BACKGROUND:Repetitive traumatic brain injury (RTBI) has gained much attention in this decade, especially in contact sports athletes and military personals. This injury is correlated with early neurodegenerative changes that are marked with the increased of tau protein. Turmeric extract (TE) is a well-known anti-inflammation and antioxidant that decreases tau protein expression in neurodegenerative disease.AIM:This study aimed to prove the effect of TE on tau protein level after RTBI.METHODS:Forty Sprague Dawley mice were divided into four groups, i.e. negative sham control group, the control group, and two treatment groups. A weight drop model was used by applying a 40-gram mass that was dropped from a 1-meter height onto the vertex of the head, with a total frequency of 12 times, divided into 4 days (day 0, 1, 3, and 7; 3 traumas on each day). TE was given to all treatment groups with 500 mg/kg BW doses once daily. The first treatment group had TE for seven days along the trauma. The second treatment group had pretreatment TE extract, given from seven days before first trauma and continued along the trauma protocol days. Tau protein level was measured on brain and serum using ELISA method.RESULTS:There was a significant reduction of tau protein level in both treatment groups compared to trauma group, either in serum or brain, but we also found significant differences regarding brain tau level between the treatment and pretreatment group.CONCLUSION:This study might provide evidence of with the role of pretreatment TE in RTBI.
Background:Traumatic brain injury (TBI) is one of the major causes of death and disability. Apoptosis after TBI contributes significantly to the final extent of tissue damage. The Bcl-2 family proteins are important apoptosis modulators which increased in injured neurons. Bcl-2 has shown an antiapoptotic effect in rats and mice. ACTH4-10Pro8-Gly9-Pro10 is a synthetic short fragment of ACTH devoid of hormonal effects and has neuromodulatory properties. ACTH4-10Pro8-Gly9-Pro10 has been shown to increase levels of Bcl-2 and BDNF in vitro as well as in vivo. It has been postulated that ACTH4-10Pro8-Gly9-Pro10 will result in improved clinical outcome and reduce hospital length of stay. The goal of this study is to compare the effect of standard therapy only with standard therapy and ACTH4-10Pro8-Gly9-Pro10, the increase of Bcl-2, and clinical outcome with reduction of hospital stay.Materials and Methods:Subjects of moderate head injury (MHI) with no indication of surgery were taken consecutively (n = 40) and separated into two groups: standard treatment only and standard treatment combined with ACTH4-10Pro8-Gly9-Pro10. Blood samples were taken on day 1 and day 5 from each subject for measurements of Bcl-2 concentration. Barthel Index and MMSE were measured, at discharge and hospital length of stay was noted.Results:Forty subjects have been involved in this study, three subjects died in the standard therapy group, and one subject in ACTH4-10Pro8-Gly9-Pro10 group. Bcl-2 serum level in standard therapy was 1.39 ± 0.75 ng/mL on day 1 and 1.48 ± 0.77 ng/mL on day 5. After treatment with ACTH4-10Pro8-Gly9-Pro10, Bcl-2 level was 1.39 ± 0.70 ng/mL on day 1 and 3.70 ± 1.02 ng/mL on day 5. The serum Bcl-2 concentration was significantly increased with ACTH4-10Pro8-Gly9-Pro10 therapy with shorter hospital length of stay (P < 0.05).Conclusion:ACTH4-10Pro8-Gly9-Pro10 increased serum Bcl-2 levels and reduced hospital length of stay significantly compared with standard therapy alone.
BACKGROUND: Traumatic brain injury (TBI) is the most common problem that caused morbidity and mortality in the world. Secondary brain injury is a complex cascade that causes brain cell apoptosis. Curcumin is a natural product that has neuroprotective properties. AIM: This study aimed to investigate the effect of curcumin toward heat shock protein 70 (HSP 70) expression against the expression apoptosis marker (apoptosis-inducing factor [AIF], caspase-3, and TUNEL assay) in brain tissue after TBI. METHODS: Thirty-three Sprague Dawley rats were randomized into three treatment groups, that is, sham-operated controls, closed head trauma (CHT), and CHT with curcumin extract (treatment group). In the treatment group, curcumin was given 500 mg/kg per oral for 7 days, then brain tissues were investigated (marker AIF, caspase-3, TUNEL assay, and HSP 70) through immunohistochemistry. Statistical test using one-way ANOVA test and Tukey honestly significant difference as post hoc test. RESULTS: The mean of positive AIF stained cells in Group A was 5.36 ± 2.11, Group B was 12.82 ± 1.40, and Group C was 3.82 ± 1.40, with a significant difference of AIF expression between Groups C and B (p < 0.05). Mean of positive caspase-3 stained cells in Group A was 5.45 ± 2.30, Group B was 13.82 ± 2.44, and Group C was 3.82 ± 1.54, with a significant difference of caspase-3 expression between Groups C and B (p < 0.05). Mean of positive TUNEL assay stained cells in Group A was 4.82 ± 2.04, Group B was 11.55 ± 1.51, and Group C was 3.55 ± 1.70, with a significant difference between Groups C and B (p < 0.05). Mean of positive HSP 70 stained cells in Group A was 6.82 ± 2.14, Group B was 3.91 ± 2.26, and Group C was 10.27 ± 2.45 with a significant difference of HSP 70 expression distribution within groups (p < 0.05). CONCLUSION: Curcumin may protect brain cells from apoptosis after close head trauma by upregulated HSP 70 expression.
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