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Abstract
Lithium (Li+) ion due to its excellent bioactivity is one of the most well-studied element in bone-tissue engineering. In this study, we fabricated nanohydroxyapatite (nHAp) doped with Li+ ions (5?mol% Li+:nHAp) and co-doped with lanthanide ions. We investigated the effects of nHAp, 5?mol% Li+:nHAp or Li+ alone, on osteogenic differentiation of human Adipose Tissue-derived Stem Cells (hASCs), their proliferation, mitochondrial dynamics and apoptosis. Moreover, we monitored cell proliferation after treatment with samarium (III) (Sm3+) and europium (III) (Eu3+) ions co-doped 5?mol% Li+:nHAp as well as their luminescent property. The hASCs treated with 5?mol% Li+:nHAp and Li+ ions proliferated more rapidly and differentiated effectively than control cells without undergoing apoptosis. Both, 5?mol% Li+:nHAp and Li+ ions improved osteogenic differentiation of hASCs. Moreover they decreased expression of glycogen synthase kinase 3β (GSK3β) while increased β-catenin mRNA level. In addition, Li+, nHAp and 5?mol% Li+:nHAp improved mitochondrial dynamics and enhanced expression of neural differentiation marker genes. Collectively, the study indicates on pro-osteogenic and anti-apoptotic properties of nHAp doped with Li+ and Li+ alone. Moreover, unique properties of 5?mol% Li+:nHAp and 5?mol% Li+:nHAp co-doped with rare earth ions, such as Sm3+ and Eu3+ have shed a promising light on their potential application in theranostics.
Abstract
Epilepsy is one of the most well-known neurological conditions worldwide. One-third of adult epileptic patients do not respond to antiepileptic drugs or surgical treatment and therefore suffer from the resistant type of epilepsy. Stem cells have been given substantial consideration in the field of epilepsy therapeutics. The implication of pathologic vascular response in sustained seizures and the eminent role of endothelial progenitor cells (EPCs) in maintaining vascular integrity tempted us to investigate the potential therapeutic effects of EPCs in a pentylenetetrazole (PTZ)-induced rat model of epilepsy. Modulation of autophagy, a process that enables neurons to maintain an equilibrium of synthesis, degradation and subsequent reprocessing of cellular components, has been targeted. Intravenously administered EPCs homed into the hippocampus and amended the deficits in memory and locomotor activity. The cells mitigated neurological damage and the associated histopathological alterations and boosted the expression of brain-derived neurotrophic factor. EPCs corrected the perturbations in neurotransmitter activity and enhanced the expression of the downregulated autophagy proteins light chain protein-3 (LC-3), beclin-1, and autophagy-related gene-7 (ATG-7). Generally, these effects were comparable to those achieved by the reference antiepileptic drug, valproic acid. In conclusion, EPCs may confer therapeutic effects against epilepsy and its associated behavioural and biochemical abnormalities at least in part via the upregulation of autophagy. The study warrants further research in experimental and clinical settings to verify the prospect of using EPCs as a valid therapeutic strategy in patients with epilepsy.
Abstract
Background
Major
symptoms of chronic obstructive pulmonary disease (COPD) are chronic
bronchitis and emphysema leading from lung tissue destruction, that is
an effect of an imbalance between metalloproteinases (MMPs) and their
tissue inhibitors activity. As potential factor involved in this COPD
pathogenesis, MMP-12 is considered. We investigated the role of genetic
polymorphism and protein level of MMP-12 in the COPD development among
Poles.
Methods
We
analyzed ??82 A?>?G SNP in the promoter region of MMP-12 gene
(rs2276109) among 335 smoked COPD patients and 309 healthy individuals,
including 110 smokers. Additionally, 60 COPD patients and 61 controls
(23 smokers) were tested for serum levels of MMP-12 using ELISA. All
subjects were analyzed for lung function using spirometry (FEV1% and FEV1/FVC parameters).
