International Immunopharmacology, Journal Year: 2024, Volume and Issue: 139, P. 112699 - 112699
Published: July 17, 2024
Language: Английский
Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15
Published: Feb. 19, 2024
Introduction: Nephrotoxicity represents a major complication of using doxorubicin (DOX) in the management several types cancers. Increased oxidative stress and activation inflammatory mediators play outstanding roles development DOX-induced kidney damage. This study aimed to investigate whether two pathways incretin-based therapy, glucagon-like peptide-1 receptor agonist (presented as semaglutide, SEM) dipeptidyl peptidase-4 inhibitor alogliptin, ALO), differentially protect against nephrotoxicity rats clarify underlying molecular mechanisms. Methods: Adult male were divided into six groups: control (received vehicle), DOX (20 mg/kg, single I.P. on day 8), + ALO mg/kg/day, P.O. for 10 days), SEM (12 μg/kg/day, S.C. ALO-alone, SEM-alone groups. At end study, animals sacrificed their functions, stress, markers assessed. Kidney sections also subjected histopathological examinations. Results: The co-treatment with either or manifested an improvement evidenced by lower serum concentrations creatinine, urea, cystatin C compared group. Lower levels MDA, higher GSH, increased SOD activity observed ALO- SEM-treated groups than those administration resulted decreased renal expressions sirtuin 1 (SIRT1) Nrf2 NF-κB TNF-α expressions, these effects ameliorated treatment SEM. Discussion: Co-treatment showed renoprotective effect that was mediated antioxidant anti-inflammatory via SIRT1/Nrf2/NF-κB/TNF-α pathway. fact both therapy demonstrate equally positive alleviating damage is noteworthy.
Language: Английский
Citations
15
International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(9), P. 4972 - 4972
Published: May 2, 2024
Since we aim to test new options find medication for cognitive disorders, have begun assess the effect of semaglutide and conduct a review gathering studies that attempted this purpose. This systematic focuses on effects semaglutide, glucagon-like peptide 1 receptor agonist (GLP-1 RA), in context neurological impairment. Semaglutide, synthetic GLP-1 analog, showcased neuroprotective beyond metabolic regulation. It mitigated apoptosis improved dysfunction cerebrovascular disease, suggesting broader implications well-being. Also, highlighted RAs’ positive impact olfactory function obese individuals with type 2 diabetes, neurodegenerative multiple sclerosis, endotoxemia. In order analyze current function, literature search was conducted up February 2024 two online databases, MEDLINE (via PubMed) Web Science Core Collection, as well various websites. Fifteen mice populations cell lines were included, analyzed, assessed bias-specific tools. The anti-apoptotic properties its analogs emphasized, animal models line demonstrating enhanced function. While promising, limitations include fewer studies, highlighting need extensive research, particularly human population. Even though seems there are significant limitations, one which is lack subjects. Therefore, aims gather evidence.
Language: Английский
Citations
9
Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 7, 2025
Language: Английский
Citations
1
Inflammopharmacology, Journal Year: 2023, Volume and Issue: 32(2), P. 1499 - 1518
Published: Dec. 19, 2023
Abstract Multiple sclerosis (MS) is an incurable chronic neurodegenerative disease where autoimmunity, oxidative stress, and neuroinflammation collaboration predispose myelin sheath destruction. Interestingly, curcumin, a natural polyphenol, showed neuroprotective effect in numerous diseases, including MS. Nevertheless, the influence of curcumin against MS-induced cognitive impairment still vague. Hence, we induced experimental autoimmune encephalomyelitis (EAE) mice using spinal cord homogenate (SCH) complete Freund’s adjuvant, which eventually mimic This study aimed not only to evaluate efficacy EAE-induced motor dysfunction, but also explore novel mechanism action, by exerts its beneficial effects Curcumin (200 mg/kg/day) was evaluated behavioral tests, histopathological examination, biochemical tests. Concisely, amended impairments, as demonstrated tests examination hippocampus. activated adenosine monophosphate (AMP)-activated protein kinase/silent mating type information regulation 2 homolog 1 (AMPK/SIRT1) axis, triggered cyclic AMP response element-binding protein/brain-derived neurotrophic factor/myelin basic (CREB/BDNF/MBP) pathway, hindering demyelination corpus callosum. Furthermore, AMPK/SIRT1 activation augmented nuclear factor erythroid 2-related (Nrf2), powerful antioxidant, amending stress. Additionally, abolished inhibiting Janus kinase /signal transducers activators transcription 3 (JAK2/STAT3) various pathways, activation. JAK2/STAT3 inhibition halts inflammatory cytokines synthesis. In conclusion, curcumin’s EAE controlled, at least part, activation, ultimately minimizes neuronal demyelination, neuroinflammation. Graphical illustration putative molecular pathways implicated management curcumin. activates AMPK/SIRT1, turn multiple that hinder neurodegeneration, Moreover, conquers pathway JAK2/STAT3/NF-kβ.
