Yaygın Anksiyete Bozukluğu Olan Ilaç Kullanmayan Hastalarda Serum Nrf2 ve HO-1 Düzeylerinin Azalması

Öz

Amaç: Yaygın anksiyete bozukluğunda (YAB) psikolojik, sosyal, genetik ve biyolojik faktörler gibi birçok neden suçlansa da etiyopatogenezi tam olarak anlaşılamamıştır.
Bu çalışmanın amacı, yaygın anksiyete bozukluğu (YAB) tanısı almış yetişkinlerde serum Nükleer Faktör Eritroid 2 ile İlişkili Faktör 2 (NRF2), Heme oksijenaz 1  (HO-1) ve tau protein düzeylerini incelemek ve bu biyobelirteçlerin anksiyete belirtilerinin şiddetiyle ilişkisinin nasıl olduğunu araştırmaktır.
Materyal ve metod: Araştırmaya daha önce herhangi bir ilaç kullanmamış 44 YAB hastası ve yaş ve cinsiyete göre eşleştirilmiş 44 sağlıklı birey dahil edilmiştir. YAB grubunda anksiyete şiddeti Beck Anksiyete Envanteri (BAI) kullanılarak değerlendirilmiştir. Serum Nrf2, HO-1 ve tau konsantrasyonları bir biyokimya laboratuvarında ELISA yöntemi kullanılarak ölçülmüştür. 
Bulgular: YAB tanısı almış bireylerde serum Nrf2 ve HO-1 düzeyleri, kontrol grubunda gözlenenlerden anlamlı derecede düşüktü (sırasıyla p=0,023; p<0,001). Ancak, hasta ve kontrol grupları arasında serum tau konsantrasyonları açısından anlamlı bir fark tespit edilmedi (p=0,980). Spearman korelasyon analizine göre, hasta grubunda toplam BAI puanları ile Nrf2, HO-1 veya tau düzeyleri arasında anlamlı bir ilişki bulunmadı. 
Sonuç: Bu bulgular, YAB hastalarında antioksidan savunma sisteminin zayıfladığını göstermektedir. YAB patofizyolojisine tam katkılarını netleştirmek için Nrf2 ve HO-1'i değerlendiren daha fazla araştırmaya ihtiyaç vardır.

Anahtar Kelimeler

• Yaygın anksiyete bozukluğu
• Oksidatif stres
• Nrf2
• HO-1
• Tau

Destekleyen Kurum

Çalışmanın finansal desteği Harran Üniversitesi Bilimsel Araştırma Koordinasyon Kurulu [No: 19017] tarafından sağlanmıştır.

Etik Beyan

Ethical approval for this study was obtained from the by Harran University Faculty of Medicine Clinical Research Ethics Committee (approval no: 10, date: October 04, 2018).

Decreased Serum Levels of Nrf2 and HO-1 in Drug-Naive Patients with Generalized Anxiety Disorder

Öz

Background: Although many causes such as psychological, social, genetic and biological factors are blamed in generalized anxiety disorder (GAD), its etiopathogenesis is not fully understood.  The aim of this study was to examine the serum levels of Nuclear factor-E2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), and tau proteins in adults diagnosed with generalized anxiety disorder (GAD), and to explore the relationship between these biomarkers and anxiety severity.
Materials and Methods: The research involved 44 patients with GAD who had not previously received any medication, along with 44 healthy individuals matched by age and gender. Anxiety severity in the GAD group was assessed using the Beck Anxiety Inventory (BAI). Serum concentrations of Nrf2, HO-1, and tau were measured in a biochemistry laboratory using the enzyme-linked immunosorbent assay (ELISA) method.
Results: In individuals diagnosed with GAD, serum levels of Nrf2 and HO-1 were significantly lower than those observed in the control group (p=0.023; p<0.001, respectively). However, no significant difference was detected between the patient and control groups regarding serum tau concentrations (p=0.98). According to Spearman correlation analysis, there were no significant correlation between total BAI scores and the levels of Nrf2, HO-1, or tau in the patient group.
Conclusions: These findings suggest that the antioxidant defense system is compromised in patients with GAD. Further research assessing Nrf2 and HO-1 is required to clarify their exact contribution to the pathophysiology of GAD.

Anahtar Kelimeler

• Generalized anxiety disorder
• Oxidative stress
• Nrf2
• HO-1
• Tau

Destekleyen Kurum

Financial support for the study was provided by the Harran University Scientific Investigation Coordination Committee [No: 19017].

Etik Beyan

Ethical approval for this study was obtained from the by Harran University Faculty of Medicine Clinical Research Ethics Committee (approval no: 10, date: October 04, 2018).

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