Latar Belakang Cedera otak traumatik (COT) merupakan salah satu penyebab utama disabilitas dan kematian pada negara berkembang. Kematian neuron pada COT dapat berlangsung secara progresif akibat cedera sekunder melalui mekanisme hipoksia dan stres oksidatif. Terapi oksigen hiperbarik (TOHB) diketahui dapat meningkatkan oksigenasi jaringan dan berpotensi menurunkan stres oksidatif, namun efektivitasnya masih diperdebatkan karena kemungkinan risiko toksisitas oksigen. Penelitian ini bertujuan untuk mengevaluasi efek TOHB pada tikus dengan COT terhadap penanda stres oksidatif.Metode Model hewan COT diinduksi dengan menggunakan Marmarou weight drop device pada tikus Sprague-Dawley. Subjek dibagi menjadi kelompok kontrol model, kontrol perlakuan, normobarik, TOHB 2 ATA, dan TOHB 3 ATA. TOHB diberikan sebanyak 6x, dengan durasi 1 jam, dan interval antar terapi 12 jam. Hewan diterminasi pada hari ke-3, ke-7, dan ke-14 setelah induksi COT. Sampel jaringan otak diekstraksi untuk analisis biomarker stres oksidatif meliputi kadar malndialdehid (MDA), kadar glutation (GSH), aktivitas glutation peroksidase (GPx), aktivitas katalase, aktivitas superoksida dismutase (SOD), dan kadar Nuclear factor erythroid 2-related factor 2 (Nrf2).Hasil Pemberian TOHB meningkatkan kadar MDA, kadar GSH, kadar Nrf2, aktivitas SOD, dan aktivitas GPx. Tidak terdapat peningkatan aktivitas katalase pada kelompok TOHB. Hasil ini menunjukkan pemberian TOHB menyebabkan stres oksidatif akibat pemberian oksigen tekanan tinggi, namun TOHB juga memicu respon adaptif seluler pertahanan antioksidan melalui jalur Nrf2.Kesimpulan TOHB menimbulkan efek protektif melalui respon adaptif seluler yang meningkatkan kapasitas antioksidan yang dipicu stres oksidatif melalui jalur Nrf2.

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Introduction Traumatic brain injury (TBI) is one of the leading causes of disability and mortality in developing countries. Neuronal death in TBI may progress through secondary injury mechanisms, including hypoxia and oxidative stress. Hyperbaric oxygen therapy (HBOT) has been shown to enhance tissue oxygenation and potentially reduce oxidative stress. However, its effectiveness remains debated due to the potential risk of oxygen toxicity. This study aimed to evaluate the effects of HBOT on oxidative stress markers in a rat model of TBI.

Method A rat model of TBI was induced using the Marmarou weight-drop device. Subjects were divided into control, sham, normobaric, and HBOT groups (2 ATA and 3 ATA). HBOT was given twice daily for one hour over six sessions. Animals were sacrificed on days 3, 7, or 14 post-injury to evaluate the healing process. Brain tissue samples were collected for the assessment of oxidative stress biomarkers, including levels of malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx) activity, catalase activity, superoxide dismutase (SOD) activity, and Nuclear factor erythroid 2-related factor 2 (Nrf2) levels.

Results HBOT increased levels of MDA, GSH, Nrf2, SOD activity, and GPx activity. However, catalase activity did not increase in the HBOT groups. These findings indicate that HBOT induces oxidative stress due to high-pressure oxygen exposure but simultaneously triggers a cellular adaptive antioxidant defense response via the Nrf2 pathway.

Conclusion HBOT exerts a protective effect through a cellular adaptive response that enhances antioxidant capacity, driven by oxidative stress via Nrf2 pathway activation.