Objective: ACTH4-10Pro8Gly9Pro10 and HMG Co-A reductase inhibitor had a well-knownÂ neuroprotective effects. One important process happened in head injury is apoptotic neuronal death.Â Bcl-2 is one of anti-apoptotic protein inhibits the intrinsic pathway of apoptosis. This study aimed to
compare the effect of standard therapy, ACTH4-10Pro8Gly9Pro10, and HMG Co-A reductase inhibitor
on serum Bcl-2 levels and the potential effect to a better outcome and reduction of hospital stay.
Method: Subjects of severe head injury without any indication for surgery were taken consecutivelyÂ (n=60) and separated into three groups of; standard treatment only (control group), standard treatmentÂ combined with ACTH4-10Pro8Gly9Pro10, and standard treatment combined withInhibitor HMG CoA
Reductase. Blood samples were taken on day-1 and day-5 from each subject for measurement of Bcl-2 concentration. Barthel index and MMSE were measured at discharge and hospital length of stay wasÂ noted.
Results: Bcl-2 serum levels in control group was 1.49Â±1.01 ng/mL on day one and 1.64Â±0.61Â ng/mL on day five; and 1.72Â±1.40 ng/mL on day one and 4.02Â±1.19 ng/mL on day five after treatmentÂ with ACTH4-10Pro8Gly9Pro10. In the HMG Co-A reductase inhibitor group, Bcl-2 serum level was
1.55Â±0.98ng/mL on day one and 2.00Â±0.90ng/mL on day five. The correlation of outcome (BarthelÂ Index and MMSE) with serum Bcl-2 levels was not significant. We found the length of stay in theÂ ACTH4-10Pro8Gly9Pro10 group was significantly shorter (p<0.05; CI 95%).
Conclusion: ACTH4-10Pro8Gly9Pro10 significantly increased serum Bcl-2 concentration in head injury. Although we didnâ€™t
find any correlation between serum Bcl-2and outcome (Barthel Index and MMSE), therapy withÂ ACTH4-10Pro8Gly9Pro10 resulted in a significantly shorter hospital length of stay.