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Background:
Pramipexole is the dopamine receptor agonist commonly used for treatment of PD, the effect of which on immunity played an important role in pathological process is also deserved to be further studied.
Aim of study:
We observed the effect of pramipexole on behavior and central nervous system (CNS) inflammatory cytokines of Parkinson's...
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Citations
... The concentrations of inflammatory cytokines were evaluated in brain tissues using an ELISA kit for interleukin 6 (IL-6) (BMS625), interleukin 10 (IL-10) (BMS629), and tumor necrosis factor-α (TNF-α) (BMS622), (Invitrogen, MI, USA). Tissue supernatants were removed, and cytokine concentrations were measured through a microplate reader (Molecular Devices, CA, USA) at 450 nm according to the manufacturer's guidelines and results were expressed as pg/mL (Jiang et al. 2021). ...
Penconazole (PEN) is a systemic triazole fungicide used to control various fungal diseases on grapes, stone fruits, cucurbits, and strawberries. Still, it leaves residues on treated crops after collection with many hazardous effects on population including neurotoxicity. Withania somnifera leaves extract (WSLE) is known for its memory and brain function enhancing ability. To evoke such action efficiently, WSLE bioactive metabolites are needed to cross the blood–brain barrier, that could limit the availability of such compounds to be localized within the brain. Therefore, in the present study, the association between PEN exposure and neurotoxicity was evaluated, and formulated WSLE nanoemulsion was investigated for improving the permeability of the plant extract across the blood–brain barrier. The rats were divided into five groups (n = 6). The control group was administered distilled water, group II was treated with W. somnifera leaves extract nanoemulsion (WSLE NE), group III received PEN, group IV received PEN and WSLE, and group V received PEN and WSLE NE. All rats were gavaged daily for 6 weeks. Characterization of compounds in WSLE using LC–MS/MS analysis was estimated. Neurobehavioral disorders were evaluated in all groups. Oxidative stress biomarkers, antioxidant enzyme activities, and inflammatory cytokines were measured in brain tissue. Furthermore, the gene expression patterns of GFAP, APP, vimentin, TGF-β1, Smad2 and Bax were measured. Histopathological changes and immunohistochemical expression in the peripheral sciatic nerve and cerebral cortex were evaluated. A total of 91 compounds of different chemo-types were detected and identified in WSLE in both ionization modes. Our data showed behavioral impairment in the PEN-treated group, with significant elevation of oxidative stress biomarkers, proinflammatory cytokines, neuronal damage, and apoptosis. In contrast, the PEN-treated group with WSLE NE showed marked improvement in behavioral performance and histopathological alteration with a significant increase in antioxidant enzyme activity and anti-inflammatory cytokines compared to the group administered WSLE alone. The PEN-treated group with WSLE NE in turn significantly downregulated the expression levels of GFAP, APP, vimentin, TGF-β1, Smad2 and Bax in brain tissue. In conclusion, WSLE NE markedly enhanced the permeability of plant extract constituents through the blood brain barrier to boost its neuroprotective effect against PEN-induced neurotoxicity.
... Clinical and preclinical studies have reported that food reward responses are sensitive to inflammatory mediators, suggesting an influence of pro-inflammatory cytokine profiles in reward perception. A positive correlation between increased proinflamatrory profile such as IL-6, TNF-a and IL-1b and defective reward responses has been previously reported in the context of monetary reward tasks (Eisenberger et al., 2010), pain related inflammation (Elvemo et al., 2015;Taylor et al., 2015), depression and aging (Felger et al., 2016;White et al., 2017), Crohn's disease, psoriasis, complex regional pain syndrome (Kappelmann et al., 2018) Parkinson's disease (Liu et al., 2000;Jiang et al., 2022), drug (Brown et al., 2018), alcohol exposure (Boyadjieva and Sarkar, 2010;Lacagnina et al., 2017) and psychostimulants abuse (Beardsley and Hauser; and also maternal motivation (Aubert et al., 1997). Notably, subjects diagnosed with a reduced reward responsiveness experience pain-related inflammation showed a reduced volume in the NAc (Elvemo et al., 2015; Taylor et al., 2015). ...
Accumulation of white adipose tissue (WAT) during obesity is associated with the development of chronic low-grade inflammation, a biological process known as lipoinflammation. Systemic and central lipoinflammation accumulates pro-inflammatory cytokines including IL-6, IL-1β and TNF-α in plasma and also in brain, disrupting neurometabolism and cognitive behavior. Obesity-mediated lipoinflammation has been reported in brain regions of the mesocorticolimbic reward circuit leading to alterations in the perception and consumption of ultra-processed foods. While still under investigation, lipoinflammation targets two major outcomes of the mesocorticolimbic circuit during food reward: perception and motivation ("Wanting") and the pleasurable feeling of feeding ("Liking"). This review will provide experimental and clinical evidence supporting the contribution of obesity- or overnutrition-related lipoinflammation affecting the mesocorticolimbic reward circuit and enhancing food reward responses. We will also address neuroanatomical targets of inflammatory profiles that modulate food reward responses during obesity and describe potential cellular and molecular mechanisms of overnutrition linked to addiction-like behavior favored by brain lipoinflammation.
... IL-6, IL-1β, and TNF-α concentrations were measured in brain homogenate as pg/ml at 450 nm by interpolation from a standard curve via a micro-plate ELISA reader (Sorin Biomedica SpA., Milan, Italy) with a detection limit from 31.3-2000 pg/ml, 31.3-2000 pg/ml, and 39.1-2500 pg/ml, respectively (Jiang et al. 2021). ...
Thiacloprid (TH) is a neurotoxic agricultural insecticide and potential food contaminant. The purpose of this study was to investigate the relationship between TH exposure and memory dysfunction in rats, as well as the potential protective efect of piracetam and piracetam-loaded magnetic chitosan nanoparticles (PMC NPs). Rats were divided into fve equal groups (six rats/group). The control group received saline. Group II was treated with PMC NPs at a dose level of 200 mg/kg body weight (Bwt); Group III was treated with 1/10 LD50 of TH (65 mg/kg Bwt); Group IV was treated with TH (65 mg/kg Bwt) and piracetam (200 mg/kg Bwt); Group V was co-treated with TH (65 mg/kg Bwt) and PMC NPs (200 mg/kg Bwt). All
animal groups were dosed daily for 6 weeks by oral gavage. Footprint analysis, hanging wire test, open feld test, and Y-maze test were employed to assess behavioral defcits. Animals were euthanized, and brain tissues were analyzed for oxidative stress biomarkers, proinfammatory cytokines, and gene expression levels of glial fbrillary acidic protein (GFAP), amyloid beta precursor protein (APP), B-cell lymphoma 2 (Bcl-2), and caspase-3. Brain and sciatic nerve tissues were used for the evaluation of histopathological changes and immunohistochemical expression of tau protein and nuclear factor kappa B (NF-κB), respectively. The results revealed that TH-treated rats sufered from oxidative damage and infammatory efect on
the central and peripheral nerves. The administration of PMC NPs considerably protected against TH-induced neuronal damage, increased antioxidant enzyme activity, decreased infammatory markers, and improved behavioral performance than the group treated with piracetam. The neuroprotective efect of PMC NPs was mediated through the inhibition of GFAP, APP, caspase-3, Tau, and NF-κB gene expression with induction of Bcl-2 expression. In conclusion, TH could induce oxidative stress, infammatory and neurobehavior impairment in rats. However, PMC NPs administration markedly mitigated TH induced brain toxicity, possibly via oxidative and infammatory modulation rather than using piracetam alone.
... This finding may relate to a significant decrease of amyloid deposits observed in the hippocampus of pramipexole treated animals, compared to those treated only with LPS [23]. In another study, pramipexole administration to mice with LPS-induced PD provided a behavioural improvement that was attributed to the concomitant reduction of mRNA expression, and hence of circulating levels, of proinflammatory cytokines, such as IL6 and tumor necrosis factor (TNF)α, in the nigrostriatal region [24]. ...
Parkinson’s disease (PD) is a common neurodegenerative disease characterized by loss of dopaminergic neurons and intraneuronal accumulation of protein aggregates. The exact mechanisms leading to neuronal death in PD are not fully understood, but several different molecular pathways are involved, leading to the concept that molecular subtypes may coexist in the nosological spectrum of PD. To this respect, immune system activation, both in the periphery and inside the central nervous system, was detected as a common trait of several pathogenic pathways of PD. The current working hypothesis implies that immune cells shift towards a proinflammatory phenotype and trigger the production of neurotoxic cytokines, ultimately contributing to neurodegeneration. While it is very important to understand how commonly used antiparkinson drugs interact with such changes, the search for treatments which may directly or indirectly modulate immune function is a great opportunity for disease modification.
Spinal cord injury (SCI) has emerged as a prevalent condition with limited effective treatment options. The neuroprotective role of pramipexole (PPX) in inhibiting nerve cell apoptosis in central nervous system injuries is well established. Therefore, we investigated the effects of PPX in SCI. Adult Sprague-Dawley rats were divided into four groups (sham, SCI, PPX-0.25, and PPX-2.0 groups) according to the PPX therapy ( n = 24). Then, SCI was induced using the modified Allen method, and PPX was intravenously administered into the tail at dosages of 0.25 or 2.0 mg/kg following the injury. Motor function was evaluated using the Rivlin-modified inclined plate apparatus and the Basso Beattie Bresnahan (BBB) workout scale. Western blotting assay was used to measure protein expression levels of DRD2, NeuN, Bax/Bcl-2, and caspase-3. Furthermore, immunohistochemistry assessed the effect of PPX on the quantity of NeuN-positive cells in the spinal cord tissue after SCI. Our findings revealed that the BBB and slanting board test scores of the PPX-treated model groups were considerably higher for the SCI group and significantly lower for the sham operation group ( P < 0.001). Moreover, the PPX-2.0 group exhibited significantly higher NeuN expression levels than the SCI group ( P < 0.01). Our findings indicate that PPX exerts a neuroprotective effect in secondary neuronal injury following SCI, facilitating the recovery of hind limb function by downregulating Bax/Bcl-2, caspase-3, and IL-1β.
