Aim:To investigate the effect of 3,5-dicaffeoylquinic acid(3,5-diCQA)onlipopolysaccharide(LPS)-induced injury in human dermal microvascular endothe-lial cells(HMEC-I).Methods:The anti-oxidant effect was detected using themalondialdehyde(MDA)assay in a rat liver microsome model of lipid peroxidation.Cell viability was analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide assay.Cell lipid peroxide injury was measured bylactate dehydrogenase(LDH)release.Apoptotic cells were detected by flowcytometry,and confirmed by DNA fragmentation analysis.Caspase-3 activitywas measured using a specific assay kit.The level of intracellular reactive oxygenspecies(ROS)was determined by flow cytometry with a 2,7-dichlorodihydro-fluorescein diacetate fluorescence probe.Results:The exposure of microsomesto ascorbate-Fe~(2+)resulted in lipoperoxidation according to an increase in the levelof MDA.MDA formation decreased in a dose-dependent manner on treatmentwith 5,10,or 50μmol/L 3,5-diCQA.Treatment with LPS for 16 h resulted in a 60%decrease in cell viability and an increase in LDH release from 47.6% to 61.5%.DNA laddering was observed by agarose gel electrophoresis.The level ofapoptotic cells peaked at 27% after treatment with LPS for 12 h.Following treat-ment with LPS for 12 h,intracellular ROS and caspase-3 activity increased.Pre-treatment with 3,5-diCQA at 5,10,or 50μmol/L for 1 h attenuated LPS-mediatedendothelial cell injury.The anti-apoptotic action of 3,5-diCQA was partiallydependent on its capacity for anti-oxidation and the suppression of caspase-3activity.Conclusion:3,5-diCQA displays anti-oxidative and anti-apoptotic activ-ity in HMEC-1 due to scavenging of intracellular ROS induced by LPS,and thesuppression of caspase-3 activity. Aim: To investigate the effect of 3,5-dicaffeoylquinic acid (3,5-diCQA) onlipopolysaccharide (LPS) -induced injury in human dermal microvascular endothe-lial cells (HMEC-I). Methods: The anti-oxidant effect was detected using themalondialdehyde (MDA) assay in a rat liver microsome model of lipid peroxidation. Cell viability was analyzed using the 3- (4,5-dimethylthiazol-2-yl) -2,5diphenyltetrazolium bromide assay. Cell lipid peroxide injury was measured by lactate dehydrogenase (LDH) release. Apoptotic cells were detected by flowcytometry, and confirmed by DNA fragmentation analysis. Caspase-3 activity was measured using a specific assay kit. The level of intracellular reactive oxygenspecies (ROS) was determined by flow cytometry with a 2,7- dichlorodihydro-fluorescein diacetate fluorescence probe. Results: The exposure of microsomesto ascorbate-Fe ~ (2+) resulted in lipoperoxidation according to an increase in the level of MDA. MDDA formation decreased in a dose-dependent manner on treatment with 5, 10, or 50 μmol / L 3,5 -diCQA.Treatment with LPS resulted in a 60% decrease in cell viability and an increase in LDH release from 47.6% to 61.5%. DNA laddering was observed by agarose gel electrophoresis. The level ofapoptotic cells peaked at 27% after treatment with LPS for 12 h.Following treat-ment with LPS for 12 h, intracellular ROS and caspase-3 activity increased. Pre-treatment with 3,5-diCQA at 5,10, or 50 μmol / L for 1 h attenuated LPS-mediatedendothelial cell injury. The anti-apoptotic action of 3,5-diCQA was partially dependent on its capacity for anti-oxidation and the suppression of caspase-3 activity. Conflux: 3,5-diCQA displays anti-oxidative and anti-apoptotic activ- ity in HMEC-1 due to scavenging of intracellular ROS induced by LPS, and the depressive of caspase-3 activity.