Publications by authors named "Xiansi Zeng"

4 Publications

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Advances in stem cells transplantation for the therapy of Parkinson's disease.

Curr Stem Cell Res Ther 2021 Mar 9. Epub 2021 Mar 9.

College of Life Sciences, Huzhou University, Huzhou 313000. China.

Parkinson's disease (PD) is a common neurodegenerative disease and is a major culprit that harms the health of elderly people. The main pathological feature is the progressive loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain. The current mainstream therapeutic strategies include surgical treatment and medicine substitute therapy. However, these treatment methods sometime have limitations. Subsequently, the treatment with stem cells (SCs) transplantation has been gradually established. SCs is a kind of cell with self-renewal ability and multi-directional differentiation potential. Transplantation of SCs, including embryonic stem cells, adult stem cells (neural stem cells and mesenchymal stem cells) and induced pluripotent stem cells, have the ability to mediate nerve regeneration and restoration within the lesioned midbrain tissue, bringing hope for the treatment of PD. In this paper we summarize the progress in therapeutic strategies of different types of SCs in PD treatment, with an emphasis on the advantages and limitations.
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http://dx.doi.org/10.2174/1574888X16666210309153949DOI Listing
March 2021

The Potential Roles of Redox Enzymes in Alzheimer's Disease: Focus on Thioredoxin.

ASN Neuro 2021 Jan-Dec;13:1759091421994351

College of Life Sciences, Huzhou University, Huzhou, China.

Alzheimer's disease (AD) is the most common neurodegenerative diseases. Increasing studies have demonstrated the critical importance for redox proteins mediating neuronal protection in models of AD. This review briefly describes some of the risk factors contributing to AD, specifically highlighting the important roles of oxidative stress in the pathology of AD. Then this article concisely introduces the dysregulation and functions of two main redox enzymes, peroxiredoxins and glutaredoxins, in AD models. This review emphasizes the neuroprotective role of the third redox enzyme thioredoxin (Trx), an important multifunctional protein regulating cellular redox status. This commentary not only summarizes the alterations of Trx expression in AD patients and models, but also reviews the potential effects and mechanisms of Trx, Trx-related molecules and Trx-inducing compounds against AD. In conclusion, Trx has a potential neuroprotection in AD and may be very promising for clinical therapy of AD in the future.
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http://dx.doi.org/10.1177/1759091421994351DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7876756PMC
February 2021

Exploration of sensory and spinal neurons expressing gastrin-releasing peptide in itch and pain related behaviors.

Nat Commun 2020 03 13;11(1):1397. Epub 2020 Mar 13.

Center for the Study of Itch and Sensory Disorders, Washington University School of Medicine, St. Louis, MO, 63110, USA.

Gastrin-releasing peptide (GRP) functions as a neurotransmitter for non-histaminergic itch, but its site of action (sensory neurons vs spinal cord) remains controversial. To determine the role of GRP in sensory neurons, we generated a floxed Grp mouse line. We found that conditional knockout of Grp in sensory neurons results in attenuated non-histaminergic itch, without impairing histamine-induced itch. Using a Grp-Cre knock-in mouse line, we show that the upper epidermis of the skin is exclusively innervated by GRP fibers, whose activation via optogeneics and chemogenetics in the skin evokes itch- but not pain-related scratching or wiping behaviors. In contrast, intersectional genetic ablation of spinal Grp neurons does not affect itch nor pain transmission, demonstrating that spinal Grp neurons are dispensable for itch transmission. These data indicate that GRP is a neuropeptide in sensory neurons for non-histaminergic itch, and GRP sensory neurons are dedicated to itch transmission.
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http://dx.doi.org/10.1038/s41467-020-15230-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7070094PMC
March 2020

The decreased expression of thioredoxin-1 in brain of mice with experimental autoimmune myasthenia gravis.

Neuromuscul Disord 2014 Aug 13;24(8):726-35. Epub 2014 May 13.

Medical Faculty, Kunming University of Science and Technology, Kunming 650500, China. Electronic address:

Myasthenia gravis (MG) is an autoimmune disease caused by circulating antibodies that block acetylcholine receptor (AchR) at the neuromuscular junction. There is the cognitive and memory impairment in patients with MG. However, the molecular mechanisms underlying the alteration of central nervous system in MG remain unknown. In the present study, we found that the level of malondialdehyde (MDA) was increased in the brain of experimental autoimmune myasthenia gravis (EAMG). Furthermore, the expression of thioredoxin-1 (Trx-1) and the activity of cAMP response element-binding protein (CREB) were significantly decreased in frontal lobe and hippocampus of mice with EAMG. We also found that the expression of pro-apoptotic C/EBP homologous protein (CHOP) was increased in the frontal lobe and hippocampus of mice. However, the expressions of glucose regulated protein 78 (GRP78/Bip) was not changed in same areas. Inversely, the expressions of pro-caspase-12, pro-caspase-3 and pro-caspase-9 were decreased. These data indicate that Trx-1 mediated endoplasmic reticulum and mitochondria pathways are involved in brain damage in MG. Trx-1 may be a pivotal target for brain protective treatment in MG.
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http://dx.doi.org/10.1016/j.nmd.2014.05.001DOI Listing
August 2014