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Safflor yellow B suppresses angiotensin II-mediated human umbilical vein cell injury via regulation of Bcl-2/p22(phox) expression.
Toxicol Appl Pharmacol. 2013 Nov 15; 273(1):59-67.TA

Abstract

Intracellular reactive oxygen species (ROS) are derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Angiotensin II (Ang II) can cause endothelial dysfunction by promoting intracellular ROS generation. Safflor yellow B (SYB) effectively inhibits ROS generation by upregulating Bcl-2 expression. In this study, we examined the effects of SYB on Ang II-induced injury to human umbilical vein endothelial cells (HUVECs), and elucidated the roles of NADPH oxidase and Bcl-2. We treated cultured HUVECs with Ang II, SYB, and Bcl-2 siRNA, and determined NADPH oxidase activity and ROS levels. Furthermore, cellular and mitochondrial physiological states were evaluated, and the expression levels of target proteins were analyzed. Ang II significantly enhanced intracellular ROS levels, caused mitochondrial membrane dysfunction, and decreased cell viability, leading to apoptosis. This was associated with increased expression of AT1R and p22(phox), increased NADPH oxidase activity, and an increased ratio of Bax/Bcl-2, leading to decreases in antioxidant enzyme activities, which were further strengthened after blocking Bcl-2. Compared to Ang II treatment alone, co-treatment with SYB significantly reversed HUVEC injury. Taken together, these results demonstrate that SYB could significantly protect endothelial cells from Ang II-induced cell damage, and that it does so by upregulating Bcl-2 expression and inhibiting ROS generation.

Authors+Show Affiliations

School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, Shandong 264003, PR China; Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Key Laboratory of Environment and Genes Related to Disease, Ministry of Education, Xi'an, Shaanxi 710061, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23994555

Citation

Wang, Chaoyun, et al. "Safflor Yellow B Suppresses Angiotensin II-mediated Human Umbilical Vein Cell Injury Via Regulation of Bcl-2/p22(phox) Expression." Toxicology and Applied Pharmacology, vol. 273, no. 1, 2013, pp. 59-67.
Wang C, He Y, Yang M, et al. Safflor yellow B suppresses angiotensin II-mediated human umbilical vein cell injury via regulation of Bcl-2/p22(phox) expression. Toxicol Appl Pharmacol. 2013;273(1):59-67.
Wang, C., He, Y., Yang, M., Sun, H., Zhang, S., & Wang, C. (2013). Safflor yellow B suppresses angiotensin II-mediated human umbilical vein cell injury via regulation of Bcl-2/p22(phox) expression. Toxicology and Applied Pharmacology, 273(1), 59-67. https://doi.org/10.1016/j.taap.2013.08.018
Wang C, et al. Safflor Yellow B Suppresses Angiotensin II-mediated Human Umbilical Vein Cell Injury Via Regulation of Bcl-2/p22(phox) Expression. Toxicol Appl Pharmacol. 2013 Nov 15;273(1):59-67. PubMed PMID: 23994555.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Safflor yellow B suppresses angiotensin II-mediated human umbilical vein cell injury via regulation of Bcl-2/p22(phox) expression. AU - Wang,Chaoyun, AU - He,Yanhao, AU - Yang,Ming, AU - Sun,Hongliu, AU - Zhang,Shuping, AU - Wang,Chunhua, Y1 - 2013/08/28/ PY - 2013/05/03/received PY - 2013/08/05/revised PY - 2013/08/13/accepted PY - 2013/9/3/entrez PY - 2013/9/3/pubmed PY - 2014/1/7/medline KW - Angiotensin II KW - Bcl-2 KW - Mitochondrial membrane potential KW - NADPH oxidase KW - Safflor yellow B KW - p22(phox) SP - 59 EP - 67 JF - Toxicology and applied pharmacology JO - Toxicol Appl Pharmacol VL - 273 IS - 1 N2 - Intracellular reactive oxygen species (ROS) are derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Angiotensin II (Ang II) can cause endothelial dysfunction by promoting intracellular ROS generation. Safflor yellow B (SYB) effectively inhibits ROS generation by upregulating Bcl-2 expression. In this study, we examined the effects of SYB on Ang II-induced injury to human umbilical vein endothelial cells (HUVECs), and elucidated the roles of NADPH oxidase and Bcl-2. We treated cultured HUVECs with Ang II, SYB, and Bcl-2 siRNA, and determined NADPH oxidase activity and ROS levels. Furthermore, cellular and mitochondrial physiological states were evaluated, and the expression levels of target proteins were analyzed. Ang II significantly enhanced intracellular ROS levels, caused mitochondrial membrane dysfunction, and decreased cell viability, leading to apoptosis. This was associated with increased expression of AT1R and p22(phox), increased NADPH oxidase activity, and an increased ratio of Bax/Bcl-2, leading to decreases in antioxidant enzyme activities, which were further strengthened after blocking Bcl-2. Compared to Ang II treatment alone, co-treatment with SYB significantly reversed HUVEC injury. Taken together, these results demonstrate that SYB could significantly protect endothelial cells from Ang II-induced cell damage, and that it does so by upregulating Bcl-2 expression and inhibiting ROS generation. SN - 1096-0333 UR - https://www.unboundmedicine.com/medline/citation/23994555/Safflor_yellow_B_suppresses_angiotensin_II_mediated_human_umbilical_vein_cell_injury_via_regulation_of_Bcl_2/p22_phox__expression_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0041-008X(13)00368-2 DB - PRIME DP - Unbound Medicine ER -