Aim
This study aimed to explore the effect and related mechanisms of LncRNA 152 in acute kidney injury (AKI).
Conclusion
LncRNA 152 attenuates oxidative stress and inflammatory responses by regulating the FGF23/Klotho axis and inhibiting the MAPK signalling pathway in rat kidney tissues, thereby ameliorating LPS-induced AKI.
Methods
QRT-PCR was used to detect the expression of LncRNA 152, FGF23 and Klotho in the serum of patients with AKI. Subsequently, Sprague Dawley (SD) rats were induced into AKI animal model by lipopolysaccharide (LPS). Then, H&E staining was performed to observe the pathological changes in the rat kidney tissues; qRT-PCR to detect the expression of LncRNA 152, FGF23 and Klotho in the rat kidney tissues; biochemical assay and ELISA to assess the levels of renal function indexes and inflammatory factors in rat serum, as well as oxidative stress indexes in kidney tissues; and western blot to measure the protein expressions of FGF23, Klotho, p-p38 and p38 in rat kidney tissues.
Results
LncRNA 152 was significantly down-regulated in serum of AKI patients and kidney tissues of AKI rats. In AKI patients, LncRNA 152 was negatively correlated with FGF23 expression while positively correlated with Klotho expression. LncRNA 152 overexpression reduced the levels of blood urea nitrogen (BUN), creatinine (Cr) and cystatin C (Cys-C) and inflammatory factors in serum of AKI rats and attenuated pathological damage and oxidative stress of kidney tissues. In addition, LncRNA 152 overexpression also decreased FGF23 expression and p-p38/p38 ratio while up-regulated Klotho expression in the kidney tissues of AKI rats.