[Protective effect of heat shock protein 70 and magnesium sulfate supplementation on renal ischemia reperfusion injury].

OBJECTIVE: To investigate whether there is a protective mechanism in exogenous magnesium ions supplement in renal ischemia reperfusion injury(IRI ), and to study the expression of heat shock protein 70 (HSP70) and HSP70-mRNA in the reperfusion injury.

METHODS: A total of 90 male Japanese white rabbits (1.8-2.0 kg) were divided into three groups: ischemia reperfusion group (I-R), MgSO4 pretreatment group and sham operation group. The right kidney was cut through median abdominal incision to make solitary kidney model. The left renal artery was blocked for 1 h in I-R group and MgSO₄ group. 2.5% MgSO₄ 1 mL/(kg×h) was given through ear vein before the artery was blocked and during the blockeage in the MgSO₄ group. the kidney cortex tissue was taken 1, 2, 4, 24, 48 and 72 h after reperfusion. Immunohistochemical examination was used to determine the HSP70 expression. A modified quantitative Real time-PCR was used to quantitate HSP70-mRNA in the three groups. Pathological examination was also used to confirm the results.

RESULTS: Real time-PCR showed that HSP70-mRNA began to increase at the end of 1 h, and reached the peak at the end of 2 h in both I-R and MgSO₄ groups, but expression in I-R group which was remarkably higher than that in the MgSO₄ group at the end of 2 h and 4 h ( P<0.05). HSP70-mRNA levels decreased rapidly at the end of 24 h. In I-R group, moderate HSP70 expression could be seen in the proximal tubules during immunohistochemical examination after reperfusion for 24 h and 48 h. By contrast, there was weak HSP70 expression in the MgSO₄ group 24 h and negative 48 h after reperfusion. Epithelial shedding, border brush, inflammatory cell infiltration and protein casts were serious after 24 to 48 h reperfusion, while only slight tubular cell shedding and necrosis could be found in the MgSO₄ group at the matched time.

CONCLUSION: Magnesium supplement can significantly relieve the renal ischemia reperfusion injury. It can inhibit the upregulated expression of HSP70 and HSP70-mRNA in vivo, which demonstrates that the expression of HSP70 is not necessary in the protective mechanism.