L) showed no effect on CD54 expression, while it showed a slightly increasing trend in CD62E expression (increasing trend in CD62E expression (P>0.05). ASA at 10 mmol/L had no obvious effect on the positive rate of >0.05). ASA at 10 mmol/L had no obvious effect on the positive rate of CD62E and CD54. CD62E and CD54.

CONCLUSIONSHigh concentrations of PrG (0.1-5 mmol/L) exert its inhibitory effect on cellular High concentrations of PrG (0.1-5 mmol/L) exert its inhibitory effect on cellular adherence of PMN to HUVECs, and its mechanism may be related to inhibiting surface expression of CD54 and adherence of PMN to HUVECs, and its mechanism may be related to inhibiting surface expression of CD54 and CD62E in HUVECs. Its action concentration was lower than that of ASA. CD62E in HUVECs. Its action concentration was lower than that of ASA.

Cell Adhesion ; drug effects ; Endothelial Cells ; cytology ; drug effects ; Flow Cytometry ; Fluorescein-5-isothiocyanate ; metabolism ; Fluorescence ; Humans ; Intercellular Adhesion Molecule-1 ; metabolism ; Neutrophils ; cytology ; drug effects ; Propyl Gallate ; chemistry ; pharmacology ; Staining and Labeling ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo investigate the effects of propyl gallate (PrG) on the thrombus formation time and the coagulation/fibrinolysis system in an experimental carotid artery thrombosis model in rats.

METHODSFifty SD rats were randomly divided into 5 groups (10 animals/group): the normal group (normal saline 2 mL/kg), the model group (normal saline, 2 mL/kg), the heparin control group (1,250 IU/kg), the low dose PrG group (30 mg/kg), and the high dose PrG group (60 mg/kg). Thirty minutes after intravenous injection of saline or the corresponding drugs, a carotid artery thrombus was induced by continuous electric stimulation in all rats except for those in the normal group. The duration from the initiation of the electric stimulation to the sudden drop in carotid temperature was recorded as the thrombus formation time. Levels of plasma tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) were determined by ELISA.

RESULTSPrG (30 and 60 mg/kg) can prolong the thrombus formation time, but the effect was obviously weaker than that of heparin (P<0.05, P<0.01). Compared with the model group, PrG (30 and 60 mg/kg) elevated the plasma activity of t-PA (both P<0.05) and showed an increasing tendency in elevating the ratio of t-PA/PAI-1 (P>0.05), while it had no significant effect on the level of PAI-1.

CONCLUSIONPrG has a certain antithrombotic effect and can slightly regulate the imbalance of the t-PA /PAI-1 ratio.

Animals ; Blood Coagulation ; drug effects ; Carotid Artery Thrombosis ; drug therapy ; Female ; Fibrinolysis ; drug effects ; Male ; Plasminogen Activator Inhibitor 1 ; blood ; Propyl Gallate ; pharmacology ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Tissue Plasminogen Activator ; blood

OBJECTIVETo explore the possible target and molecular mechanism of Radix Paeoniae 801 (RP801), an effective ingredient extracted from Radix Paeoniae, the Chinese herbal medicine for activating blood circulation to remove blood stasis, using experimental in vitro method by directly detecting the interaction between RP801 and endothelin-1 (ET-1).

METHODSPiezoelectric quartz crystal biosensor, namely, the quartz crystal microbalance (QCM) was used to detect the specific combining between RP801 and ET-1 by binding avidin to the pre-activated Au surface of electrode of QCM, followed by immobilizing biotinylated ET-1 to it, and adding RP801, then the binding curve was recorded. PBS washing was applied at the end of every steps of combining reaction for dissociate the non-specific absorption.

RESULTSSpecific combining of RP801 and ET-1 was found.

CONCLUSIONET-1 could possibly be one of the acting targets of RP801 in the body, that is, RP801 could combine with ET-1 to impede the binding of ET-1 with its receptor, so as to counteract the action of ET-1, dilate blood vessels and inhibit platelet aggregation.

Biosensing Techniques ; methods ; Drugs, Chinese Herbal ; pharmacology ; Electrochemistry ; Endothelin-1 ; chemistry ; drug effects ; Humans ; Models, Chemical ; Paeonia ; chemistry ; Platelet Aggregation Inhibitors ; pharmacology ; Propyl Gallate ; isolation & purification ; pharmacology ; Protein Binding ; Quartz

AIMTo explore the protective effect of propyl gallate against neuronal injury in the boundary zone of the infarction area in the rat cerebral ischemia-reperfusion model and its possible mechanism.

METHODSTransient focal ischemia induced by middle cerebral artery occlusion in the rats was established by ligation of the left internal carotid artery for 2 h. Rats were treated by propyl gallate with different doses (23.5, 47 and 94 micromol x kg(-1)) for three days before operation. Coronal brain sections were collected after 1 , 2, 4, 6, 12 and 24 h of reperfusion, neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Nissl staining. The expression of activated Caspase-3, total SAPK/JNK, p38MAPK and their phosphorylation (Thr183/Tyr185, Thr180/Tyr182) was investigated by immunohistochemistry and Western blotting with corresponding antibodies.

RESULTSAlthough SAPK/JNK immunoreactivity did not increase at each time point in the boundary zone of the infarction area after reperfusion, p-SAPK/JNK immunoreactivity increased significantly at 1 h and then decreased gradually, and p38MAPK immunoreactivity was enhanced at each time point, peaked at 6 h. Expression of p-p38MAPK peaked at 6 h. Activated Caspase-3 immunoreactivity appeared at 6 h in the boundary zone of the infarction area and peaked at 12 h. TUNEL positive neurons were observed at 12 h and became more abundant at 24 h. The number of Nissl positive neurons decreased gradually and apoptosis ratio of neurons peaked at 24 h. Propyl gallate reduced the immunoreactivity of SAPK/JNK, p-SAPK/JNK, p38MAPK and p-p38MAPK markedly at 1 and 6 h. Propyl gallate with doses of 47 and 94 micromol x kg(-1) were more effective.

CONCLUSIONInhibition on the activation of SAPK/JNK and p38MAPK is the possible protective mechanism of propyl gallate against neuronal injury induced by cerebral ischemia-reperfusion.

Animals ; Apoptosis ; drug effects ; Brain Ischemia ; etiology ; Caspase 3 ; metabolism ; Enzyme Activation ; drug effects ; Infarction, Middle Cerebral Artery ; complications ; MAP Kinase Kinase 4 ; metabolism ; Male ; Neurons ; pathology ; Neuroprotective Agents ; pharmacology ; Propyl Gallate ; pharmacology ; Putamen ; pathology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; enzymology ; etiology ; pathology ; p38 Mitogen-Activated Protein Kinases ; metabolism