摘要
We observed changes of intermedin （IMD） and its re- ceptor system mRNA expressed with renal ischemiaJreperfusion （I/R） injury in the rat and explored the protective effects of IMD pretreatment on renal injury. In comparison with sham group kid- neys, I/R-injured rats had severe pathological changes; renal su- peroxide dismutase （SOD） was decreased （-34.8%） and tissue malondialdehyde （MDA） was increased （＋34%; both p^0.01）; renal IMD content and mRNA levels were decreased by 63.5% and 48.2%, respectively （both p〈0.01）; and CRLR, RAMP1, and RAMP3 mRNA levels were decreased by 39.5%, 11.2%, and 21.2%, respectively （all p〈0.01）. After pretreatment with IMD （1.0 and 5.0 nmol/kg） and ADM （5.0 nmol/kg）, MDA content was lowered by 49.2%, 37.3%, and 36.9% respectively （all p^O.O1） and SOD activity was increased by 37.2%, 22.1%, and 19.7%, respectively （all p 〈 0.01）. Thus, renal I/R injury in rat downregu- lated IMD and its receptor system and pretreatment with IMD attenuated I/R-induced renal functional and structural damage.
We observed changes of intermedin （IMD） and its re- ceptor system mRNA expressed with renal ischemiaJreperfusion （I/R） injury in the rat and explored the protective effects of IMD pretreatment on renal injury. In comparison with sham group kid- neys, I/R-injured rats had severe pathological changes; renal su- peroxide dismutase （SOD） was decreased （-34.8%） and tissue malondialdehyde （MDA） was increased （＋34%; both p^0.01）; renal IMD content and mRNA levels were decreased by 63.5% and 48.2%, respectively （both p〈0.01）; and CRLR, RAMP1, and RAMP3 mRNA levels were decreased by 39.5%, 11.2%, and 21.2%, respectively （all p〈0.01）. After pretreatment with IMD （1.0 and 5.0 nmol/kg） and ADM （5.0 nmol/kg）, MDA content was lowered by 49.2%, 37.3%, and 36.9% respectively （all p^O.O1） and SOD activity was increased by 37.2%, 22.1%, and 19.7%, respectively （all p 〈 0.01）. Thus, renal I/R injury in rat downregu- lated IMD and its receptor system and pretreatment with IMD attenuated I/R-induced renal functional and structural damage.
基金
Supported by the Hubei Provincial Department of Education Science Foundation(B200524007)
the Xiangfan Central Hospital Science Foundation(XFCH200601)
