Objective To investigate the role of LIGHT/TNFSF14 (TNF superfamily
protein 14) in
cisplatin-induced
acute kidney injury (Cis-AKI) in mice and explore the underlying mechanism. Methods Male wild-type (WT) and LIGHT gene knockout (LIGHT-/-) C57BL/6 mice were selected and divided into four groups: saline- and
cisplatin-treated WT mice, saline- and
cisplatin-treated LIGHT-/- mice. The
cisplatin groups were given a single
intraperitoneal injection of
cisplatin (20 mg/kg, 200 μL), and the saline groups were injected with equal volume of
normal saline (9 g/L). After 72 hours, the mice were sacrificed, blood was taken from the eyeball, and kidney tissues were collected. Blood
urea nitrogen (BUN) and serum
creatinine (Scr) were measured by automatic biochemical analyzer. HE staining was used to detect the histopathological changes of kidney tissues, The
mRNA levels of LIGHT, kidney injury molecule 1 (KIM-1),
interleukin-6 (IL-6),
monocyte chemotactic protein 1 (MCP-1), and
tumor necrosis factor (TNF-α) were detected by real-time quantitative PCR. The
protein levels of LIGHT, Bcl2, BAX and
cytochrome C were detected by Western blot analysis or immunohistochemical staining. Results Compared with saline-treated WT mice, the expression of LIGHT in renal tissue of
cisplatin-treated WT mice significantly increased. Compared with
cisplatin-treated WT mice, the kidney injury in
cisplatin-treated LIGHT-/- mice was more serious; BUN and Scr increased; and the pathological damage of kidney tissue was more obvious. Moreover, the
mRNA levels of
IL-6, MCP-1 and TNF-α, as well as the
protein levels of BAX and
cytochrome C increased, while the
protein levels of Bcl2 decreased. Conclusion LIGHT plays a protective role in Cis-AKI, which may be related to down-regulated secretion of inflammatory factors and decreased apoptosis.