| Abstrak/Abstract |
Introduction: Kidney ischemia/reperfusion injury (IRI) is the
leading cause of acute kidney injury (AKI). Kidney IRI
demonstrated apoptosis of epithelial cells in acute phase
followed by proliferation of interstitial cells in chronic
episode, and cellular senescence may contribute to
development of AKI, however, its occurrence within acute or
chronic episodes is still not completely understood.
Methods: Kidney IRI was performed with bilateral pediculus
clamping in Swiss Background mice (3 months, 30-40g).
Mice were euthanised on day one (I/R1, n=6), day eight (I/R8,
n=6), and day twelve (I/R12, n=6) to exam acute and chronic
episodes. Sham operation procedure was performed in the
control. Tubular injury was assessed based on periodic acid-
Schift (PAS) staining. Reverse transcriptase PCR (RT-PCR)
was done to quantify mRNA expression of Bax, Bcl-2, and
p16. Immunohistostaining (IHC) was performed to examine
localisation of apoptosis (p53) and proliferation (Bcl-2).
Results: RT-PCR analysis showed upregulation of mRNA
expression of Bcl-2, Bax, and p16 (p<0.05). The data showed
that ischemia/reperfusion induces upregulation of Bax
(p=0.20), Bcl-2 (p=0.45), p16 (p=0.18). Apoptosis and
proliferation occurred in the epithelial cells in acute
episodes, but occurred in interstitial areas in chronic
episodes.
Conclusions: Ischemia/reperfusion injury induces
upregulation proliferation, apoptosis, and cellular
senescence in acute kidney injury. Apoptosis reached its
peak on day 1, proliferation on day 8, and cellular
senescence on day 12. |
