| 초록 |
It has been known that hypothermia attenuates acute renal injury after ischemia reperfusion. We evaluated the hypothermic protection against renal ischemia reperfusion injury(IRI), and investigated the molecular mechanisms involved. We used renal fibrosis model after ischemia reperfusion injury in mice. C57BL/6 mice were divided into the following groups: sham mice and ischemia reperfusion injury mice (37°C vs. 32°C). The kidneys were harvested at day 1, day 3, day 7 after IRI. HK2 cells, a human kidney proximal tubular cell-2, were incubated at 33°C and 37°C incubator during 24 h. We knocked down PGC-1α by using siRNA in order to clarify the role of PGC-1α in renal fibrosis. The blood urea nitrogen (BUN) levels, and serum creatinine (s-Cr) levels, and the histologic renal injury scores were significantly lower in the 32°C IRI groups, compared to the 37°C ischemia reperfusion injury groups. In hypothermic IR group, TGF-β and α-SMA were significantly decreased, while the PGC-1α level was significantly increased. Cold preparation increased the PGC-1α in HK2 cell. In TGF-β treated HK2 cell, cold preperation decreased α-SMA and type 4 collagen. In addition, siPGC-1α in HK2 cells increased α-SMA and type 4 collagen in spite of cold preparation. Hypothermia attenuates renal function deterioration and renal fibrosis in renal IRI mice kidneys. PGC-1α may play a role in hypothermic protection in renal fibrosis after IRI. |