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1.
Plant Physiol Biochem ; 192: 129-140, 2022 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-36228444

RESUMEN

Stripe rust instigated by Puccinia striiformis f. sp. tritici causes major yield loss in wheat. In this study, disease resistance was induced in wheat by pre-activation of pathogenesis related (PR) genes using two different nano-formulations (NFs) i.e. Chitosan- Salicylic acid (SA) NFs (CH-NFs) and Zinc sulphate NFs (Zn-NFs). These NFs were synthesized using green approach and were characterized using various techniques. Both NFs effectively controlled stripe rust in wheat genotypes (WH 711 and WH 1123) by significantly increasing activities of phenylalanine ammonia lyase, tyrosine ammonia lyase and polyphenol oxidase enzymes when compared with disease free-control and diseased plants. Total soluble sugar (TSS) level was highest in CH-NF treated plants. TSS was also relatively higher in diseased plants than disease free-control as well as Zn-NF treated plants. Both CH-NFs and Zn-NFs induced the expression of PR genes. In CH-NF treated plants, the relative expression of PR genes was higher on the 3rd day after spraying (DAS) of NFs as compared to diseased and Zn-NF treated plants in both the genotypes. While in case of Zn-NF treated plants, relative expression of PR genes was higher on 5th DAS as compared to diseased and disease free-control plants. Early rise in expression of PR genes due to NF treatments was responsible for disease resistance in both the wheat genotypes as evidenced by a lower average coefficient of infection. These NFs can be synthesized easily with low cost input, are eco-friendly and can be effectively used against yellow rust as well as other wheat diseases.

2.
Pharmaceutics ; 14(6)2022 May 25.
Artículo en Inglés | MEDLINE | ID: mdl-35745697

RESUMEN

Excitotoxicity is a type of neurodegenerative disorder. It caused by excessive glutamate receptor activation, which leads to neuronal malfunction and fatality. The N-methyl-D-aspartate (NMDA) receptors are found in glutamatergic neurons, and their excessive activation is primarily responsible for excitotoxicity. They are activated by both glutamate binding and postsynaptic depolarization, facilitating Ca2+ entry upon activation. Therefore, they are now widely acknowledged as being essential targets for excitotoxicity issues. Molecular docking and molecular dynamics (MD) simulation analyses have demonstrated that nobiletin efficiently targets the binding pocket of the NMDA receptor protein and exhibits stable dynamic behavior at the binding site. In this study, five potential neuroprotectants, nobiletin, silibinin, ononin, ginkgolide B, and epigallocatechin gallate (EGCG), were screened against the glutamate NMDA receptors in humans via computational methods. An in silico ADMET study was also performed, to predict the pharmacokinetics and toxicity profile for the expression of good drug-like behavior and a non-toxic nature. It was revealed that nobiletin fulfills the criteria for all of the drug-likeness rules (Veber, Lipinski, Ghose, Muegge, and Egan) and has neither PAINS nor structural alerts (Brenks). In conclusion, nobiletin demonstrated a possible promising neuroprotectant activities compared to other selected phytochemicals. Further, it can be evaluated in the laboratory for promising therapeutic approaches for in vitro and in vivo studies.

3.
Pharmaceuticals (Basel) ; 15(5)2022 May 12.
Artículo en Inglés | MEDLINE | ID: mdl-35631419

RESUMEN

Environmental exposure to arsenic has been profoundly associated with chronic systemic disorders, such as neurodegeneration, in both experimental models and clinical studies. The neuronal cells of the brain and the nervous system have a limited regeneration capacity, thus making them more vulnerable to exposure to xenobiotics, leading to long-lasting disabilities. The functional and anatomical complexity of these cells hinders the complete understanding of the mechanisms of neurodegeneration and neuroprotection. The present investigations aimed to evaluate the neuroprotective efficacy of a herbal formulation of Nobiletin (NOB) against the toxic insult induced by sodium arsenate (NA) in human neural progenitor cells (hNPCs) derived from human induced pluripotent stem cells (hiPSCs). Prior to the neuroprotective experiments, biologically safe doses of both NOB and NA were ascertained using standard endpoints of cytotoxicity. Thereafter, the hNPCs were exposed to either NOB (50 µM) or NA (50 µM) and co-exposed to biologically safe concentrations of NA (50 µM) with NOB (50 µM) for a period of up to 48 h. NOB treatment restored the morphological damage (neurite damage), the levels of stress granule G3BP1 (Ras-GTPase-activating protein (SH3 domain)-binding protein) and TIA1 (T cell-restricted intracellular antigen), and the expression of neuronal markers (Tuj1, Nestin, MAP2, and PAX6) when compared to NA-exposed cells. A substantial restoration of reactive oxygen species and mitochondrial membrane potential was also witnessed in the co-exposure group (NA + NOB) in comparison to the NA-exposed group. The findings suggest that NOB possesses a significant restorative/protective potential against the NA challenge in hNPCs under experimental conditions and imply that nobiletin may impart a potential therapeutic impact if studied adequately using in vivo studies.

4.
Mol Neurobiol ; 58(7): 3417-3434, 2021 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-33715108

RESUMEN

There are regular reports of extrapulmonary infections and manifestations related to the ongoing COVID-19 pandemic. Coronaviruses are potentially neurotropic, which renders neuronal tissue vulnerable to infection, especially in elderly individuals or in those with neuro-comorbid conditions. Complaints of ageusia, anosmia, myalgia, and headache; reports of diseases such as stroke, encephalopathy, seizure, and encephalitis; and loss of consciousness in patients with COVID-19 confirm the neuropathophysiological aspect of this disease. The brain is linked to pulmonary organs, physiologically through blood circulation, and functionally through the nervous system. The interdependence of these vital organs may further aggravate the pathophysiological aspects of COVID-19. The induction of a cytokine storm in systemic circulation can trigger a neuroinflammatory cascade, which can subsequently compromise the blood-brain barrier and activate microglia- and astrocyte-borne Toll-like receptors, thereby leading to neuronal tissue damage. Hence, a holistic approach should be adopted by healthcare professionals while treating COVID-19 patients with a history of neurodegenerative disorders, neuropsychological complications, or any other neuro-compromised conditions. Imperatively, vaccines are being developed at top priority to contain the spread of the severe acute respiratory syndrome coronavirus 2, and different vaccines are at different stages of development globally. This review discusses the concerns regarding the neuronal complications of COVID-19 and the possible mechanisms of amelioration.


Asunto(s)
Encéfalo/virología , COVID-19/complicaciones , Síndrome de Liberación de Citoquinas/virología , Encefalitis/virología , Inflamación/virología , Accidente Cerebrovascular/virología , Humanos , SARS-CoV-2
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