Language: Английский
Citations
20
Current Issues in Molecular Biology, Journal Year: 2024, Volume and Issue: 46(6), P. 5929 - 5949
Published: June 13, 2024
Semaglutide (SEM), a glucagon-like peptide-1 receptor agonist, has garnered increasing interest for its potential therapeutic effects in neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s (PD). This review provides comprehensive description of SEM’s mechanism action preclinical studies these debilitating conditions. In animal models AD, SEM proved beneficial on multiple pathological hallmarks the disease. administration been associated with reductions amyloid-beta plaque deposition mitigation neuroinflammation. Moreover, treatment shown to ameliorate behavioral deficits related anxiety social interaction. SEM-treated animals exhibit improvements spatial learning memory retention tasks, evidenced by enhanced performance maze navigation tests novel object recognition assays. Similarly, PD, demonstrated promising neuroprotective through various mechanisms. These include modulation neuroinflammation, enhancement mitochondrial function, promotion neurogenesis. Additionally, improve motor function dopaminergic neuronal loss, offering disease-modifying strategies. Overall, accumulating evidence from suggests that holds promise approach AD PD. Further research is warranted elucidate underlying mechanisms translate findings into clinical applications devastating disorders.
Language: Английский
Citations
5
Behavioural Brain Research, Journal Year: 2024, Volume and Issue: unknown, P. 115280 - 115280
Published: Oct. 1, 2024
Language: Английский
Citations
5
Drug Development Research, Journal Year: 2023, Volume and Issue: 84(6), P. 1159 - 1174
Published: May 12, 2023
Growing evidence points to impaired autophagy as one of the major factors implicated in pathophysiology Parkinson's disease (PD). Autophagy is a downstream target adenosine monophosphate-activated protein kinase (AMPK). Inosine has already demonstrated neuroprotective effect against neuronal loss neurodegenerative diseases, mainly due its anti-inflammatory and antioxidant properties. We, herein, aimed at investigating effects inosine rotenone-induced PD rats focus on activation AMPK-mediated autophagy. successfully increased p-AMPK/AMPK ratio improved their motor performance muscular co-ordination (assessed by rotarod, open field, grip strength tests, well manual gait analysis). Furthermore, was able mitigate histopathological alterations restore tyrosine hydroxylase immunoreactivity rats' substantia nigra. Inosine-induced AMPK resulted an enhancement, striatal Unc-S1-like kinase1 beclin-1 expression, also increment light chain 3II 3I ratio, along with decline mammalian rapamycin p62 expressions. The inosine-induced stimulation attenuated apoptosis promoted activity. Unsurprisingly, these were antagonized preadministration dorsomorphin (an inhibitor). In conclusion, exerted via through restoration imbalance between apoptosis. These findings support potential application treatment.
Language: Английский
Citations
11
European Journal of Pharmacology, Journal Year: 2024, Volume and Issue: 982, P. 176929 - 176929
Published: Aug. 23, 2024
Language: Английский
Citations
4
Neural Regeneration Research, Journal Year: 2023, Volume and Issue: 19(8), P. 1671 - 1677
Published: Dec. 11, 2023
The glucagon-like peptide 1 is a pleiotropic hormone that has potent insulinotropic effects and key in treating metabolic diseases such as diabetes obesity. Glucagon-like exerts its by activating membrane receptor identified many tissues, including different brain regions. activates several signaling pathways related to neuroprotection, like the support of cell growth/survival, enhancement promotion synapse formation, autophagy, inhibition secretion proinflammatory cytokines, microglial activation, apoptosis during neural morphogenesis. glial cells, astrocytes microglia, maintain homeostasis defense against pathogens central nervous system. After insult, microglia are first cells respond, followed reactive astrocytosis. These activated produce mediators cytokines or chemokines react insult. Furthermore, under these circumstances, can become chronically inflammatory losing their homeostatic molecular signature and, consequently, functions diseases. Several processes promote development neurological disorders influence pathological evolution: formation protein aggregates, accumulation abnormally modified cellular constituents, release injured neurons synapses molecules dampen function, critical importance, dysregulation control mechanisms. agonist emerges tool brain-related pathologies, restoring conditions, modulating activity, decreasing response. This review summarizes recent advances linked anti-inflammatory properties activation multiple sclerosis, Alzheimer's disease, Parkinson's vascular dementia, chronic migraine.
Language: Английский
Citations
11
Frontiers in Neuroscience, Journal Year: 2025, Volume and Issue: 18
Published: Jan. 9, 2025
Acupoint catgut embedding (ACE) is a traditional Chinese medicine technique commonly used for managing various disorders, including chronic inflammatory pain and allergic asthma. Despite its growing use, the neuroimmunological mechanisms underlying ACE treatment effects remain unclear. This study investigated roles potential of in treating experimental autoimmune encephalomyelitis (EAE), frequently animal model neuroinflammation. The were evaluated by monitoring body weight EAE severity scores. Behavioral tests, histopathological analysis, ELISA, flow cytometry conducted to assess therapeutic efficacy ACE. RNA sequencing was performed uncover ACE-associated transcriptional signatures spinal cords mice. results validated through western blotting, qRT-PCR, immunofluorescence (IF) staining. In ACE-treated mice, disease significantly ameliorated, along with improvements anxiety-like behaviors reduced inflammation demyelination. restored immune imbalance mice decreasing Th17 Th1 cells, while increasing Treg cells peripheral organs reducing serum cytokine levels. revealed significant suppression genes pathways associated reactive microglial astrocytic activation, corroborated IF studies. Additionally, could suppress ERK JNK signaling at both protein These findings confirm protective role mitigating symptoms modulating activity regulating cytokines.
Language: Английский
Citations
0