Results
We
observed that -82G allele and -82GG homozygous genotype frequencies of
the SNP rs2276109 were significantly lower in COPD patients than in
controls (12.5% vs 16.9%, respectively; X2?=?4.742, p?=?0.02 for allele and 0.5% vs 3.9%, respectively; X2?=?9.0331,
p?=?0.01 for genotype). Moreover, -82G allele was more frequent in
controls smokers than in non-smokers (22.3% vs 14.1%, X2?=?6.7588,
p?=?0.01). Serum level of MMP-12 was significantly higher in COPD
patients than in controls groups (6.8?ng/ml vs 3.3?ng/ml, respectively;
F?=?7.433, p?<?0.0001), although independently of analyzed gene
polymorphisms. Additionally, no correlation between parameters of lung
function (FEV1% and FEV1/FVC) and protein level was found.
Conclusions
We
found that -82G allele of SNP rs2276109 was associated with reduced
risk of COPD, and COPD patients released more MMP-12 than healthy
individuals, but independently on this SNP.
Keywords
COPD Metalloproteinase 12 Genetics SNP ELISA
Abstract
Evidence indicates that adverse experiences in early life may be a factor for immune disturbances leading to the depression in adulthood. Recently, a pivotal role in the pathogenesis of depression has been assigned to the activation of the brain Nod-like receptor pyrin-containing 3 (NLRP3) inflammasome. We investigated the impact of chronic treatment with antidepressant drugs on the behavioral disturbances and the levels of proinflammatory factors in the hippocampus and frontal cortex of adult male rats after prenatal stress exposure. Next, we explored the involvement of the NLRP3 inflammasome-related pathways in the mechanism of antidepressant action. Our study confirmed that chronic antidepressant treatment attenuated depression-like disturbances and exerted an anxiolytic action. All antidepressants diminished the prenatal stress-induced increase in IL-1beta in both brain areas, while IL-18 only in the hippocampus. Moreover, tianeptine administration diminished the increase in CCR2 levels in both brain areas, while in the hippocampus, tianeptine, along with venlafaxine CCL2 and iNOS levels. Next, we observed that in the hippocampus, tianeptine and fluoxetine suppressed upregulation of TLR4. Furthermore, venlafaxine suppressed NFkB p65-subunit phosphorylation, while fluoxetine enhanced the IкB level. Importantly, in the hippocampus, all antidepressants normalized evoked by stress changes in caspase-1 level, while tianeptine and venlafaxine also affect the levels of ASC and NLRP3 subunits. Our results provide new evidence that chronic administration of antidepressants exerts anti-inflammatory effects more pronounced in the hippocampus, through suppression of the NLRP3 inflammasome activation. These effects are accompanied by an improvement in the behavioral dysfunctions evoked by prenatal stress.
Abstract
Objective
The
combination of pharmacological hypothermia - dihydrocapsaicin (DHC) and
intra-arterial regional cooling infusions (RCI) was found to enhance
the efficiency of hypothermia and efficacy of hypothermia-induced
neuroprotection in acute ischemic stroke. The aim of this study was to
explore whether the combination could induce a long-term neuroprotective
effects, as well as the underlying mechanism.
Methods
Sprague-Dawley
rats were subjected to middle cerebral artery occlusion (MCAO) for 2?h
using intraluminal hollow filament. The ischemic rats were randomized to
receive pharmacological hypothermia by intraperitoneal (i.p.) injection
of DHC, physical hypothermia by RCI of 6?ml cold saline (4℃), the
combination, and no treatment. Over a 21-day period, brain damage was
determined by infarct volume with MRI, and neurological deficit with
grid-walking and beam balance tests. Blood brain barrier (BBB) was
assessed by Evans-Blue (EB) contents. Inflammatory cytokines were
determined in peri-infarct area by antibody array and ELISA.
Results
The combination of DHC and RCI reduced (p?
Conclusions
The
combination approach enhanced the efficacy of hypothermia-induced
neuroprotection following ischemic stroke. Our findings provide a hint
to translate the combination method from bench to bedside.
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