ArticleFrontiers in cellular neuroscience2017
Administration of Tauroursodeoxycholic Acid Attenuates Early Brain Injury via Akt Pathway Activation.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Endoplasmic Reticulum-Mitochondrial Crosstalk in Calcium Regulation: Mechanistic Insights and Therapeutic Implications in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Targeting mitofusin 1-mediated mitochondrial dynamics to suppress neuroinflammation and pyroptosis after traumatic brain injury.Burns & trauma · 2026Article
- Tauroursodeoxycholic acid reduces brain lesion volume and cortical edema in a rat model of Traumatic brain injury.Brain research · 2025Article
- An antioxidant and anti-ER stress combination therapy elevates phosphorylation of α-Syn at serine 129 and alleviates post-TBI PD-like pathology in a sex-specific manner in mice.Experimental neurology · 2024Article
- Endoplasmic reticulum stress and the unfolded protein response: emerging regulators in progression of traumatic brain injury.Cell death & disease · 2024Review
- The alteration of serum bile acid profile among traumatic brain injury patients: a small-scale prospective study.Journal of clinical biochemistry and nutrition · 2023Article
- Neutrophil extracellular traps aggravate neuronal endoplasmic reticulum stress and apoptosis via TLR9 after traumatic brain injury.Cell death & disease · 2023Article
- The mechanism and relevant mediators associated with neuronal apoptosis and potential therapeutic targets in subarachnoid hemorrhage.Neural regeneration research · 2023Review
- The gut-brain axis in ischemic stroke: its relevance in pathology and as a therapeutic target.Neurological research and practice · 2022Review
- Tauroursodeoxycholic Acid Reduces Neuroinflammation but Does Not Support Long Term Functional Recovery of Rats with Spinal Cord Injury.Biomedicines · 2022Article
- The Role of Bile Acids in the Human Body and in the Development of Diseases.Molecules (Basel, Switzerland) · 2022Review
- Activation of Sigma-1 Receptor Alleviates ER-Associated Cell Death and Microglia Activation in Traumatically Injured Mice.Journal of clinical medicine · 2022Article
- Synergistic effects of brain injury and aging: common mechanisms of proteostatic dysfunction.Trends in neurosciences · 2021Review
- Revisiting promising preclinical intracerebral hemorrhage studies to highlight repurposable drugs for translation.International journal of stroke : official journal of the International Stroke Society · 2021Article
- The Complexity of Secondary Cascade Consequent to Traumatic Brain Injury: Pathobiology and Potential Treatments.Current neuropharmacology · 2021Article
- A Retrospective Clinical Analysis of the Serum Bile Acid Alteration Caused by Traumatic Brain Injury.Frontiers in neurology · 2021Article
- Redox-Dependent Effects in the Physiopathological Role of Bile Acids.Oxidative medicine and cellular longevity · 2021Review
- Endoplasmic Reticulum Stress-Associated Neuronal Death and Innate Immune Response in Neurological Diseases.Frontiers in immunology · 2021Review
- Bile Acid Signaling in Neurodegenerative and Neurological Disorders.International journal of molecular sciences · 2020Review
- Probiotics ameliorate intestinal pathophysiology in a mouse model of Alzheimer's disease.Neurobiology of aging · 2020Article
Corrections and comments
- Retracted
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is one of the leading causes of trauma-induced mortality and disability, and emerging studies have shown that endoplasmic reticulum (ER) stress plays an important role in the pathophysiology of TBI. Tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, has been reported to act as an ER stress inhibitor and chemical chaperone and to have the potential to attenuate apoptosis and inflammation. To study the effects of TUDCA on brain injury, we subjected mice to TBI with a controlled cortical impact (CCI) device. Using western blotting, we first examined TBI-induced changes in the expression levels of GRP78, an ER stress marker, p-PERK, PERK, p-eIF2a, eIF2a, ATF4, p-Akt, Akt, Pten, Bax, Bcl-2, Caspase-12 and CHOP, as well as changes in the mRNA levels of Akt, GRP78, Caspase-12 and CHOP using RT-PCR. Neuronal cell death was assessed by a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, and CHOP expression in neuronal cells was detected by double-immunofluorescence staining. Neurological and motor deficits were assessed by modified neurological severity scores (mNSS) and beam balance and beam walking tests, and brain water content was also assessed. Our results indicated that ER stress peaked at 72 h after TBI and that TUDCA abolished ER stress and inhibited p-PERK, p-eIF2a, ATF4, Pten, Caspase-12 and CHOP expression levels. Moreover, our results show that TUDCA also improved neurological function and alleviated brain oedema. Additionally, TUDCA increased p-Akt expression and the Bcl-2/Bax ratio. However, the administration of the Akt inhibitor MK2206 or siRNA targeting of Akt abolished the beneficial effects of TUDCA. Taken together, our results indicate that TUDCA may attenuate early brain injury via Akt pathway activation.
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