Monosialotetrahexosylganglioside Sodium Research Articles

Monosialotetrahexosylganglioside Sodium Promotes the Cortical Neurogenesis in Traumatic Brain Injury Rats

To explore the effect of monosialotetrahexosylganglioside sodium on cortical neurogenesis in traumatic brain injury rats. Thirty Sprague–Dawley rats were randomly divided into the control group, the saline group and the monosialotetrahexosylganglioside sodium group. The rats traumatic brain injury model of saline group and the monosialotetrahexosylganglioside sodium group, control group rats was prepared with hydraulic controllable injury device and control group received sham operation. The levels of oxidative stress, nerve damage, cortical new born neurons, learning and memory capabilities of rats were assessed with serum malondialdehyde and superoxide dismutase levels, serum neurofilament light level and terminal deoxynucleotidyl transferase dUTP nick end labeling, neuronal nuclear protein/ bromodeoxyuridine cells and Morris water maze respectively. Compared with the control group, the level of oxidative stress was significantly increased, the nerve damage was obvious, the number of new born neurons increased, and the ability of learning and memory decreased in the other two groups. Compared with the normal saline group, the oxidative stress level was lower, the nerve damage was reduced, the number of new born neurons increases more obviously and the decline in learning and memory ability was reduced in the monosialotetrahexosylganglioside sodium group. Monosialotetrahexosylganglioside sodium can reduce the oxidative stress level, protect the nerve cells from damage and promote the neurogenesis in the cortex and promote the improvement of cognitive functions such as learning and memory in traumatic brain injury rats.

Effect of Xingnaojing Injection in treatment of cerebral hemorrhage based on Tabu search algorithm:a real world study

In this study, Tabu search algorithm was used to analyze the effect of Xingnaojing Injection in the treatment of cerebral hemorrhage in the real world. Through the analysis of the results, the therapies based on the pathogeny of cerebral hemorrhage were screened out: Xingnaojing Injection+hemostatic drugs for promoting blood circulation and removing stasis. Cerebral hemorrhage complicated with brain edema: combined with mannitol or mannitol+aescin. The patients with relevant complications in the acute stage of cerebral hemorrhage could select according to the indications: ①Aminocycline+Oxiracetam+Piperacillin Sodium Sulbactam Sodium+Sodium Lactate Ringer; ②Aminocycline+Oxiracetam+Nifedipine+Captopril+Metoclopramide+Cimetidine; ③Insulin+Pantoprazole+So-dium Nitroprusside. The combined therapies for patients of the stable stage with complicating diseases could select according to the indications: ① Monosialotetrahexosyl Ganglioside Sodium+Deproteinized Calf Blood Serum+Nitroglycerin+Compound Potassium Dihydrogn Phosphate; ② Edaravone+Gangliosides+Captopril+Levofloxacin+Tanreqing Injection+Aminophylline. The analysis of subgroup module of drugs for promoting blood circulation and removing blood stasis suggested that the safety of traditional Chinese medicine should be paid attention to in the treatment of cerebral hemorrhage. This study was based on the data of the real world, but with some problems, such as lack of data and confounding factors. The summarized medication plan is only for the reference of clinicians. The clinical application shall be based on the specific situation of patients and the clinical benefits and risks, and pay attention to the incompatibility.

Diammonium glycyrrhizinate promotes the regeneration and repair of central nervous system in rats with severe traumatic brain injury by Wnt/β-catenin signaling pathway

To observe the effects of diammonium glycyrrhizinate (DG) on nerve regeneration repair in rats with severe traumatic brain injury (STBI) from the perspective of Wnt/β-catenin signaling pathway. Seventy-two Sprague-Dawle (SD) male rats were randomly divided into normal group, STBI model group, ganglioside (GA) treatment group and DG treatment group. The STBI animal model was reproduced referring to modified Feeney free fall impact model. No injury was made in normal group. Six hours after modeling, monosialotetrahexosylganglioside sodium injection and DG injection were injected via tail vein of rats in GA treatment group and DG treatment group respectively, once a day for 7 days. Normal group and STBI model group were given the same amount of normal saline. Six rats in each group were sacrificed on the 1st, 3rd and 7th day after the challenge for neurological severity score (NSS), and then the blood of abdominal aorta was drawn and brain tissue was harvested. The contents of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in serum were detected by enzyme linked immunosorbent assay (ELISA). The pathological changes of sub-granular zone (SGZ) were observed under light microscope after hematoxylin eosin (HE) staining. Real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the mRNA expressions of Wnt3a, β-catenin, glycogen synthetase kinase-3β (GSK-3β) and Axin. (1) There was no neurological deficit in the normal group and NSS was 0. NSS score of rats increased significantly on the first day after modeling, and then decreased gradually over time. NSS of the rats treated with GA and DG were significantly lower than that of the STBI model rats (score: 7.33±2.07, 6.17±2.23 vs. 9.33±1.63, both P < 0.01). Though NSS gradually decreased over time, the differences were still statistically significant on the 7th day (score: 2.67±0.82, 1.00±0.00 vs. 6.17±2.23, both P < 0.01), and NSS of DG treatment group was significantly lower than that of GA treatment group. (2) In SGZ of rats, cells were arranged in a compact and orderly way in the normal group, but neurons and tissues were damaged and destroyed at different time points in the STBI model group. After either GA or DG treatment, the damage of nerve tissue was improved gradually over time, and the effect of DG was more obvious. (3) In the normal group, the mRNA expressions of Wnt3a and β-catenin were almost not expressed, the mRNA expressions of GSK-3β and Axin were higher, and the contents of BDNF and NGF in serum were less. On the 1st day after STBI, the mRNA expressions of Wnt3a and β-catenin in hippocampus, the contents of BDNF and NGF in serum were significantly increased, and the mRNA expressions of GSK-3β and Axin were significantly decreased. The mRNA expressions of Wnt3a and β-catenin in the hippocampus and the contents of BDNF and NGF in serum were significantly higher than those in the model group 1 day after GA or DG was added, the mRNA expressions of GSK-3β and Axin were significantly decreased, and the effect of DG was more significant than that of GA [Wnt3a mRNA (2-ΔΔCt): 3.51±0.14 vs. 2.93±0.05, β-catenin mRNA (2-ΔΔCt): 1.90±0.08 vs. 1.75±0.04, BDNF (ng/L): 4.06±0.55 vs. 3.16±0.64, NGF (ng/L): 9.53±1.08 vs. 7.26±0.43, GSK-3β mRNA (2-ΔΔCt): 0.75±0.01 vs. 0.79±0.01, Axin mRNA (2-ΔΔCt): 0.74±0.02 vs. 0.76±0.02, all P < 0.05]. It was gradually increasing or decreasing over time and the difference was still statistically significant up to the 7th day. DG can promote the recovery of nerve function in rats with STBI, and its mechanism may be related to the regeneration of nerve cells proliferation and differentiation by Wnt/β-catenin signaling pathway and the reconstruction of nerve tissue in SGZ of hippocampus.

