Oxidative stress promotes ventilator-induced lung injury through activating NLRP3 inflammasome and TRPM2 channel.

An X, Sun X, Yang X, Liu D, Hou Y, Chen H, Wu J

Artificial cells, nanomedicine, and biotechnology1 Dec 2019Cited by 20 (Europe PMC)

PMID31411068DOI10.1080/21691401.2019.1652631PepBankPUB-31411068

Summary

Ventilator has been widely used for life support, but ventilator-induced lung injury (VILI) is still a major problem. Oxidative stress has been considered as a key contributor for VILI, but the specific mechanism remains unclear. The expression of NLRP3 inflammasome in cells and inflammatory factors in the supernatant were measured. Mitochondrial ROS and TRPM2 channel currents were investigated using flow cytometry and Patch-clamp technique, respectively. TRPM2^-/- and NLRP3^-/- mice were used for animal experiments. Lung tissues were stained by HE and the wet-dry ratio, bronchoalveolar lavage fluid (BALF) protein, MPO (marrow peroxidase), NLRP3 inflammasome were also investigated. Knockdown of NLRP3 or Caspase-1 or treatments with SS-31 or YVAD inhibited the expression of the NLRP3 inflammasome, and reduced IL-1β and IL-18 levels in cell supernatant. These treatments suppressed the production of ROS and lowered the TRPM2 channel currents, but Rotenone exerted an opposite effect. High-tidal volume ventilation significantly increased the levels of IL-1β, IL-18, NLRP3 inflammasome, wet-dry ratio of lung, MPO and BALF protein. However, these parameters were down-regulated in TRPM2^-/- and NLRP3^-/- mice. These parameters were suppressed in TRPM2^-/- and NLRP3^-/- mice indicate that oxidative stress might promote VILI through activating NLRP3 inflammasome and TRPM2 channel.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone5

In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Elamipretide (SS-31).

01LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism
In cells, knockdown of NLRP3 or caspase-1 and treatment with SS‑31 or YVAD inhibited expression of the NLRP3 inflammasome.
In plain wordsIn lab cells, blocking NLRP3 or caspase-1, or treating with SS‑31 or YVAD, lowered NLRP3 inflammasome levels.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseNLRP3 inflammasome expression
Study
n: not reported in source
Cells (type not stated)
Outcome group
Inflammation markers · Respiratory
Source sentences
Summary
Knockdown of NLRP3 or Caspase-1 or treatments with SS-31 or YVAD inhibited the expression of the NLRP3 inflammasome, and reduced IL-1β and IL-18 levels in cell supernatant.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Show in the study text Report a problemFND-3141106801
02LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism
In cells, knockdown of NLRP3 or caspase-1 and treatment with SS‑31 or YVAD reduced IL-1beta levels.
In plain wordsIn lab cells, blocking NLRP3 or caspase-1, or treating with SS‑31 or YVAD, lowered IL-1beta.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseIL-1beta in cell supernatant
Study
n: not reported in source
Cells (type not stated)
Outcome group
Inflammation markers · Respiratory
Source sentences
Summary
Knockdown of NLRP3 or Caspase-1 or treatments with SS-31 or YVAD inhibited the expression of the NLRP3 inflammasome, and reduced IL-1β and IL-18 levels in cell supernatant.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Show in the study text Report a problemFND-3141106802
03LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism
In cells, knockdown of NLRP3 or caspase-1 and treatment with SS‑31 or YVAD reduced IL-18 levels.
In plain wordsIn lab cells, blocking NLRP3 or caspase-1, or treating with SS‑31 or YVAD, lowered IL-18.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseIL-18 in cell supernatant
Study
n: not reported in source
Cells (type not stated)
Outcome group
Inflammation markers · Respiratory
Source sentences
Summary
Knockdown of NLRP3 or Caspase-1 or treatments with SS-31 or YVAD inhibited the expression of the NLRP3 inflammasome, and reduced IL-1β and IL-18 levels in cell supernatant.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Show in the study text Report a problemFND-3141106803
04LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism
In cells, these treatments (knockdown of NLRP3 or caspase-1, SS‑31, YVAD) suppressed the production of ROS.
In plain wordsIn lab cells, these treatments, including SS‑31, lowered reactive oxygen species.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseROS production
Study
n: not reported in source
Cells (type not stated)
Outcome group
Mitochondrial function · Respiratory
Source sentences
Summary
These treatments suppressed the production of ROS and lowered the TRPM2 channel currents, but Rotenone exerted an opposite effect.
1 context sentence(design, population, supporting numbers)
Summary · context
Knockdown of NLRP3 or Caspase-1 or treatments with SS-31 or YVAD inhibited the expression of the NLRP3 inflammasome, and reduced IL-1β and IL-18 levels in cell supernatant.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Show in the study text Report a problemFND-3141106804
05LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism
In cells, these treatments (knockdown of NLRP3 or caspase-1, SS‑31, YVAD) lowered TRPM2 channel currents.
In plain wordsIn lab cells, these treatments, including SS‑31, lowered TRPM2 channel currents.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseTRPM2 channel currents
Study
n: not reported in source
Cells (type not stated)
Outcome group
Receptor activity and mechanism · Respiratory
Source sentences
Summary
These treatments suppressed the production of ROS and lowered the TRPM2 channel currents, but Rotenone exerted an opposite effect.
1 context sentence(design, population, supporting numbers)
Summary · context
Knockdown of NLRP3 or Caspase-1 or treatments with SS-31 or YVAD inhibited the expression of the NLRP3 inflammasome, and reduced IL-1β and IL-18 levels in cell supernatant.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Show in the study text Report a problemFND-3141106805

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
10 Oct 2026, 08:19 UTC
Study results updated
Version 1
9 Oct 2026, 02:47 UTC
First added · source update from Europe PMC

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