STUDY ON ROLES OF PROTEIN
KINASE C AND INOSITOL1,4,5-TRISPHOSPHATE IN THE PATHOGENESIS OF
HYPOXIC-ISCHEMIC BRAIN INJURY IN NEONATAL RATS
Wang
H, Han YK and Wu BM
Department
of Pediatrics, The Second Clinical College, China Medical University,
Shenyang, China
Methods: The protein concentration was determined by Lowry’s
method. PKC activity was measured by the incorporation of [γ-32P] into a specific substrate peptide in
the cytosolic and particulate fraction respectively. IP3 was
determined by the radioreceptor binding assay.
Results: Compared with control, PKC activities in particulate
fractions in both cerebral cortex and hippocampus decreased, whereas
increased in cytosol in cerebral cortex and remained within normal range in
cytosol in hippocampus at 0, 4, 12, 24, 48, 72 hours, 7, 14 days after
hypoxic-ischemia for 20 minutes. All these changes restored to normal
levels at 21 days post hypoxic-ischemia. Similarly, a decrease in IP3
in cerebral cortex and hippocampus was noted and increase in IP3
in thalamus after hypoxic-ischemia, respectively. Changes in cytosolic PKC
activity were not related with those of IP3 as evaluated
statistically.
Conclusions: The hypoxia-ischemia induced disturbance of the second
messenger IP3 and PKC, which may play important roles in the
pathogenesis of hypoxic-ischemic brain injury.