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Pretreatment with granulocyte colony‐stimulating factor attenuated renal ischaemia and reperfusion injury via activation of PI3/Akt signal pathway
Author(s) -
LI YIWEN,
WU JIANYONG,
SHOU ZHANGFEI,
HE QIANG,
ZHANG PING,
HAN FEI,
LI HEN,
CHEN JIANGHUA
Publication year - 2008
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.2008.00928.x
Subject(s) - wortmannin , medicine , kidney , granulocyte colony stimulating factor , reperfusion injury , ischemia , pharmacology , granulocyte , acute kidney injury , endocrinology , apoptosis , protein kinase b , chemotherapy , biology , biochemistry
SUMMARY: Aim: Granulocyte colony‐stimulating factor (G‐CSF) has been shown to exert protective effects in various tissues and experimental models of ischaemia‐induced injury. However, the mechanism of renoprotective action in ischaemia/reperfusion (I/R) renal injury of G‐CSF was unknown. Methods: Male C57BL/6J mice, subjected to renal ischaemia for 45 min, 48 h and 7 days reperfusion, were administered either saline, wortmannin, G‐CSF, and G‐CSF plus wortmannin 3 days prior to I/R. Saline‐treated group served as the control. At 48 h and 7 days of reperfusion, the mice were killed. Results: Significantly, renal dysfunction and morphological injury were identified at 48 h and 7 days after I/R. Wortmannin pretreatment worsened the renal injury significantly. However, G‐CSF pretreatment significantly attenuated renal injury, reduced the terminal deoxynucleotidyl transferase‐mediated dUTP nick end labeling‐positive ratio of renal tubular epithelial cells and inflammation cytokine expression in the kidney. Moreover, G‐CSF pretreatment inhibited the expression of Bax and increased the expression of bcl‐2 and p‐Akt in the kidney. Wortmannin blunted the beneficial effects of G‐CSF. Conclusion: The cytoprotective action of G‐CSF against I/R injury seems to be associated with its anti‐apoptotic action mediated by upregulation of p‐Akt signal pathway.