Journal of Korean Orthopaedic Research Society  2004;7(2):184-190

Alteration of PKC, PKC theta, NF-kappa B and AP-1 in Ischemic-reperfused Soleus Muscle of Rat with Ischemic Preconditioning.

Tai Seung KIM 1 ; Joo Hak KIM ; Kang Wook KIM

Affiliations

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Keywords

Skeletal muscle; PKC; NF-kappa B; Ischemic preconditioning

Country

Republic of Korea

Language

Korean

Abstract

PURPOSE: This study was designed to examine the expression patterns of PKC, PKC theta which is a house-keeping member of PKC family in the skeletal muscle, and two redox sensitive transcription factors, NF-kappa B and AP-1. MATERIALS AND METHODS: Male Sprague-Dawley rats, 9, 30 and 65 weeks old, were divided into 4 groups, such as normal controls, ischemic preconditioning controls, subjects receiving 4 hours of ischemia, and subjects receiving 4 hours of ischemia with ischemic preconditioning. Each group was divided into 5 subgroups based on reperfusion time. For ischemic preconditioning, left common iliac artery was occluded three times for 5 minutes of ischemia followed by 5 minutes of reperfusion using rodent vascular clamps. Ischemia was induced by occluding the same artery for 4 hours. The soleus muscles were removed at hours 0, 1, 3, 6, and 24 after the onset of reperfusion. Muscle samples were embedded in paraffin and 6 micrometer sections were made. The expression levels of PKC, PKC theta, NF-kappa B, and AP-1 were examined using immunohistochemical methods. RESULTS: Treatment of ischemia for 4 hours followed by reperfusion, resulted in the decrease in PKC, PKC theta, NF-kappa B, and AP-1 in 9 week-old rats, but consistant increase in 30 week-old rats. These factors were highly enhanced in the muscle from 65 week-old rats receiving 3 hours of reperfusion, followed by declined expression. And ischemic preconditioning reduced the expression variability. CONCLUSION: Ischemic precoditioning reduces the expression variabilities that activated by reperfusion after ischemia, such as PKC, PKC theta, NF-kappa B, and AP-1. But we couldn't predict the tissue damage by the patterns of expression of those factors.