Publications by authors named "Hai-fei Zhang"

Background: Ghost cell odontogenic carcinoma (GCOC) is a rare malignancy characterized by the presence of ghost cells, preferably in the maxilla. Only slightly more than 50 case reports of GCOC have been documented to date. Due to the rarity of this tumor and its nonspecific clinical criteria, there is a heightened risk of misdiagnosis in clinical examination, imaging findings, and pathology interpretation.

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Objective: Studies have shown that Wuzi Yanzong Pill (WYP) can be used to treat neurological diseases, but its mechanisms for multiple sclerosis (MS) remain unclear. This study aims to determine the effect of WYP on MS in an animal model of experimental autoimmune encephalomyelitis (EAE), and explore its mechanism. To provide theoretical basis for the clinical treatment of MS with WYP.

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Parkinson's disease (PD) is a neurodegenerative disease characterized by the pathological loss of nigrostriatal dopaminergic neurons, which causes an insufficient release of dopamine (DA) and then induces motor and nonmotor symptoms. Hyperoside (HYP) is a lignan component with anti-inflammatory, antioxidant, and neuroprotective effects. In this study, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its active neurotoxic metabolite 1-methyl-4-phenylpyridinium ion (MPP) were used to induce dopaminergic neurodegeneration.

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Objective: To investigate the protective effects and its possible mechanism of Wuzi Yanzong Pill (WYP) on Parkinson's disease (PD) model mice.

Methods: Thirty-six C57BL/6 male mice were randomly assigned to 3 groups including normal, PD, and PD+WYP groups, 12 mice in each group. One week of intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to establish the classical PD model in mice.

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FSD-C10, a Fasudil derivative, was shown to reduce severity of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), through the modulation of the immune response and induction of neuroprotective molecules in the central nervous system (CNS). However, whether FSD-C10 can promote neuroregeneration remains unknown. In this study, we further analyzed the effect of FSD-C10 on neuroprotection and remyelination.

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Article Synopsis
  • - Bone marrow-derived mesenchymal stem cells (MSCs) are promising candidates for cellular therapy aimed at neuroprotection and neurorestoration, but optimizing their effectiveness and improving their surrounding environment remains challenging.
  • - In a study involving a mouse model of experimental autoimmune encephalomyelitis (EAE), the combination of MSCs and the drug Fasudil demonstrated a greater reduction in the severity of the condition compared to either treatment alone, suggesting a synergistic effect.
  • - The combination therapy reduced inflammatory signaling and increased levels of neurotrophic factors (BDNF and GDNF), indicating that MSCs and Fasudil together may enhance neuroprotective mechanisms, though further research is needed to understand their interaction in treating
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The ROCK signaling pathway is involved in numerous fundamental cellular functions such as cell migration, apoptosis, inflammatory responses, and neurite outgrowth. Previous studies demonstrate that Fasudil exhibited therapeutic potential of experimental autoimmune encephalomyelitis (EAE) possibly through immune-modulation and anti-inflammation. In this study, we observed the effect of Fasudil on synaptic protection of EAE mice.

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Viewing multiple sclerosis (MS) as both neuroinflammation and neurodegeneration has major implications for therapy, with neuroprotection and neurorepair needed in addition to controlling neuroinflammation in the central nervous system (CNS). While Fasudil, an inhibitor of Rho kinase (ROCK), is known to suppress experimental autoimmune encephalomyelitis (EAE), an animal model of MS, it relies on multiple, short-term injections, with a narrow safety window. In this study, we explored the therapeutic effect of a novel ROCK inhibitor FSD-C10, a Fasudil derivative, on EAE.

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Aim: To explore the therapeutic effect of Fasudil and its possible mechanisms in experimental autoimmune encephalomyelitis (EAE) mice, mainly focusing on the roles of microglia and astrocytes in the treatment.

Methods: Female adult C57BL/6 mice were immunized with MOG35-55 to induce chronic EAE. Fasudil was injected on day 3 p.

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Aim: The purpose of this investigation was to further explore the mechanism(s) underlying the amelioration in EAE caused by Fasudil, particularly focusing on anti-inflammatory effect.

Methods: We induced a chronic-progressive experimental autoimmune encephalomyelitis (EAE) in B6 mice immunized with myelin oligodendrocyte glycoprotein(35-55) and performed Fasudil intervention in early and late stages of the disease.

Results: The administration of Fasudil (40 mg/kg, i.

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Aim: To explore the effect of Fasudil on LPS-stimulated BV-2 microglia in inflammatory reaction and phenotype conversion.

Methods: The routinely cultured BV-2 microglia in vitro were divided into PBS control group, PBS plus Fasudil treatment group, LPS stimulation group and LPS plus Fasudil group. We determined the production of NO by Griess reaction, the level of TNF-α by ELISA, and analyzed the M1 and M2 phenotypes of microglia by flow cytometry.

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Aim: To examine the involvement of K(+) channels and endothelium in the vascular effects of magnesium lithospermate B (MLB), a hydrophilic active component of Salviae miltiorrhiza Radix.

Methods: Isolated rat mesenteric artery rings were employed to investigate the effects of MLB on KCl- or norepinephrine-induced contractions. Conventional whole-cell patch-clamp technique was used to study the effects of MLB on K(+) currents in single isolated mesenteric artery myocytes.

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The present paper investigates Raman spectral characters of 1-hexanol by the SiC anvil cell at the pressure of 163.4-793.4 MPa and the temperature of 25 degrees C.

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