Pengaruh Pemberian Propofol Intravena terhadap Ekspresi Kaspase 3 Hipokampus pada Mencit Balb/C dengan Cedera Kepala

Yusri Yani, Ardana Tri Arianto, M.H Sudjito

Abstract


Latar Belakang dan Tujuan: Cedera kepala masih menjadi penyebab utama kecacatan dan kematian. Dalam cedera kepala terjadi proses biomolekuler dan biokimiawi patologik yang dapat menyebabkan nekrosis maupun apoptosis melalui aktivasi kaspase 3. Propofol obat anestesi intravena mempunyai mekanisme neuroproteksi dengan pengaturan pada kaspase 3. Tujuan penelitian ini adalah meneliti keefektifan pemberian propofol 10 mg/kgbb, 25 mg/kgbb dan 50 mg/kgbb terhadap ekspresi kaspase 3 pada mencit balb/c dengan cedera kepala.

Subjek dan Metode: Penelitian eksperimental laboratorik dengan desain randomized controlled trial group pada 32 ekor mencit Balb/c yang disuntik propofol intravena. Mencit dibagi menjadi 4 kelompok secara random, yaitu kelompok K1 sebagai kontrol. Semua kelompok diberi perlakuan cedera kepala dengan metode weight drop dan kemudian diberi propofol 10 mg; 25 mg; 50 mg/kgBB intravena untuk kelompok K2, K3, K4. Pemeriksaan aktivasi kaspase 3 menggunakan pengecatan khusus immunohistokimia setelah 6 jam pemberian propofol. Hasil dinilai dengan SPSS 19 dengan derajat kemaknaan p<0,05.

Hasil: Rata-rata persentase ekspresi kaspase 3: K1=4,08, K2= 2,95, K3= 2,52, K4=1,77. Perhitungan statistik dari semua kelompok menunjukkan signifikan (P=0,000). Perbandingan antar kelompok menujukkan: K1-K2 (p=000), K1-K3 (p=0,000), K1-K4 (p=0,000), K2-K4 (p=0,000), K3-K4 (p=0,000), sedangkan antara K2-K3 tidak ada perbedaan signifikan (P=0,232).

Simpulan: Pemberian propofol 10,25,50 mg/kgbb menunjukkan hasil yang signifikan menghambat ekspresi kaspase 3 aktif dibandingkan dengan kontrol pada mencit yang diberi cedera kepala. Dari penelitian ini dapat ditarik simpulan bahwa pemberian propofol dosis 50 mg/kgbb merupakan dosis yang efektif untuk menurunkan ekspresi kaspase 3 aktif pada mencit dengan cedera kepala

 

The Effect of Propofol Intravena to Expression of Caspase 3 in Hipocampus Mice Balb/C with Brain Injury

Background and Objective: Head injury is a leading cause of disability and death. In head injury occurs biomolecular and biochemical processes that can lead to pathologic necrosis or apoptosis through the expression of caspase 3. Propofol an intravenous anesthetic drug has neuroprotective mechanism by setting the caspase 3. The objective of the research is to identify effect of propofol 10 mg/kg,25 mg/kg, and 50 mg/kg dose toward activation caspase 3 in Balb/c mice hipocampus with brain injury.

Subject and Methods: This is a laboratory setting experiment with randomized post test only controlled group design. Thirty two balb/c mice makes head injury by given of weight drop and intravenous propofol. The mice were given the same procedure weight drop and intravenous propofol 10,25,50 mg/kg 6 hours after injury for the K2, K3, K4 group respectively. Activation of caspase 3 was studied by immunohistochemistry method 6 hours after intravenous propofol administration. Data was analized using Kruskal Wallis Test, cross-tabulation chi square, one way ANOVA and processed by SPSS program.

Result: Means expression of caspase 3: K1= 4.08; K2 = 2.95; K3 =2.52; K4 = 1.77. The statistic result test among all groups show significant differences (p=0.000). The comparation of groups that have significant 82 Jurnal Neuroanestesia Indonesia outcome are: K1-K2 (p=0.00), K1-K3 (p=0.000), K1-K4 (p=0.000), K2-K4 (p=0.000), K3-K4 (p=0.000).There is no significant difference between K2-K3 (p=0.232). Conclusion: Administration of propofol 10, 25, 50 mg/kg intravenous after traumatic head injury show significant difference in hipocampus caspase 3 activation compared to control, group. From this research, we can also conclude that administering propofol in 50 mg is the effective dose to lowering expression of caspase 3 to mice, with given brain injury.


Keywords


Cedera kepala; ekspresi kaspase 3; propofolBrain injury; expression of caspase 3; propofol

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References


Dawodu ST. Definition, epidemiology, pathophysiology. Traumatic brain injury. Available from: URL: Dalam: Yadav RR,Talavera F, penyunting. 2005;diakses 15 Juli 2011.

McGarry LJ. Outcomes and costs of acute treatment of traumatic brain injury. Journal of traumatologi critical care 2002; 45:1152-1159.

Salinas P. Closed head trauma. Traumatic brain injury. Available from: URL: Dalam: Penar PL, Talavera F, penyunting. 2006; Diakses 10 Oktober 2011.

Zauner A, Muizelaar JP. Brain metabolism and cerebral blood flow. Head injury. London: Chapman and Hall Medical; 2004,229-36.

Pelinka LE, Kroepfl A. Glial fibrilary acidic protein in serum after traumatic brain injury. Dalam: Biochemical markers for brain damage. Available from:URL: http://www.ijccm.org/article.asp?issn=09725229.2003.

Abbas AK. Cellular and molecular immunology. 4th ed. Philadelphia: Elsevier Saunders Company; 2006, 143-56

Danial NN, Korsmeyer SJ. Cell death: critical control points. Dalam: Cell 2004;36:205-19.

Peter ME, Krammer PH. The CD95 (APO1/Fas) DISC and beyond. Cell Death Differ 2003; 10:26-35.

Kresno SB. Imunologi: diagnosis dan prosedur laboratorium. 3th ed, Jakarta: Universitas Indonesia; 2003.

Moe GW, Marin J. In vivo TNF- inhibition ameliorates cardiac mitochondrial dysfunction, oxidative stress, and apoptosis in experimental heart failure. AJP- Heart Circulatory Physiology 2004;35: 90-95.

Lou A. Inhibition of caspase mediated apoptosis by peroxynitrite in traumatic brain injury. The Journal of neuroscience 2006;45:95-98.

Chainlee Y. Subanesthetic doses of propofol induce neuroapoptosis in the infant mouse brain. International Anesthesia Research. 2008;36: 143-50.

Xu H, Zang C, Chunxiao Z. Effect of propofol pretreatment on apotosis in rat brain cortex after focal cerebral ischemi and reperfusion. Neural Regeneration Research 2011; 6:90-97.

Jill W. Apoptosis and traumatic brain injury. Neurocritical care. Singapore: Departement of Neurosurgery; 2009.




DOI: https://doi.org/10.24244/jni.vol2i2.160

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