2022  1,200
2021  1,540
2020  1,374
2019  1,023
2018  0,932
2017  0,977
2016  0,799
2015  0,662
2014  0,740
2013  0,739
2012  0,637
2011  0,658
2010  0,654
2009  0,570
2008  0,849
2007  0,805
2006  0,330
2005  0,435
2004  0,623
2003  0,567
2002  0,641
2001  0,490
2000  0,477
1999  0,762
1998  0,785
1997  0,507
1996  0,518
1995  0,502
Vol 58(2024) N 2 p. 279-288; DOI 10.1134/S002689332402002X Full Text

L. An1,2,3, M.-Y. Liu2, Y. Zhong1,2*, H. Gao1,5, Y.-Q. Liu4, Y. Liu1,2, S.-Z. Wang2, T.-Y. Yang2, H. Wu2, J.-L. Yu2

Sestrin2 Alleviates Sepsis-Induced Renal Injury by Inhibiting NLRP3 Activation and Reactive Oxygen Species Production

1Department of Anaesthesiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, 550004 P.R. China
2School of Anesthesiology, Guizhou Medical University, Guiyang, Guizhou, 550025 P.R. China
3Translational Medicine Research Center of Guizhou Medical University, Guiyang, Guizhou, 550025 P.R. China
4Department of Anaesthesiology, Guiyang Fourth People's Hospital, Guiyang, Guizhou, 550007P.R. China
5Guizhou Hospital of The 1st Affiliated Hospital, Sun Yat-sen University, Guiyang, Guizhou, 510080 P.R. China

Received - 2023-05-09; Revised - 2023-09-22; Accepted - 2023-09-23

Sepsis is a life-threatening disorder that develops in response to an infection. Kidneys are one of the most common organs affected by sepsis. This study explored the influence of Sestrin2 regulating NLRP3 inflammasome activation on sepsis-induced renal injury. A sepsis mouse model was established by intraperitoneal injection of LPS. Adenoviral transduction was used to upregulate Sestrin2 expression. H&E staining, TUNEL staining, DHE staining, ELISA, RT-PCR, and western blotting were applied to the detections of pathological changes, ROS, oxidative stress markers, Sestrin2 expression, apoptosis-related proteins, and NLRP3 inflammasome-related factors in renal tissues. A HK-2 cell model of LPS-induced injury was constructed, and the release of IL-6 and TNF-α and expression of NLRP3 were detected using ELISA and immunofluorescence, respectively. Sestrin2 overexpression suppressed inflammation and reduced renal injury and apoptosis in LPS-treated mice. Moreover, overexpressed Sestrin2 resulted in inhibited levels of ROS, NLRP3, caspase-1, and IL-1β in renal tissues, as well as reduced TNF-α and IL-6 secretion and NLRP3 expression in LPS-stimulated HK-2 cells. Collectively, Sestrin2 can inhibit inflammation and reduce sepsis-induced renal injury, which may be associated with NLRP3 inflammasome inactivation and oxidative stress reduction.

Sestrin2, sepsis-induced renal injury, NLRP3 inflammasome, reactive oxygen species