Abstract:

PIM1 is a serine/threonine kinase that participates in the regulation of multiple signal pathways and plays an important role in many diseases. In order to explore the role of PIM1 kinase in cisplatin-induced acute kidney injury， C57BL/6 mice and renal tubular cells were selected as experimental objects. Cisplatin-induced acute kidney injury in mice was established by intraperitoneal injection of cisplatin. The levels of urea nitrogen and creatinine in serum were measured， renal pathology change was assayed by HE staining， qRT-PCR and Western blot were used to detect the expression levels of PIM1 mRNA and PIM1 protein. Renal tubular cells were infected by Adenovirus for overexpression of PIM1， the expression levels of p62、Beclin-1、LC3B were detected by Western blot， CCK-8 and flow cytometry were used to detect the renal tubular cell injury. Results showed that in vivo model， after injection of cisplatin， the levels of serum creatinine， urea nitrogen and tubular injury were significantly increased， the PIM1 mRNA and PIM1 protein expression in kidney tissues were dramatically increased. In vitro model， PIM1 mRNA and PIM1 protein expression levels significantly increased after Adenovirus infection. After cisplatin treated， the cell viability was decreased and the apoptosis was increased， while in the PIM1 overexpression group， the cell viability was increased and the apoptosis was decreased. After cisplatin treated， the expression level of p62 was decreased， the expression levels of Beclin-1， LC3B were increased， and autophagy was activated. Compared with the cisplatin treated group， the expression level of p62 was increased， the expression levels of Beclin-1， LC3B were decreased， and autophagy was weakened in the PIM1 overexpression group. In conclusion， PIM1 was activated in cisplatin-induced acute kidney injury， overexpression of PIM1 alleviated the cisplatin-induced renal tubular cells injury by inhibiting excessive autophagy.

Key words: PIM1 kinase, acute kidney injury, cisplatin, autophagy