Key result
IL-35 pretreatment preserves cardiac function and blunts myocardial inflammation in LPS-induced heart injury.
Why the study?
Targeting inflammation is promising for treating LPS-induced sepsis and heart injury, but the role of interleukin-35 remained obscure.
Does pretreatment with a plasmid encoding IL-35 prevent lipopolysaccharide-induced heart injury in mice?
Population
Mice and mouse myocardial fibroblasts
Comparison
Plasmid encoding IL-35 pretreatment followed by LPS vs LPS alone
Design
Preclinical animal and in vitro study
Follow-up
12 h
Authors
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IL-35 may protect against LPS-induced cardiac injury in mice; hypothesis-generating and should not yet inform clinical practice.
Does pretreatment with a plasmid encoding IL-35 prevent lipopolysaccharide-induced heart injury in mice?
p-value: p=<0.05
IL-35 pretreatment attenuates cardiac inflammation, apoptosis, and fibrosis in LPS-induced sepsis models, suggesting it as a potential therapeutic target for sepsis-related cardiac injury.
Fu et al. (2020) studied Lipopolysaccharide (LPS)-induced heart injury (n=40). Interleukin-35 (IL-35) pretreatment vs. PBS (Control) was evaluated on Cardiac function (EF% and FS%) and pathological changes (p=<0.05). Interleukin-35 pretreatment significantly improved cardiac function and attenuated inflammation, apoptosis, and fibrosis in a mouse model of lipopolysaccharide-induced heart injury.
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