[Impacts of invasion on the benthic food web in the Yellow River Delta during autumn].

was introduced into the Yellow River Delta (YRD) in 1990 with the purpose of shore protection and siltation accretion. However, it spread rapidly and became a severe threat to the local coastal wetland ecosystem. To assess the impacts of invasion on the benthic food web, we sampled the potential food sources of macrobenthos in November 2020, analyzed the trophic level and the benthic food web structure based on stable isotope technique.

Nasal delivery of Fasudil-modified immune cells exhibits therapeutic potential in experimental autoimmune encephalomyelitis.

Aim: Multiple sclerosis (MS) is a relapsing-remitting inflammatory demyelinating disease that requires long-term treatment. Although Rho kinase inhibitor Fasudil shows good therapeutic effect in experimental autoimmune encephalomyelitis (EAE), an animal model of MS, certain side effects may limit its clinical use. This study aimed at observing the therapeutic potential of Fasudil-modified encephalitogenic mononuclear cells (MNCs) via nasal delivery in EAE and exploring possible mechanisms of action.

Therapeutic effect of Rho kinase inhibitor FSD-C10 in a mouse model of Alzheimer's disease.

Fasudil, a Rho kinase (ROCK) inhibitor, effectively inhibits disease severity in a mouse model of Alzheimer's disease (AD). However, given its significant limitations, including a relatively narrow safety window and poor oral bioavailability, Fasudil is not suitable for long-term use. Thus, screening for ROCK inhibitor(s) that are more efficient, safer, can be used orally and suitable for long-term use in the treatment of neurodegenerative disorders is required.

Multitarget Therapeutic Effect of Fasudil in APP/PS1transgenic Mice.

Introduction: Therapeutic strategies targeting Alzheimer's disease-related molecule β- amyloid (Aβ), Tau protein and β-site amyloid precursor protein cleaving enzyme (BACE) have been recently explored. However, the treatment effect for single target is not ideal. Based on multiaspect roles of Rho kinase inhibitor Fasudil on neuroprotection, neurorepair and immunomodulation, we observed therapeutic potential of Fasudil and explored possible mechanisms in amyloid precursor protein/ presenilin-1 transgenic (APP/PS1 Tg) mice, an animal model of Alzheimer's disease.

Safflower Yellow regulates microglial polarization and inhibits inflammatory response in LPS-stimulated Bv2 cells.

Activated microglia, especially polarized M1 cells, produce pro-inflammatory cytokines and free radicals, thereby contributing directly to neuroinflammation and various brain disorders. Given that excessive or chronic neuroinflammation within the central nervous system (CNS) exacerbates neuronal damage, molecules that modulate neuroinflammation are candidates as neuroprotective agents. In this study, we provide evidence that Safflor yellow (SY), the main active component in the traditional Chinese medicine safflower, modulates inflammatory responses by acting directly on BV2 microglia.

Role of Rho Kinase and Fasudil on Synaptic Plasticity in Multiple Sclerosis.

In addition to myelin loss and oligodendrocyte injury, axonal damage is a major cause of irreversible neurological disability in multiple sclerosis (MS). A series of studies have demonstrated that Rho kinase (ROCK) is involved in synaptic plasticity of neurons. Here, we found that ROCK activity in MS serum was elevated compared with serum from healthy controls.

FSD-C10: A more promising novel ROCK inhibitor than Fasudil for treatment of CNS autoimmunity.

Rho-Rho kinase (Rho-ROCK) triggers an intracellular signalling cascade that regulates cell survival, death, adhesion, migration, neurite outgrowth and retraction and influences the generation and development of several neurological disorders. Although Fasudil, a ROCK inhibitor, effectively suppressed encephalomyelitis (EAE), certain side effects may limit its clinical use. A novel and efficient ROCK inhibitor, FSD-C10, has been explored.

Lipoic acid protects dopaminergic neurons in LPS-induced Parkinson's disease model.

