Vasoactive intestinal peptide inhibits toll-like receptor 3-induced nitric oxide production in Schwann cells and subsequent sensory neuronal cell death in vitro

Three polyisoprenoid alcohols were isolated from the leaves of Tournefortia hirsutissima by a bioassay-guided phytochemical investigation. The compounds were identified as 16-hydroxy-lycopersene (Compound 1), (Z8,E3,ω)-dodecaprenol (Compound 2) and (Z9,E3,ω)-tridecaprenol (Compound 3). Compound 1, an unusual polyisoprenoid, was characterized by 1D and 2D NMR. We also determined the absolute configuration at C-16 by the modified Mosher’s method. The in vitro antiproliferative and anti-inflammatory activities of the isolated compounds were evaluated. Among isolates, Compound 1 moderately inhibited the nitric oxide production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. On the other hand, Compound 1 displayed selective antiproliferative activity against HeLa, PC3, HepG2 and Hep3B cancer cells and was less potent against IHH non-cancerous cells. Compound 1 in Hep3B cells showed significant inhibition of cell cycle progression increasing the sub-G1 phase, suggesting cell death. Acridine orange/ethidium bromide staining and Annexin V-FITC/PI staining demonstrated that cell death induced by Compound 1 in cells Hep3B was by apoptosis. Further study showed that apoptosis induced by Compound 1 in Hep3b cells is associated with the increase of the ratio of Bax/Bcl-2, and caspase 3/7 activation. These results suggest that Compound 1 induce apoptotic cell death by the mitochondrial pathway. To our knowledge, this is the first report about the presence of polyprenol Compounds 1–3 in T. hirsutissima, and the apoptotic and anti-inflammatory action of Compound 1.

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502: Pressure Induces Nitric Oxide Production by Human Ureteral Cells in Vitro

The Journal of Urology ◽

10.1016/s0022-5347(18)34742-6 ◽

2005 ◽

Vol 173 (4S) ◽

pp. 137-137

Author(s):

Michael M. Ohebshalom ◽

Stella K. Maeng ◽

Jie Chen ◽

Dix P. Poppas ◽

Diane Felsen

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Production ◽

Oxide Production

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Resveratrol and grape juice: Effects on redox status and nitric oxide production of endothelial cells in in vitro preeclampsia model

Pregnancy Hypertension ◽

10.1016/j.preghy.2021.01.001 ◽

2021 ◽

Vol 23 ◽

pp. 205-210

Author(s):

Mayara Caldeira-Dias ◽

Sarah Viana-Mattioli ◽

Jackeline de Souza Rangel Machado ◽

Mattias Carlström ◽

Ricardo de Carvalho Cavalli ◽

...

Keyword(s):

Nitric Oxide ◽

Endothelial Cells ◽

Grape Juice ◽

Redox Status ◽

Nitric Oxide Production ◽

Oxide Production

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Cytokinin Plant Hormones Have Neuroprotective Activity in In Vitro Models of Parkinson’s Disease

Molecules ