جستجوی مقالات مرتبط با کلیدواژه "microglia" در نشریات گروه "پزشکی"

Macrophages and glial activation contribute to the pathophysiology of spinal cord injury (SCI). Some preclinical studies have shown the anti-inflammatory effects of aripiprazole (ARP). In the current study, we evaluated the anti-inflammatory effects of ARP in a rat SCI model. Forty male Wistar rats underwent either T9 vertebra laminectomy or were used as a sham-operated group without laminectomy. There were four major groups in this study: a sham-operated, three treatments (normal saline [vehicle] control versus ARP 10 and 20 mg/kg/day for three days after surgery, first dose 30 minutes post-surgery) SCI groups. We evaluated locomotor scaling and neuropathic pain behavioral tests over 28 days. On Day 28, tissue samples were investigated for neuroinflammatory and histopathology changes through flow cytometry and ELISA. ARP (10 and 20 mg/kg/day, 3 days) treatment significantly reduced locomotors disability (P<0.01) and mechanical (P<0.01) and thermal allodynia (P<0.001) scores. Additionally, Levels of tumor necrosis factor (TNF)-α level and interleukin (IL)-10 were significantly altered in ARP-treated spinal cord tissues 28 days after SCI (P<0.01). Moreover, spinal cord tissue expression of M1 and M2 macrophages, as well as M1/M2 ratio, were reduced in ARP-treated SCI animals, concurrent with decreased M1 and increased M2 and M1/M2 in dorsal root ganglion (P<0.001). Our study indicates that ARP has therapeutic effects on SCI via the reduction of neuroinflammation and SCI sensory and locomotor abnormalities.

Ecstasy is a popular recreational psychostimulant with side effects on the central nervous system. This study examined the corpus striatum tissue of adult rats that received ecstasy during the embryonic period for histological and molecular studies.

Rats were divided into control and ecstasy groups. The ecstasy group was given MDMA 15 mg/kg intraperitoneally twice daily at 8-hour intervals on days 7–15 of gestation. At the age of 15 weeks, adult offspring of both groups were examined for learning and memory study by the Morris water maze test. Then, ventral striatum tissue was harvested for TUNEL assay, Nissl staining, and real-time PCR for the expression of the GFAP and CD11b. 

Ecstasy up-regulated the GFAP and CD11b expression in the striatum of offspring (*P˂0.05). Furthermore, the Morris water maze test showed that exposure to ecstasy significantly impaired learning and spatial memory (*P˂0.05). TUNEL assay results did not show any significant change in the number of apoptotic cells in the striatum tissue of ecstasy offspring compared with controls, while Nissl staining showed a significant decrease in the number of neurons in the ecstasy group (*P˂0.05).

Exposure to ecstasy during pregnancy causes long-lasting changes in brain regions underlying learning and memory, including the striatum, and impaired working memory in the offspring. In addition, these data provide the first evidence that exposure to ecstasy during the embryonic period causes a persistent change in the activity of microglial cells and the number of astrocyte cells in the striatum.

To elucidate the mechanism of Respiratory Syncytial Virus (RSV) infection and central neuronal disease and to understand the role of microglia in neuronal injuries during RSV infection.

The effects of RSV and the cytokines produced by RSV-infected CHME-5 microglial cells on SY5Y neuronal cells were evaluated based on an in vitro Transwell coculture system. Five treatment groups were established in this study, including the normal control SY5Y group, RSV+SY5Y infection group, (cytokine+CHME-5)+SY5Y Transwell group, (RSV+CHME-5)+SY5Y Transwell group, and (RSV+cytokine+CHME-5)+SY5Y Transwell group. The morphological and physical alterations in SY5Y cells and their synapses were analyzed by confocal microscopy. The mRNA and protein expression levels of TLR3/RIG-I, as well as the expression of Hv1, in microglia were measured by qRT-PCR and Western blot assays. In addition, the apoptosis ratio of neuronal cells was determined by flow cytometry.

RSV infection activated the protein expression of Hv1 protein in microglia in vitro (p <0.05), induced morphological changes in SY5Y cells, lengthened synapses (73.36±0.12 μm vs 38.10±0.11 μm), simultaneously activated TLR3 and RIG-I protein expression (p <0.05), upregulated the secretion of the inflammatory cytokines TNF-α, IL-6, and IL-8 (p <0.01), and increased the apoptosis rate of SY5Y cells (p <0.01).

The results demonstrate that RSV infection of microglia can induce SY5Y neuronal cell injury and stimulate apoptosis through inflammatory cytokine release.

Microglia, small glial cells, i.e. mesodermal in origin and found in the brain and spinal cord, play a key role in the maintenance of neurons and immune defense. Haloperidol, an antipsychotic drug, is used to treat numerous neurological and neurodegenerative disorders. Its mechanism is not understood; however, haloperidol may result in Wnt signaling pathway activation. This study aimed to activate the Wnt signaling pathway using haloperidol and determining the effect of GSK3 inhibition on the expression of TGFB, NT-3, and BDNF genes in cultured rat microglia. 

Microglia isolation was conducted, and the immunohistochemistry technique was performed to confirm microglia purity. The RNA extraction was followed by cDNA synthesis. Real-time RT-PCR was used to evaluate any significant changes in the expression level of these genes. 

The three gene expressions in microglia were proportional to the different concentrations of the drug. More concentration of drugs resulted in higher levels of expression of these genes. Besides, the haloperidol did not affect the expression of the beta-actin gene as the reference gene. 

The obtained results supported the beneficial use of haloperidol in targeted microglia therapy. This study can be a breakthrough in neurology research.

The pathophysiology of neurodegenerative diseases is complicated, in which inflammatory reactions play a vital role. Microglia cells activation, an essential process of neuroinflammation, can produce neurotoxic molecules and neurotrophic factors, which aggravate inflammation and neuronal injury. Monascin, a major component of red yeast rice, is an azaphilonoid pigment with potential anti-inflammatory effects; however, the effects in central nervous system have not been evaluated. Our goal in this project was to explore the therapeutic effect and the underlying mechanism of Monascin, which may be via anti-inflammatory action.

We used lipopolysaccharide to induce BV-2 microglial cells in order to form an inflammation model in vitro. The anti-inflammatory effects of Monascin were measured by enzyme-linked immunosorbent assay (ELISA), real time-polymerase chain reaction (RT-PCR), Western Blot and Immunofluorescent staining.

Our data indicated that inflammatory cytokines including interleukin-1β (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α) and nitric oxide were suppressed by Monascin treatment. Furthermore, the related pro-inflammatory genes were inhibited consistent with the results of ELISA assay. Western blotting results showed that the phosphorylation of nuclear factor kappa B (NF-κB/p65) was reduced by Monascin treatment may be through suppressing the activation of IκB. Furthermore, immunofluorescence staining showed that the translocation of NF-κB/p65 to the cellular nuclear was blockaded after Monascin treatment.

Taken together, Monascin exerts anti-inflammatory effect and suppressed microglia activation, which suggested its potential therapeutic effect for inflammation-related diseases.