Objective      To investigate the expression changes of transient receptor potential melastatin related 7 (TRPM7)

poly(ADP-ribose) polymerase 1 (PARP-1)

and necroptosis marker receptor interacting protein-1 (RIP1) in rat kidneys after ischemia/reperfusion (I/R) injury and their relationship with nephridial tissue injury so as to preliminarily explo

re the role of TRPM7 in the kidney I/R injury of programmed cell necrosis and its possible mechanism.       Methods      Renal I/R injury models of 55 male SD rats were established. Serum creatinine (SCr) and urea nitrogen (BUN) were detected on days 1

2

5 and 7 after kidney I/R. Renal injury was observed under a light microscope with PAS staining. TRPM7

PARP-1

and RIP1 were tested by immunohistochemistry and Western blotting.       Results      Comparing the control group with the sham operation group

the levels of SCr and BUN and the renal morphology had no significant difference. The levels of SCr and BUN were significantly higher in the I/R group than in the sham operation group. The levels of SCr and BUN in the I/R group reached the peak at the time point of 24 h after reperfusion

and then gradually declined

falling to be nearly normal levels about 7 d. HE staining results showed that nephridial injury appeared obviously at the time points of 24 and 48 h after reperfusion

and started to repair on day 5 and recovered on day 7. Immunohistochemistry and Western blot results showed that TRPM7 was expressed mainly in the renal tubular epithelial cells. In the I/R group

TRPM7 expression in kidney tissue started to rise significantly after reperfusion

reached the peak at the time point of 24 h after reperfusion

and then declined gradually. The changes of PARP-1 and RIP1 expression were similar to TRPM7 expression. Correlation analysis showed that there was a positive relation between the changes of TRPM7 expression and acute renal tubular injury grading (

r

=0.71

P

0.05).       Conclusion      TRPM7 expression rises in the early period of kidney I/R injury

and then returns to the normal level gradually. The expression of PARP-1 and RIP1 and nephridial tissue injury have similar change trends. TRPM7 may participate in the kidney I/R injury through the downstream calcium-dependent signal pathways regulating PARP 1 and RIP1 to influence necroptosis.