Application of Tauroursodeoxycholic Acid for Treatment of Neurological and Non-neurological Diseases: Is There a Potential for Treating Traumatic Brain Injury?

被引:33
作者
Gronbeck, Kyle R. [1 ,2 ]
Rodrigues, Cecilia M. P. [3 ]
Mahmoudi, Javad [4 ]
Bershad, Eric M. [5 ]
Ling, Geoffrey [6 ]
Bachour, Salam P. [1 ]
Divani, Afshin A. [1 ,7 ,8 ]
机构
[1] Univ Minnesota, Dept Neurol, MMC 295,420 Delaware St SE, Minneapolis, MN 55455 USA
[2] Univ Minnesota, Sch Med, Twin Cites Campus, Minneapolis, MN 55455 USA
[3] Univ Lisbon, Res Inst Med IMed ULisboa, Fac Pharm, Lisbon, Portugal
[4] Tabriz Univ Med Sci, Neurosci Res Ctr, Tabriz, Iran
[5] Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA
[6] Uniformed Serv Univ Hlth Sci, Dept Neurol, Bethesda, MD 20814 USA
[7] Univ Minnesota, Dept Neurol Surg, Minneapolis, MN 55455 USA
[8] Univ Minnesota, Dept Biomed Engn, Minneapolis, MN 55455 USA
关键词
Traumatic brain injury; Tauroursodeoxycholic acid; Apoptosis; Neuroprotection; Intracranial pressure; Edema; Neuroinflammation; Blast injury; Stroke; Intracerebral hemorrhage; PRIMARY BILIARY-CIRRHOSIS; ENDOPLASMIC-RETICULUM STRESS; ISCHEMIA-REPERFUSION INJURY; PEPTIDE-INDUCED APOPTOSIS; INDUCED NEURONAL DEATH; URSODEOXYCHOLIC ACID; BILE-ACIDS; RAT HEPATOCYTES; CELL-DEATH; ALZHEIMERS-DISEASE;
D O I
10.1007/s12028-015-0225-7
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
The objective of this review was to evaluate the potential of tauroursodeoxycholic acid (TUDCA) for neuroprotection in traumatic brain injury (TBI) patients in the neurocritical care setting. Specifically, we surveyed preclinical studies describing the neuroprotective and systemic effects of TUDCA, and the potential therapeutic application of TUDCA. Preclinical studies have provided promising data supporting its use in neurological disease characterized by apoptosis-induced neuronal loss. TUDCA inhibits multiple proteins involved in apoptosis and upregulates cell survival pathways. In addition, TUDCA exhibits anti-inflammatory effects in models of neuroinflammation and attenuates neuronal loss in chronic neurodegenerative diseases. This may be applicable to TBI, which also triggers inflammatory and apoptotic processes. Additionally, preliminary data support the use of pharmacological therapies that reduce apoptosis and inflammation associated with TBI. The anti-apoptotic and anti-inflammatory mechanisms of TUDCA could prove promising in the treatment of TBI. Currently, there are no published data supporting improvement in clinical outcomes of TBI by treatment with TUDCA, but future studies should be considered.
引用
收藏
页码:153 / 166
页数:14
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