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IL-10 ameliorates PM2.5-induced lung injury by activating the AMPK/SIRT1/PGC-1α pathway
Ning Zhang1, Ping Li2, Hua Lin2
1Department of Respiratory Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, 050051, Hebei, China; Department of Gerontology, Hebei General Hospital, Shijiazhuang, 050051, Hebei, China.
Abstract:
Exposure to fine particulate matter with a diameter ≤2.5 μm (PM2.5) can cause a number of respiratory diseases. However, there is currently no safe treatment for PM2.5-induced lung damage. This study investigated the protective effect of IL-10 against lung injury and the possible involvement of AMPK/SIRT1/PGC-1α signaling. The mean diameter, particle size distribution, and zeta potential of PM2.5 samples were assessed using a Zetasizer Nano ZS90 analyzer. Thereafter, Wistar rats were exposed to PM2.5 (1.8, 5.4, or 16.2 mg/kg) alone or high-dose PM2.5 with recombinant rat IL-10 (rrIL-10; 5 μg/rat). Treatment with rrIL-10 ameliorated PM2.5-induced acute lung injury, reduced mitochondrial damage, and inhibited inflammation, oxidative stress, and apoptosis in the PM2.5-treated rats. Moreover, the mRNA and protein expression of AMPK, SIRT1, and PGC-1α were upregulated by rrIL-10 treatment. In conclusion, rrIL-10 protected lung tissues against PM2.5-induced inflammation by reducing oxidative stress and apoptosis via activating AMPK/SIRT1/PGC-1α signaling.
Insights
Interleukin-10 (IL-10) treatment protects against lung injury caused by fine particulate matter (PM2.5). This protective effect involves reducing inflammation, oxidative stress, and apoptosis via the AMPK/SIRT1/PGC-1α pathway.
Area of Science:
- Environmental Health
- Toxicology
- Molecular Biology
Background:
- Fine particulate matter (PM2.5) exposure is a significant risk factor for respiratory diseases.
- Current treatments for PM2.5-induced lung damage are limited.
- Understanding the molecular mechanisms underlying PM2.5 toxicity is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the protective effects of Interleukin-10 (IL-10) against PM2.5-induced lung injury.
- To explore the potential involvement of the AMPK/SIRT1/PGC-1α signaling pathway in IL-10's protective mechanism.
Main Methods:
- Characterization of PM2.5 particle properties (size, distribution, zeta potential).
- Induction of acute lung injury in Wistar rats via PM2.5 exposure.
- Administration of recombinant rat IL-10 (rrIL-10) to PM2.5-exposed rats.
- Assessment of lung injury markers, inflammation, oxidative stress, apoptosis, and AMPK/SIRT1/PGC-1α signaling pathway activation.
Main Results:
- rrIL-10 treatment significantly ameliorated PM2.5-induced acute lung injury.
- IL-10 administration reduced inflammation, oxidative stress, and apoptosis in lung tissues.
- The expression of AMPK, SIRT1, and PGC-1α (mRNA and protein) was upregulated by rrIL-10.
Conclusions:
- Recombinant rat IL-10 (rrIL-10) demonstrates significant protective effects against PM2.5-induced lung inflammation.
- IL-10 mitigates PM2.5 toxicity by reducing oxidative stress and apoptosis.
- The protective mechanism of IL-10 is mediated through the activation of the AMPK/SIRT1/PGC-1α signaling pathway.
