ABSTRACT
Traumatic brain injury (TBI) is a major reason for temporary or permanent dyskinesia and cognitive impairment of the organism. Generally, TBI induces subsequent neuroinflammation to assist cell debris removal and tissue repair and regeneration after injury. However, overactivation or long-term activation of immune cells will exacerbate nerve damage or death, cause cognitive dysfunction, and ultimately lead to neurodegenerative diseases. Therefore, secondary damage caused by persistent inflammation is a key component of TBI pathological process. As the main metabolite of anaerobic glycolysis, lactate is increased after TBI and participates in brain inflammation as an important immune regulatory molecule rather than a metabolic waste. Importantly, histone lysine lactylation as a novel type of histone post-translational modifications (HPTM) derived from lactate allows lactate to participate in the regulation of complex immunopathophysiological processes of the central nervous system after TBI. Further study on the process of histone lactylation and its immune regulation mechanism during TBI may provide new insights for early intervention and improvement of TBI prognosis. Thus, the authors reviewed the role of histone lactylation in the immune regulation of TBI, so as to further elucidate the mechanism of TBI and the explore new warning and prevention measures from the perspective of HPTM.
ABSTRACT
Posttraumatic stress disorder (PTSD) refers to the sudden, threatening or catastrophic life events leading to delay and long-term persistence of mental disorders. Hippocampus, amygdala, prefrontal cortex and hypothalamus-pituitary-adrenal axis (HPA) may be involved in PTSD, but the exact pathogenesis is not entirely clear. Traditional Chinese Medicine, including Chinese herbs, acupuncture and emotion-thought therapy, are considered as the main methods for PTSD, which may play a role in neuroprotection, adjustment of learn-ing-memory, anti-stress, adjusting HPA, etc.
ABSTRACT
It is difficult for regeneration of central nervous system (CNS) in adult mammals, and myelin-associated inhibitors (MAIs) are believed to be major contributors. Paired immunoglobulin-like receptor B (PirB), as a co-receptor of MAIs, and expresses highly in CNS after injury, plays a vital role in the signal transduction of inhibition in the injured CNS. Knockout or block of PirB in vitro and in vivo may promote the neuro-regeneration after spinal cord injury or hypoxic-ischemic brain damage, release the damage induced byβ-amyloid in Al-zheimer's disease, recover the neural function in brain inflammation models, improve the reconstruction of vision after optic nerve injury, and so on. PirB may be a potential therapeutic target for neuro-regeneration and synaptic plasticity.
ABSTRACT
BACKGROUND: To summarize the progress of tissue engineering in repairing spinal cord injury in recent years.DATA SOURCES: A computer-based online search of PubMed database (http://www.ncbi.nlm.nih.gov/PubMed) and CNKI database (www.cnki.net/index.htm) was performed for articles published between September 1999 and September 2009 with the key words of "spinal cord injury, tissue engineering" in English and Chinese, respectively. Articles published recently or in authoritative journals in the same field were selected.DATA SELECTION: Inclusion criteria: clinical or experimental study about tissue engineering in repairing spinal cord injury.Repetitive studies were excluded. A total of 29 articles were included.MAIN OUTCOME MEASURES: Seed cell selection of tissue engineering; requirements of scaffold materials of tissue-engineered spinal cord, neurotrophic factor for regeneration, special internal environment construction for regeneration.RESULTS: Seed cells of tissue-engineered spinal cord include Schwann cells, olfactory ensheathing cells, embryonic stem cells, neural stem cells and bone marrow stromal stem cells. Scaffold materials involve synthetic or modified natural materials, such as polyglycolic acid, polylactic acid, and lactic acid/glycolic acid copolymer, which benefit cell attachment and nutrition factor aggregation following surface modification. Antibodies that promote or inhibit nerve growth factor in combination with polyoxyl are coupled to function as tissue-engineered scaffold, which may be approaches to repair spinal cord injury by tissue engineering in combination with stem cell transplantation and electric field/magnetic field stimulation.CONCLUSION: The optimal elements for tissue engineering are the key role in repairing spinal cord injury by tissue engineering.
ABSTRACT
@# Myelin of the adult mammalian central nervous system(CNS)has been attributed to affect nerve structural plasticity and suppress regeneration of nerve fibers.Nogo-A is possibly the best characterized of a variety of neurite growth inhibitors in CNS myelin.Neutralizing its activity results in improved axon regrowth and functional recovery in experimental spinal cord injury(SCI)models of animals.Nogo-A and its receptors,especially Nogo-66 receptor(NgR),p75 neurotrophin receptor(p75NTR),and LINGO-1 increasingly become the hot spot in the study of SCI repair,and have become the major targets for therapeutic intervention to promote axon regeneration after SCI.Inhibition of Nogo-A and its receptors NgR/p75NTR/LINGO-1 may be promote the regeneration of axon and maximize functional recovery after SCI.