Clinical Characteristics of Intravenous Injection of Monosialotetrahexosyl Ganglioside Sodium-Related Guillain-Barre Syndrome.

Introduction: Guillain Barre Syndrome (GBS) is an acute inflammatory immune-mediated multiple nerve root neuropathy. GBS primarily damages the spinal nerve root and peripheral nerves, but can also affect the cranial nerves and cause acute demyelination. This study analyzed the clinical features of intravenous injection of monosialotetrahexosyl ganglioside sodium-related Guillain-Barre syndrome (GRD-GBS).Methods: We retrospectively studied 12 patients who developed GRD-GBS after receiving monosialotetrahexosyl ganglioside sodium treatment in association with recent trauma, surgery, acute cerebrovascular disease, or chronic peripheral neuropathy. Clinical characteristics, electrophysiological examinations, serum-specific antibodies, and prognosis were assessed. As controls, we selected 12 patients hospitalized with non-ganglioside-related (NGRD)-GBS.Results: The positive rate of the ganglioside antibody test was significantly higher in the GRD-GBS group (66.67%) than in the NGRD-GBS group (8.33%). CSF protein levels were similar between the groups, but the incidence of blood-nerve-barrier (BNB) disruption was higher in the GRD-GBS group. Patient scores for the Hughes Functional Grading Scale (HFGS), a disability scale, were higher (more severe disability) in the GRD-GBS group than in the NGRD-GBS group. The HFGS scores of the GRD-GBS group did not change between peak onset and 30 days after discharge, but did change significantly by 90 days after discharge, while scores were significantly lower at both 30 and 90 days after discharge in the NGRD-GBS group.Conclusions: GRD-GBS patients showed more severe clinical manifestations, poorer prognosis, and slower recovery than patients with NGRD-GBS. Ganglioside treatment should be used with extreme caution in patients with trauma that damages the BNB.

Protective effects of monosialotetrahexosylganglioside sodium on H2O2-induced human vascular endothelial cells.

Monosialotetrahexosylganglioside sodium (GM1) is widely used in the treatment of central and peripheral neurological injuries. In addition to its neuroprotective activity, GM1 exerts protective effects on brain microvascular endothelial cells, although the mechanisms underlying these effects remain unclear. The aim of the present study was to clarify the protective effects and underlying mechanisms of GM1 on human umbilical vein endothelial cells (HUVECs). In this study, hydrogen peroxide (H2O2) was applied to induce the HUVEC injury. HUVECs in a logarithmic growth phase were divided into five groups, namely the control, H2O2-treated, 10-mg/l GM1, 5-mg/l GM1 and 1-mg/l GM1 groups. In all the groups, cell proliferation was detected using a Cell Counting Kit-8 assay, a flow cytometric method was applied to analyze the cell cycle and nuclear factor (NF)-κB expression was evaluated using immunofluorescence analysis. In addition, the protein expression levels of NF-κB, phosphatidylinositol 3-kinase (PI3K) and glycogen synthase kinase (GSK)-3 were detected via western blot analysis. The results indicated that GM1 exerted significant protective effects on H2O2-injured cells by increasing the ratio of cells in the S/G2 phase. Furthermore, western blot analysis revealed that PI3K expression levels were markedly increased after 24 h, as a result of the GM1 treatment, while the expression of both GSK-3 markedly decreased. In addition, the ratio of nuclear-to-cytoplasmic NF-κB expression increased in the GM1-treated cells. In summary, GM1 exhibited marked protective effects on the HUVECs, possibly due to the ability of GM1 in maintaining the integrity of the endothelium and increasing the proportion of cells undergoing mitosis, a process in which the PI3K/GSK-3 and NF-κB pathways are crucially involved.