FSTL1 aggravates sepsis-induced acute kidney injury through regulating TLR4/MyD88/NF-κB pathway in newborn rats

Background: The aim of this work was to investigate whether Follistatin like 1 (FSTL1) exerted an effect on acute kidney injury (AKI) induced by sepsis, and explore the molecular mechanism. Methods: A cecal ligation puncture (CLP) model established adenoviral solution administrated newborn rats achieve FSTL1 knockdown. Colorimetric assays measured concentrations serum creatinine blood urea nitrogen (BUN) ELISA were performed examine TNF-α, IL-1β IL-6 levels in tissues. Kidney histological analysis using hematoxylin-eosin (HE) staining. Protein toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), phosphorylated p65 (p-p65) total (p65) determined western blotting. Results: significantly up-regulated kidneys following CLP, but subsequent inhibition alleviated AKI. knockdown CLP inhibited production IL-1β, inactivated TLR4/MyD88/NF-κB pathway. Furthermore, overexpression activated pathway TLR4 inhibitor TAK242 abolished effect. Conclusions: aggravates sepsis-induced through regulating