Education, Science, Technology, Innovation and Life
Open Access
Sign In

Study on the Molecular Mechanism of Traditional Medical Postural Intervention Therapy in the Treatment of Sepsis ARDS

Download as PDF

DOI: 10.23977/medsc.2022.030416 | Downloads: 9 | Views: 570

Author(s)

Wenhan Xia 1, Qiong Ouyang 2, Tingyu Li 3, Chunli Yang 1, Zhiru Zhong 1, Fang Liu 1, Zhiping Chen 4

Affiliation(s)

1 Department of Critical Medicine, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China
2 Ji'an First People's Hospital, Ji'an, China
3 School of Humanities, Jiangxi University of Chinese Medicine, Nanchang, China
4 Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China

Corresponding Author

Zhiping Chen

ABSTRACT

Acute respiratory distress syndrome caused by sepsis has become a clinical syndrome that seriously threatens the life of severe patients. Taking cecal ligation and perforation leading to Escherichia coli peritonitis and septic ARDS rats as the model, this paper discusses the molecular pathogenesis of ARDS and the effect of prone position on RIPK3 signal pathway, in order to put forward a possible new way for the prevention and treatment of septic ARDS. A rat model of ARDS caused by sepsis was established. The supine position was maintained for 3 hours in the sham operation group; The operation group was given placebo or RIPK3 inhibitor 30 minutes before modeling; The supine position was maintained for 3h after modeling in the operation + supine position group, and the prone position was maintained for 3h after modeling in the operation + prone position group. Three hours after modeling, blood was collected from inferior vena cava, and the supernatant was taken for preservation after low-temperature centrifugation. After taking blood, take lung tissue for standby. The wet dry ratio of the left lung was measured, and the pathological conditions were observed by HE staining after partial right lung fixation. The expression of RIPK3 protein was detected by immunohistochemistry. The expression of RIPK3 protein was detected by WB in some right lung tissues. The expression level of RIPK3 protein in ARDS model rats is high. RIPK3 inhibitor can effectively reduce the expression level of RIPK3 protein in ARDS model rats, and the therapeutic effect of prone position is better than that of supine position.

KEYWORDS

acute respiratory distress syndrome, sepsis, prone position, supine position, ripk3

CITE THIS PAPER

Wenhan Xia, Qiong Ouyang, Tingyu Li, Chunli Yang, Zhiru Zhong, Fang Liu, Zhiping Chen, Study on the Molecular Mechanism of Traditional Medical Postural Intervention Therapy in the Treatment of Sepsis ARDS. MEDS Clinical Medicine (2022) Vol. 3: 100-109. DOI: http://dx.doi.org/10.23977/medsc.2022.030416.

REFERENCES

[1] Wang L, Wang T, Li H, Liu Q, Zhang Z, Xie W, Feng Y, Socorburam T, Wu G, Xia Z et al. (2016) Receptor interacting protein 3-mediated Necroptosis promotes lipopolysaccharideinduced inflammation and acute respiratory distress syndrome in mice. PLoS One, 11:e0155723.
[2] Shashaty M G S, Reilly J P, Faust H E. et al. (2019) Plasma receptor interacting protein kinase-3 levels are associated with acute respiratory distress syndrome in sepsis and trauma: a cohort study. Crit Care 23, 235.
[3] Long P, Dun-Chen Y, Yu-Zhong Y, et al. (2016) Activation of necroptosis in a rat model of acute respiratory distress syndrome induced by oleic acid. Sheng li xue bao: Acta physiologica Sinica, 68, 5, 661-668.
[4] Linkermann A, Brasen JH, De Zen F, Weinlich R, Schwendener RA, Green DR, et al. (2012) Dichotomy between RIP1- and RIP3-mediated necroptosis in tumor necrosis factor- alpha-induced shock. Mol Med, 18:577–86.
[5] Linkermann A, Green DR. (2014) Necroptosis. N Engl J Med, 370, 5, 455–65.
[6] Wang L, Wang T, Li H, Liu Q, Zhang Z, Xie W, et al. (2016) Receptor interacting protein 3-mediated necroptosis promotes lipopolysaccharide-induced inflammation and acute respiratory distress syndrome in mice. PLoS One, 11, 5, e0155723.
[7] Qing DY, Conegliano D, Shashaty MG, Seo J, Reilly JP, Worthen GS, et al. (2014) Red blood cells induce necroptosis of lung endothelial cells and increase susceptibility to lung inflammation. Am J Respir Crit Care Med, 190, 11, 1243–54.
[8] Vandenabeele P, Galluzzi L, Vanden Berghe T, Kroemer G. (2010) Molecular mechanisms of necroptosis: an ordered cellular explosion. Nat Rev Mol Cell Biol, 11, 10, 700–14.
[9] Linkermann A, Chen G, Dong G, Kunzendorf U, Krautwald S, Dong Z. (2014) Regulated cell death in AKI. J Am Soc Nephrol, 25, 12, 2689–701.
[10] Moreno-Gonzalez G, Vandenabeele P, Krysko DV. (2016) Necroptosis: a novel cell death modality and its potential relevance for critical care medicine. Am J Respir Crit Care Med, 194, 4, 415– 28.
[11] Kaczmarek A, Vandenabeele P, Krysko DV. (2013) Necroptosis: the release of damage-associated molecular patterns and its physiological relevance. Immunity, 38, 2, 209–23.
[12] Pasparakis M, Vandenabeele P. (2015) Necroptosis and its role in inflammation. Nature, 517, 7534, 311–20.

Downloads: 4395
Visits: 193308

Sponsors, Associates, and Links


All published work is licensed under a Creative Commons Attribution 4.0 International License.

Copyright © 2016 - 2031 Clausius Scientific Press Inc. All Rights Reserved.