Objective    To observe the protection and underlying mechanism of preconditioning with endoplasmic reticulum stress (ERS) by tunicamycin on rat acute ischemic kidney injury.     Methods    Twenty-four SD rats were divided into 4 groups randomly

sham operation group

tunicamycin group

ischemia reperfusion (I/R) group

tunicamycin pretreatment + I/R group. The renal ischemia and reperfusion model was developed by bilateral clamping of the renal pedicle for 40 min and then reperfusing for 12 h. Tunicamycin was intraperitoneally administered to rats 24 h prior to I/R at a dosage of 0.6 mg/kg. Serum creatinine (SCr) and blood urea nitrogen (BUN) were detected with automatic biochemistry analyzer. Renal tubular injury was measured by PAS staining in the kidney tissue samples at 36 h after operation and evaluated with kidney tubules scoring. The expression of GRP78 in the ischemic renal tissue was detected by Western blotting and    immunohistochemical assay.     Results    Compared with sham operation group（0.20±0.03）

the expression of GRP78 protein was increased significantly in I/R group（2.40±0.17

P0.05）

and the levels of SCr and BUN were increased significantly in this group [（186.83±20.21）μmol/L

（21.73±2.33）mmol/L] compared with sham operation group[（47.42±6.02）μmol/L

（4.75±1.77）mmol/L] (P0.05). I/R group had a higher kidney tubule score than sham operation group (3.69±0.45 vs 0

P0.05). Tunicamycin induced the expression of GRP78 protein to elevate but had no effect on SCr and BUN

or kidney tubule injury. Compared with I/R group

the expression of GRP78 protein of TM+I/R group(3.2±0.24) was increased（P0.05）

The levels of SCr

BUN were decreased significantly in TM+I/R group[(98.72±14.55) μmol/L and（13.22±2.45）mmol/L] compared with I/R group（P0.05）

and the score of renal tubular injury was decreased significantly in TM+I/R group(2.45±0.33) compared with I/R group(3.69±0.45) （P0.05）.     Conclusion    Pretreatment with ERS protects the rats from acute ischemic kidney injury. The mechanism may be through activating ERS and up-regulating the expression of GRP78

then inhibiting the excessive ERS and increasing the kidney tolerance to ischemia and alleviating cellular and tissue injury. In this way

pretreatment with ERS exerts a protective effect against renal ischemia reperfusion injury.