Parkinson's disease (PD) is a chronic neurodegenerative disease of the central nervous system (CNS), characterized by a loss of dopaminergic neurons, which is thought to be caused by both genetic and environmental factors. Recent findings suggest that neuroinflammation may be a pathogenic factor in the onset and progression of sporadic PD. Here we explore the potential therapeutic effect of lipoic acid (LA) on a lipolysaccharide (LPS)-induced inflammatory PD model.

Fasudil mediates cell therapy of EAE by immunomodulating encephalomyelitic T cells and macrophages.

Although Fasudil has shown therapeutic potential in EAE mice, the mechanism of action are still not fully understood. Here, we examined the immunomodulatory effect of Fasudil on encephalitogenic mononuclear cells (MNCs), and tested the therapeutic potential of Fasudil-treated MNCs in active EAE. Fasudil inhibited expression of CCL20 on T cells and migration of T cells, decreased CD4(+) IFN-γ(+) and CD4(+) IL-17(+) T cells, but increased CD4(+) IL-10(+) and CD4(+) TGF-β(+) T cells.

The therapeutic potential of Rho kinase inhibitor fasudil derivative FaD-1 in experimental autoimmune encephalomyelitis.

Although therapeutic potential of fasudil in EAE is promising, action mechanism and clinical limitations are still not fully understood and resolved. In this study, we observed the therapeutic potential of a novel Rho kinase (ROCK) inhibitor FaD-1, a fasudil derivative, and explored possible mechanism in MOG35-55-induced EAE. Experimental autoimmune encephalomyelitis (EAE) was induced by myelin oligodendrocyte glycoprotein (MOG35-55) immunization.

The inhibition of Rho kinase blocks cell migration and accumulation possibly by challenging inflammatory cytokines and chemokines on astrocytes.

Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune diseases characterized by the immune-mediated demyelination and neurodegeneration of the CNS. Our previous studies showed that Rho kinase inhibitor Fasudil can delay onset, and ameliorate severity of EAE, accompanied by the improvement in myelination and the inhibition of inflammatory responses in the CNS. In this study, we found that Fasudil inhibited the migration of T cells indirectly by affecting the production of inflammatory factors and the expression of chemokines in astrocytes functions, indicating that Fasudil treatment reduced inflammatory cytokines such as TNF-α and IL-6, reactive oxygen species (NO) and chemokines like MIP-3α (CCL-20), RANTES (CCL5), MIP-1α (CCL-3) and MCP-1 (CCL2) in vitro, and blocked the chemotaxis of reactive mononuclear cells in EAE mice.

Intranasal delivery of FSD-C10, a novel Rho kinase inhibitor, exhibits therapeutic potential in experimental autoimmune encephalomyelitis.

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.

[The extraction technology of epigoitri from isatidis radix by supercritical CO2 fluid].

Objective: To study the extraction technology of epigoitri from Isatidis Radix by supercritical CO2 fluid.

Methods: The effects of pressure, temperature, time, concentration and dosage of alcohol were studied by single factor analysis and orthogonal test.

Results: The optimized conditions were as follows: The pressure was 20 MPs, the temperature was 50 degrees C, the time was 2 h, concentration of alcohol was 100%, dosage was 80 mL.

[Effect of Fasudil on miroglia and astrocytes in experimental autoimmune encephalomyelitis mice].

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.

Fasudil ameliorates disease progression in experimental autoimmune encephalomyelitis, acting possibly through antiinflammatory effect.

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.

[Effect of Fasudil on the phenotype conversion of LPS-stimulated BV-2 microglia].

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.

[Prokaryotic expression of LMoV CP gene and preparation of its antiserum].

Objective: To prepare antiserum against the CP of Lilg mottle virus (LMoV).

Methods: Specific primer was designed according to Genbank to amplify CP gene of LMoV of Fritillaria thumbergii and its sequence was analyzed. Then the CP gene was inserted into pSBET and expressed in Escherichia coli BL21 (DE3) plys E strain.