| Summary: | 碩士 === 慈濟大學 === 藥理暨毒理學研究所 === 97 === Ischemia coupled with reperfusion (ischemia/reperfusion) in the kidney
results in cell death, which can ultimately lead to severe renal injury. In patients
with severe renal injury, the levels of adiponectin (APN), a member of
adipocyte-derived cytokine, and its isoforms are increased. Adiponectin is
known to exert anti-inflammatory and anti-apoptotic effects. However, the
physiological function of adiponectin in severe renal disease is not clear.
We have previously shown that serum adiponectin was greatly reduced in
mice kidney I/R model serum. In this study, we further demonstrated that
I/R-induced renal dysfunction, as evidenced by elevated serum creatinine and
urea levels, was significantly reduced following i.v. injection of E. Coli
carrying active with adiponectin, suggesting that adiponectin may play a
protection role for kidney upon I/R. On pathology examination, we observed
that adiponectin treated mice had more mild renal damage with renal cell
disruption, tubular cell apoptosis, and neutrophil infiltration than sham operated
mice. Furthermore, we found that administration of adiponectin to peroxisome
proliferators activated receptor (PPARα) siRNA treated cells or PPARα
knockout mice activated heme oxygenase-1 (HO-1) expression via
PPARα-dependent pathway. Collectively, these results demonstrated that
adiponectin reverses I/R-mediated renal tubule cell death through an
PPARα-induced HO-1 mechanism, which may thus have therapeutic potential
for diminishing I/R-dependent kidney injury and inflammation.
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