Tesis

Pengaruh Terapi Oksigen Hiperbarik Intermiten terhadap Neuroplastisitas dan Memori Spasial pada Model Tikus Cedera Otak Traumatis Difus dan Akut = Effect of Intermittent Hyperbaric Oxygen Therapy on Neuroplasticity and Spatial Memory in Rat Models of Diffuse and Acute Traumatic Brain Injury.

Latar Belakang: Cedera otak traumatis (COT) difus akut menyebabkan hipoksia, kerusakan jaringan, dan gangguan memori spasial, dengan tingkat mortalitas tinggi. Terapi oksigen hiperbarik intermiten (TOHBI) diketahui meningkatkan ekspresi BDNF, neurotrophin utama dalam neuroplastisitas, serta memperbaiki fungsi kognitif. TOHBI pada fase akut terbukti mencegah kerusakan neurologis, namun belum ada studi yang mengeksplorasi jalur hilir efeknya terhadap COT difus akut. Metode: Penelitian in vivo ini menggunakan model tikus COT difus yang diinduksi dengan Marmarou Weight Drop Device, kemudian diberikan TOHBI dengan tekanan 1, 2, dan 3 ATA selama tiga hari pertama pascacedera, sebanyak dua kali sehari selama satu jam per sesi. Evaluasi dilakukan pada hari ke-3, ke-7, dan ke-14, menggunakan Force Alternation Y-maze, pewarnaan Golgi-Cox untuk visualisasi spina dendrit, dan ELISA untuk mengukur konsentrasi PSD-95. Hasil: TOHBI tidak meningkatkan memori spasial secara statistik (p=0,4539), namun terdapat tren peningkatan pada tekanan 2 dan 3 ATA di hari ke-7 dan ke-14. Kepadatan spina dendrit meningkat signifikan berdasarkan waktu (p < 0,05), terutama pada hari ke- 14. Konsentrasi PSD-95 meningkat signifikan pada tekanan 2 ATA di hari ke-14 (p < 0,0001), dengan interaksi bermakna antara waktu dan tekanan (p=0,0005). Kesimpulan: TOHBI berpotensi menginduksi neuroplastisitas dan perbaikan fungsi memori spasial melalui peningkatan kepadatan spina dendrit dan kadar PSD-95.
Kata Kunci: Cedera Otak Traumatis; Memori Spasial; Neuroplastisitas; Terapi Oksigen hiperbarik.


Background: Acute diffuse traumatic brain injury (TBI) leads to hypoxia, tissue damage, and spatial memory impairment, with a high mortality rate. Intermittent hyperbaric oxygen therapy (IHBOT) has been shown to increase BDNF expression and improve cognitive function. IHBOT administered in the acute phase has been found to prevent neurological damage, but no studies have explored its downstream effects on acute diffuse TBI. Methods: This in vivo study used a diffuse TBI rat model induced via the Marmarou Weight Drop Device. IHBOT was administered at pressures of 1, 2, and 3 ATA during the first three days post-injury, with two sessions per day, each lasting one hour. Assessments were conducted on days 3, 7, and 14 post-injury, including Force Alternation Y-maze for spatial memory, Golgi-Cox staining for dendritic spine visualization, and ELISA for PSD-95 quantification Result: TOHBI did not significantly improve spatial memory (p=0.4539), but 2 and 3 ATA showed a trend of improved performance on days 7 and 14. Dendritic spine density increased significantly over time (p < 0.05), particularly on day 14. PSD-95 expression increased significantly at 2 ATA on day 14 (p < 0.0001), with a significant interaction between time and pressure (p=0.0005) Conclusion: IHBOT promotes neuroplasticity and spatial memory recovery by enhancing dendritic spine density and PSD-95 levels, suggesting its potential as a supportive therapy for acute diffuse TBI.
Keywords: Intermitten Hyperbaric Oxygen Therapy; Neuroplasticity; Spatial Memory; Traumatic Brain Injury