Alpha lipoic acid inhibits neural apoptosis via a mitochondrial pathway in rats following traumatic brain injury

Wei, Wen Jun; Wang, Handong; Wu, Yong; Ding, Ke; Li, Tao; Cong, Zixiang; Xu, Jianguo; Zhou, Meifang; Huang, Linke; Ding, Hui; Wu, Heming

doi:10.1016/j.neuint.2015.06.003

Cited by 42 publications

(35 citation statements)

References 38 publications

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“…Mitochondria are crucial to central nervous system function and their susceptibility to free radical damage might be the initiating event for apoptosis and necrosis after TBI (Wei et al 2015). Mitochondria are composed of an outer and inner membrane, both with different characteristics and functions.…”

Section: Introductionmentioning

confidence: 99%

The use of antioxidants in the treatment of traumatic brain injury

Venegoni¹,

Shen

Thimmesch

et al. 2017

Journal of Advanced Nursing

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Aims The aim of this study was to discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. Background One of the leading causes of death globally is traumatic brain injury, affecting individuals in all demographics. Traumatic brain injury is produced by an external blunt force or penetration resulting in alterations in brain function or pathology. Often, with a traumatic brain injury, secondary injury causes additional damage to the brain tissue that can have further impact on recovery and the quality of life. Secondary injury occurs when metabolic and physiologic processes alter after initial injury and includes increased release of toxic free radicals that cause damage to adjacent tissues and can eventually lead to neuronal necrosis. Although antioxidants in the tissues can reduce free radical damage, the magnitude of increased free radicals overwhelms the body's reduced defence mechanisms. Supplementing the body's natural supply of antioxidants, such as coenzyme Q10, can attenuate oxidative damage caused by reactive oxygen species. Design Discussion paper. Data sources Research literature published from 2011–2016 in PubMed, CINAHL and Cochrane. Implications for nursing Prompt and accurate assessment of patients with traumatic brain injury by nurses is important to ensure optimal recovery and reduced lasting disability. Thus, it is imperative that nurses be knowledgeable about the secondary injury that occurs after a traumatic brain injury and aware of possible antioxidant treatments. Conclusion The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury.

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Section: Introductionmentioning

confidence: 99%

The use of antioxidants in the treatment of traumatic brain injury

Venegoni¹,

Shen

Thimmesch

et al. 2017

Journal of Advanced Nursing

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“…Alpha lipoic acid (ALA) which is characterized by its therapeutic effects, is described as a potent antioxidant derived from octanoic acid [1]. ALA which has 8 carbons containing 2 sulfur atoms in the dithiol ring structure is an essential substrate for energy metabolism of carbohydrates, proteins and fats [2].…”

Section: Introductionmentioning

confidence: 99%

Potential Therapeutic Agent In Psychiatric And Neurological Diseases: Alpha Lipoic Acid

Çekici¹,

BakÃ„Â±rhan²

2018

Acta Psychopathol

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“…The primary injury is the main factor determining patient outcomes. In addition, secondary brain damage induces various pathological processes including oxidative stress, autophagy, inflammatory responses, etc., which may aggravate side effects [3-5]. Although great efforts have been made in fundamental and clinical research, to date, no effective treatment has emerged.…”

Section: Introductionmentioning

confidence: 99%

Tetrahydrocurcumin Provides Neuroprotection in Experimental Traumatic Brain Injury and the Nrf2 Signaling Pathway as a Potential Mechanism

Guan

Chen

Lin

et al. 2017

Neuroimmunomodulation

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The protective effect of tetrahydrocurcumin (THC) after experimental traumatic brain injury (TBI) has been demonstrated, as demonstrated by the inhibition of oxidative stress, mitochondrial dysfunction, and apoptosis. However, the mechanisms underlying this effect are still not well understood. This study was to investigate the neuroprotective effects of THC, and its potential mechanisms, in a rat model of TBI. To this end, rats were divided into 4 groups: the sham group, the TBI group, the TBI + vehicle (V) group, and the TBI + THC group. THC or V was administered via intraperitoneal injection to rats in the TBI + V and TBI + THC groups 30 min after TBI. After euthanasia (24 h after TBI), neurological scores, brain water content, and neuronal cell death in the cerebral cortex were recorded. Brain samples were collected after neurological scoring for further analysis. THC treatment alleviated brain edema, attenuated TBI-induced neuronal cell apoptosis, and improved neurobehavioral function. In addition, NFE2-related factor 2 (Nrf2) expression was upregulated following TBI. These results suggest that THC improves neurological outcome after TBI, possibly by activating the Nrf2 signaling pathway.

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Alpha lipoic acid inhibits neural apoptosis via a mitochondrial pathway in rats following traumatic brain injury

Cited by 42 publications

References 38 publications

The use of antioxidants in the treatment of traumatic brain injury

The use of antioxidants in the treatment of traumatic brain injury

Potential Therapeutic Agent In Psychiatric And Neurological Diseases: Alpha Lipoic Acid

Tetrahydrocurcumin Provides Neuroprotection in Experimental Traumatic Brain Injury and the Nrf2 Signaling Pathway as a Potential Mechanism

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