Li-Na Zhou1, Wei-Feng Yao2, Jia Liu2, Jing Shang2, Ming-Qiu Shan2, Li Zhang2, An-Wei Ding2. 1. Key Laboratory of Prescription High-Tech Research of Jiangsu Province, Nanjing University of Chinese Medicine, Nanjing 210023, China. zln5566.0k@163.com 2. Key Laboratory of Prescription High-Tech Research of Jiangsu Province, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Abstract
OBJECTIVE: To study the protective effect of different solvent extracts from Platycladi Cacumen Carbonisatum (PCC) on LPS-induced human umbilical vein endothelial cell damage, and discuss the effective extracts from PCC for protecting vascular endothelial cells and their possible active substances. METHOD: HUVECs were cultured in vitro; And LPS was adopted to establish the human umbilical vein endothelial cell damage model. MTT colorimetric method was used to determine cell activity; Xanthine oxidase method was adopted to detect the activity of superoxide dismutases (SOD) in the cell culture fluid; The TBA method was adopted to determine the content of malondialdehyde (MDA); The nitrate reductase method was used to detect the content of nitric oxide (NO); And UPLC/Q-TOF-MS was used to analyze the difference in flavonoids components among different solvent extracts from PCC. RESULT: Compared with the model group, N-butanol extract (100 mg x L(-1)) and ethylacetate extract (100, 50 mg x L(-1)) could significantly enhance the cell activity (P < 0.05), significantly reduce MDA and NO content, and increase SOD activity (P < 0.05). Among the four solvent extracts, the content of total flavonids were the highest in ethyl acetate extract, the lowest in water extract and equivalent in N-butanol and petroleum benzene extract. In terms of the contents of quercitrin and myricitrin, N-butanol extract were second only to ethyl acetate extract. CONCLUSION: Ethylacetate extract from PCC has a notable antagonistic effect in the damage induced by LPS to HUVECs, and thus is the most effective extract from PCC in protecting vascular endothelial cells. Quercitrin, myricitrin or multiple flavonoids that it contains may be their active substances for protecting vascular endothelial cells. Its mechanism may be related to the decrease in the production of NO and the inhibition of lipid peroxidation in cells.
OBJECTIVE: To study the protective effect of different solvent extracts from Platycladi Cacumen Carbonisatum (PCC) on LPS-induced human umbilical vein endothelial cell damage, and discuss the effective extracts from PCC for protecting vascular endothelial cells and their possible active substances. METHOD: HUVECs were cultured in vitro; And LPS was adopted to establish the human umbilical vein endothelial cell damage model. MTT colorimetric method was used to determine cell activity; Xanthine oxidase method was adopted to detect the activity of superoxide dismutases (SOD) in the cell culture fluid; The TBA method was adopted to determine the content of malondialdehyde (MDA); The nitrate reductase method was used to detect the content of nitric oxide (NO); And UPLC/Q-TOF-MS was used to analyze the difference in flavonoids components among different solvent extracts from PCC. RESULT: Compared with the model group, N-butanol extract (100 mg x L(-1)) and ethylacetate extract (100, 50 mg x L(-1)) could significantly enhance the cell activity (P < 0.05), significantly reduce MDA and NO content, and increase SOD activity (P < 0.05). Among the four solvent extracts, the content of total flavonids were the highest in ethyl acetate extract, the lowest in water extract and equivalent in N-butanol and petroleum benzene extract. In terms of the contents of quercitrin and myricitrin, N-butanol extract were second only to ethyl acetate extract. CONCLUSION:Ethylacetate extract from PCC has a notable antagonistic effect in the damage induced by LPS to HUVECs, and thus is the most effective extract from PCC in protecting vascular endothelial cells. Quercitrin, myricitrin or multiple flavonoids that it contains may be their active substances for protecting vascular endothelial cells. Its mechanism may be related to the decrease in the production of NO and the inhibition of lipid peroxidation in cells.