Publications by authors named "Runnan Xu"

3 Publications

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Neuroprotective effect of magnesium supplementation on cerebral ischemic diseases.

Life Sci 2021 May 22;272:119257. Epub 2021 Feb 22.

College of Biotechnology, Guilin Medical University, Guilin, Guangxi 541100, China. Electronic address:

Ischemic encephalopathy is associated with a high mortality and rate of disability. The most common type of ischemic encephalopathy, ischemic stroke, is the second leading cause of death in the world. At present, the main treatment for ischemic stroke is to reopen blocked blood vessels. However, despite revascularization, many patients are not able to achieve good functional results. At the same time, the strict time window (<4.5 h) of thrombolytic therapy limits clinical application. Therefore, it is important to explore effective neuroprotective drugs for the treatment of ischemic stroke. Magnesium is a natural calcium antagonist, which exerts neuroprotective effects through various mechanisms. However, while most basic studies have shown that magnesium supplementation can help treat cerebral ischemia, intravenous magnesium supplementation in large clinical trials has failed to improve prognosis of ischemic patients. Therefore, we review the basic and clinical studies of magnesium supplementation for cerebral ischemia. According to the route of administration, treatment can be divided into intraperitoneal magnesium supplementation, intravenous magnesium supplementation, arterial magnesium supplementation and intracranial magnesium supplementation. We also summarized the potential influencing factors of magnesium ion intervention in cerebral ischemia injury. Finally, in combination with influencing factors derived from basic research, this article proposes three future research directions, including magnesium supplementation into the circulatory system combined with magnesium supplementation in the lateral ventricle, magnesium supplementation in the lateral ventricle combined with hypothermia therapy, and lateral ventricle magnesium supplementation combined with intracarotid magnesium supplementation combined with selective hypothermia.
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May 2021

The Expression of GLAST and GLT1 in a Transient Cerebral Ischemia Mongolian Gerbil Model.

Neuropsychiatr Dis Treat 2020 23;16:789-800. Epub 2020 Mar 23.

Department of Guangxi Key Laboratory of Brain and Cognitive Neuroscience, Guilin Medical University, Guilin, Guangxi 541004, People's Republic of China.

Purpose: Excitatory amino acid transporters (EAATs) have an indispensable function in the reuptake of extracellular glutamate. To investigate the relationship and the expression of neuronal and astrocytic markers after brain ischemia, the temporal profile of glial EAATs in both peripheral and core regions of the cortex was examined.

Methods: Transient common carotid artery occlusion was used to induce unilateral transient forebrain ischemia of Mongolian gerbils, and post-ischemic brains (6 h to 2 w) were collected and prepared for immunohistochemical and Western blotting analysis of glutamine synthetase (GS), GLT-1, GLAST, S100β, and NeuN, and for Alizarin red staining of calcium deposits.

Results: The expression of GLAST and GLT-1 were significantly escalated at 6 h both in the core and periphery regions, while reduced from 12 h to 2 w in the core region post-ischemia. GS-positive cells increased at 6 h both in the core and periphery regions, while the density of Alizarin red-positive cells increased and peaked at 12 h in the ischemic cortex. The density of S100β-positive cells decreased in the ischemic core and increased in the periphery region. Immunofluorescence staining showed that S100β and TUNEL double-positive cells increased at 12 h in the core region.

Conclusion: The results of GLT-1 and GLAST expression in the cortex indicate that their up-regulation was time-dependent and occurred in the acute post-ischemia period, whereas their down-regulation was region-dependent and it is involved in the pathological progress of nerve cell and glial cell death, and has a series of cascade reactions.
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March 2020

Treatment Of Magnesium-L-Threonate Elevates The Magnesium Level In The Cerebrospinal Fluid And Attenuates Motor Deficits And Dopamine Neuron Loss In A Mouse Model Of Parkinson's disease.

Neuropsychiatr Dis Treat 2019 11;15:3143-3153. Epub 2019 Nov 11.

Department of Guangxi Key Laboratory of Brain and Cognitive Neuroscience, Guilin Medical University, Guilin 541004, Guangxi, People's Republic of China.

Purpose: Epidemiology research has demonstrated that magnesium (Mg) deficiency is associated with a high incidence of Parkinson's disease (PD). It is known that the systemic administration of MgSO is not able to elevate the Mg concentration in cerebrospinal fluid (CSF). This study aims to verify the protective effect of magnesium-L-threonate (MgT) in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) mouse model.

Methods: C57BL/6J mice were orally administered MgT or MgSO for 4 weeks, and received MPTP in the third week. After analysis of open-field and rotarod tests on the last day, tyrosine hydroxylase (TH) immunopositive cells and protein levels were quantified in the substantia nigra pars compacta (SNpc) and striatum. The expression of inducible nitric oxide synthase (iNOS) level was evaluated. Mg concentration in serum and CSF was measured after oral administration of MgSO or MgT in normal mice. Mg concentration in the CSF was increased in the mice treated with MgT but not MgSO.

Results: The total distance and mean speed in open-field tests, and the time spent on rotarod in the MgT group were increased, compared with MPTP group. The MgT treatment but not MgSO dose-dependently attenuated the loss of TH-positive neurons, and the reduction of the TH expression in the SNpc. The MgT treatment also inhibited the expression of iNOS as measured by immunohistochemistry and Western blots. Double-immunofluorescence staining of TH and iNOS showed iNOS-positive cells were collocalized for TH-positive cells.

Conclusion: The treatment with MgT is associated with an increase of Mg in the CSF. MgT, rather than MgSO4, can significantly attenuate MPTP-induced motor deficits and dopamine (DA) neuron loss.
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November 2019