Docosahexaenoic Acid (DHA) Provides Neuroprotection in Traumatic Brain Injury Models via Activating Nrf2-ARE Signaling
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ORIGINAL ARTICLE
Docosahexaenoic Acid (DHA) Provides Neuroprotection in Traumatic Brain Injury Models via Activating Nrf2-ARE Signaling Wei Zhu ,1,3 Yuexia Ding,2 Wei Kong,1 Tuo Li,1 and Hongguang Chen1
In this study, we explored the neuroprotective effects of docosahexaenoic acid (DHA) in traumatic brain injury (TBI) models. In this study, we first confirmed that DHA was neuroprotective against TBI via the NSS test and Morris water maze experiment. Western blot was conducted to identify the expression of Bax, caspase-3, and Bcl-2. And the cell apoptosis of the TBI models was validated by TUNEL staining. Relationships between nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) pathway-related genes and DHA were explored by RT-PCR and Western blot. Rats of the DHA group performed remarkably better than those of the TBI group in both NSS test and water maze experiment. DHA conspicuously promoted the expression of Bcl-2 and diminished that of cleaved caspase-3 and Bax, indicating the anti-apoptotic role of DHA. Superoxide dismutase (SOD) activity and cortical malondialdehyde content, glutathione peroxidase (GPx) activity were renovated in rats receiving DHA treatment, implying that the neuroprotective influence of DHA was derived from lightening the oxidative stress caused by TBI. Moreover, immunofluorescence and Western blot experiments revealed that DHA facilitated the translocation of Nrf2 to the nucleus. DHA administration also notably increased the expression of the downstream factors NAD(P)H:quinone oxidoreductase (NQO-1) and heme oxygenase 1(HO-1). DHA exerted neuroprotective influence on the TBI models, potentially through activating the Nrf2- ARE pathway.
Abstract—
KEY WORDS: traumatic brain injury; Nrf2/ARE pathway; docosahexaenoic acid (DHA); immunofluorescence.
BACKGROUND Traumatic brain injury (TBI), a primary cause of death and disability among the young population, has Wei Zhu and Yuexia Ding contributed equally to this work. 1
Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, No. 20 East Yuhuangding Road, Zhifu District, Yantai, 264000, Shandong, China 2 Department of Pharmacy, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, Shandong, China 3 To whom correspondence should be addressed at Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, No. 20 East Yuhuangding Road, Zhifu District, Yantai, 264000, Shandong, China. E-mail: [email protected]
now become a primary public health issue [1]. TBI induces primary mechanical injury of brain cells and triggers secondary damage such as inflammation, apoptosis, and oxidative stress that appear gradually after the primary damage [2, 3]. Although the primary brain injury is the major factor determining the outcomes, the secondary brain injury exacerbates TBI [4, 5]. Regardless of endeavors of searching for valid approaches to mitigate the secondary damage, up to now, the majority of treatments for TBI fo
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