Published Paper Details:

Brain injury is a problem faced by many neurosurgeons and is a major cause of disability, death and requires high costs to treat in Indonesia. Neurological damage in brain injury does not only occur at the time of impact injury, but develops in the hours and days that follow due to secondary brain injury. The mechanisms of secondary brain injury include oxygen free radicals, neuroinflammation, brain edema, and brain cell death. Kencur extract has antioxidant potential with total phenolic and flavonoid content including luteolin apigenin and is expected to reduce MDA expression. This study is an experimental laboratory with simple random sampling so that the experimental animals, experimental sites and research materials are homogeneous. The treatment of all samples was carried out simultaneously using post-test only control group design which allowed researchers to measure the effect of treatment on the experimental group by comparing the experimental group with the control group. Based on the ANOVA test, the significance value of the Kencur extract treatment group was 0.000 (p<0.05) indicating that there was a difference in MDA expression in brain-injured rats without kencur extract with brain-injured rats and given kencur extract. The 24-hour and 48-hour time groups, a significance value of 0.488 (p> 0.05) showed no significant difference in MDA expression. Then the Kencur extract treatment group with a time group of 0.117 (p> 0.05) showed no significant difference in MDA expression. There was a significant difference in the expression of MDA in brain injured rats without kencur extract with brain injured rats and given kencur extract. There were no significant differences in the MDA expression in the 24-hour and 48-hour time groups and the Kencur extract treatment group and the 24-hour and 48-hour time groups.