Ginsenoside Rb1 ameliorates neutrophil extracellular traps-induced vascular endothelial damage by suppressing apoptosis
DOI:
https://doi.org/10.3329/bjp.v19i3.76490Keywords:
Apoptosis, Ginsenoside Rb1, Immunofluorescence detection, Neutrophil extracellular traps, Vascular endothelial injuryAbstract
The study aims to investigate the effect of ginsenoside Rb1 on improving neutrophil extracellular traps-induced vascular endothelial damage. The CCK8 assay was used to evaluate the impact of ginsenoside Rb1 on cell activity. Flow cytometry was used to assess cell apoptosis. E-cadherin was used to determine the damage to endothelial cells, and caspase 3 was used to detect apoptosis-related proteins. Ginsenoside Rb1 (100 μmol/L) could significantly increase the cell viability (p<0.05). At this concentration, the damage caused by neutrophil extracellular traps to human umbilical vein endothelial cells could be reversed (p<0.05). Ginsenoside Rb1 (100 μmol/L) could significantly inhibit the apoptosis and the expression of caspase3 protein caused by neutrophil extracellular traps (p<0.05). Ginsenoside Rb1 can reduce vascular endothelial injury induced by neutrophil extracellular traps, ginsenoside Rb1 protects vascular endothelium by inhibiting cell apoptosis.
Downloads
28
19
References
Blanco LP, Wang X, Carlucci PM, Torres-Ruiz JJ, Romo-Tena J, Sun HW, Hafner M, Kaplan MJ. RNA externalized by neutrophil extracellular traps promotes inflammatory path-ways in endothelial cells. Arthritis Rheumatol. 2021; 73: 2282-92.
Carmona-Rivera C, Zhao W, Yalavarthi S, Kaplan MJ. Neutrophil extracellular traps induce endothelial dysfunction in systemic lupus erythematosus through the activation of matrix metalloproteinase-2. Ann Rheum Dis. 2015; 74: 1417-24.
Chen Z, Tang H, Gan S, Yang C, Li S, Li J, Yao L. Ferroptosis mediates airway epithelial E-cadherin dysfunction in LPS-induced acute lung injury. Pulm Pharmacol Ther. 2024; 84: 102284.
Guo ZF, Tongmuang N, Li C, Zhang C, Hu L, Capreri D, Zuo MX, Summer R, Sun J. Inhibiting endothelial cell Mst1 attenuates acute lung injury in mice. JCI Insight. 2024; 9: e178208.
Hoste E, Maueroder C, van Hove L, Catrysse L, Vikkula HK, Sze M, Maes B, Karjosukarso D, Martens L, Goncalves A, Parthoens E, Roelandt R, Declercq W, Fuentes I, Palisson F, Gonzalez S, Salas-Alanis JC, Boon L, Huebener P, Mulder KW, Ravichandran K, Saeys Y, Schwabe RF, van Loo G. Epithelial HMGB1 delays skin wound healing and drives tumor initiation by priming neutrophils for NET formation. Cell Rep. 2019; 29: 2689-701.
Ke SY, Yu SJ, Liu DH, Shi GY, Wang M, Zhou B, Wu L, Song ZM, Zhu JM, Wu CD, Qian XX. Ginsenoside Rb1 protects human umbilical vein endothelial cells against high glucose-induced mitochondria-related apoptosis through activating SIRT3 signaling pathway. Chin J Integr Med. 2021; 27: 336-44.
Leon M, Moya C, Rivera-Concha R, Pezo F, Uribe P, Schulz M, Sánchez R, Taubert A, Hermosilla C, Zambrano F. Extrusion of neutrophil extracellular traps (NETs) negatively impacts canine sperm functions: Implications in reproductive failure. Int J Mol Sci. 2024; 25: 6216.
Qin GW, Lu P, Peng L, Jiang W. Ginsenoside Rb1 inhibits cardiomyocyte autophagy via PI3K/Akt/mTOR signaling pathway and reduces myocardial ischemia/reperfusion injury. Am J Chin Med. 2021; 49: 1913-27.
Wang H, Kim SJ, Lei Y, Wang S, Wang H, Huang H, Zhang H, Tsung A. Neutrophil extracellular traps in homeostasis and disease. Signal Transduct Target Ther. 2024; 9: 235.
Cai H, Han XJ, Luo ZR, Wang QL, Lu PP, Mou FF, Zhao ZN, Hu D, Guo HD. Pretreatment with notoginsenoside R1 enhances the efficacy of neonatal rat mesenchymal stem cell transplantation in model of myocardial infarction through regulating PI3K/Akt/FoxO1 signaling pathways. Stem Cell Res Ther. 2024; 15: 419.
Xie J, Zhu CL, Wan XJ, Zhao ZZ, Meng Y, Li P, Guo Y, Liu Q, Bian JJ, Deng XM, Wang JF. GSDMD-mediated NETosis promotes the development of acute respiratory distress syndrome. Eur J Immunol. 2023; 53: e2250011.
Yang X, Ma Y, Chen X, Zhu J, Xue W, Ning K. Mechanisms of neutrophil extracellular trap in chronic inflammation of endothelium in atherosclerosis. Life Sci. 2023; 328: 121867.
Yu S, Liu J, Yan N. Endothelial dysfunction induced by extra-cellular neutrophil traps plays important role in the occurrence and treatment of extracellular neutrophil traps-related disease. Int J Mol Sci. 2022; 23: 5626.
Zhang Y, Wang Y, Ma Z, Liang Q, Tang X, Tan H, Xiao C, Gao Y. Ginsenoside Rb1 inhibits doxorubicin-triggered H9C2 cell apoptosis via aryl hydrocarbon receptor. Biomol Ther (Seoul). 2017; 25: 202-12.
Zheng Z, Wang M, Cheng C, Liu D, Wu L, Zhu J, Qian X. Ginsenoside Rb1 reduces H2O2‑induced HUVEC dysfunction by stimulating the sirtuin‑1/AMP‑activated protein kinase pathway. Mol Med Rep. 2020; 22: 247-56.
Zhou P, Lu S, Luo Y, Wang S, Yang K, Zhai Y, Sun G, Sun X. Attenuation of TNF-α-induced inflammatory injury in endothelial cells by ginsenoside Rb1 via inhibiting NF-κB, JNK and p38 signaling pathways. Front Pharmacol. 2017; 8: 464.
Zhou X, Jin J, Lv T, Song Y. A narrative review: The role of NETs in acute respiratory distress syndrome/acute lung injury. Int J Mol Sci. 2024; 25: 1464.
Zhu S, Yu Y, Hong Q, Li C, Zhang H, Guo K. Neutrophil extracellular traps upregulate p21 and suppress cell cycle progression to impair endothelial regeneration after inflammatory lung injury. J Clin Med. 2024; 13: 1204.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2024 Biao Zhang, Junkai Zhao, Jiamin Yin, Jiaping Chen, Lingqi Xu
This work is licensed under a Creative Commons Attribution 4.0 International License.
Authors who publish with this journal agree to the following terms:
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).