2010Zhongguo Yike Daxue xuebaoRequires access

mTOR in ischemic postconditioning-induced attenuation of ischemia/reperfusion injury in rat skeletal muscle.

Jun Yang, Xinhua Hu, Zhishen Zhang, Liu Cheng-wei, Yi ZhengGui, Zhang Qiang

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Abstract

Objective To study the expression of mammalian target of rapamycin(mTOR)in ischemic postconditioning(I-postC)-induced attenuation of ischemia/reperfusion (I/R)injury in rat skeletal muscle. Methods A total of 48 healthy male Wistar rats were randomly divided into 3 groups (n =16 each group):I/R group (4-hour ischemia followed by 12or 24-hour reperfusion),ischemic preconditioning (IPC)group(3 cycles of 5-minute ischemia followed by 5-minute reperfusion),and I-postC group(3 cycles of 1-minute reperfusion followed by l-minute ischemia). The rat model of I/R injury in right hind limb model was established by clamping the right femoral artery. The changes in the morphology,wet-to-dry weight ratio(W/D),malondialdehyde(MDA),and myeloperoxidase(MPO)in skeletal muscle were compared. The expression of mTOR was detected by Western blot and immunohistochemistry. Results In I-postC and IPC groups,the skeletal muscle edema was less severe,the levels of MDA and MPO significantly decreased,and the expression of mTOR significantly increased,compared with I/R group (all P 0.05). There was no significant difference between I-postC and IPC groups. Conclusion IpostC may attenuate I/R injury in rat hind limbs by activating mTOR signal pathway,which is similar to the mechanism of IPC.

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Objective To study the expression of mammalian target of rapamycin(mTOR)in ischemic postconditioning(I-postC)-induced attenuation of ischemia/reperfusion (I/R)injury in rat skeletal muscle. Methods A total of 48 healthy male Wistar rats were randomly divided into 3 groups (n =16 each group):I/R group (4-hour ischemia followed by 12or 24-hour reperfusion),ischemic preconditioning (IPC)group(3 cycles of 5-minute ischemia followed by 5-minute reperfusion),and I-postC group(3 cycles of 1-minute reperfusion followed by l-minute ischemia). The rat model of I/R injury in right hind limb model was established by clamping the right femoral artery. The changes in the morphology,wet-to-dry weight ratio(W/D),malondialdehyde(MDA),and myeloperoxidase(MPO)in skeletal muscle were compared. The expression of mTOR was detected by Western blot and immunohistochemistry. Results In I-postC and IPC groups,the skeletal muscle edema was less severe,the levels of MDA and MPO significantly decreased,and the expression of mTOR significantly increased,compared with I/R group (all P 0.05). There was no significant difference between I-postC and IPC groups. Conclusion IpostC may attenuate I/R injury in rat hind limbs by activating mTOR signal pathway,which is similar to the mechanism of IPC.

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Available abstract

Objective To study the expression of mammalian target of rapamycin(mTOR)in ischemic postconditioning(I-postC)-induced attenuation of ischemia/reperfusion (I/R)injury in rat skeletal muscle. Methods A total of 48 healthy male Wistar rats were randomly divided into 3 groups (n =16 each group):I/R group (4-hour ischemia followed by 12or 24-hour reperfusion),ischemic preconditioning (IPC)group(3 cycles of 5-minute ischemia followed by 5-minute reperfusion),and I-postC group(3 cycles of 1-minute reperfusion followed by l-minute ischemia). The rat model of I/R injury in right hind limb model was established by clamping the right femoral artery. The changes in the morphology,wet-to-dry weight ratio(W/D),malondialdehyde(MDA),and myeloperoxidase(MPO)in skeletal muscle were compared. The expression of mTOR was detected by Western blot and immunohistochemistry. Results In I-postC and IPC groups,the skeletal muscle edema was less severe,the levels of MDA and MPO significantly decreased,and the expression of mTOR significantly increased,compared with I/R group (all P 0.05). There was no significant difference between I-postC and IPC groups. Conclusion IpostC may attenuate I/R injury in rat hind limbs by activating mTOR signal pathway,which is similar to the mechanism of IPC.

Key concepts: Medicine, Skeletal muscle, Malondialdehyde, Ischemia, Reperfusion injury, PI3K/AKT/mTOR pathway, Hindlimb, Ischemic preconditioning

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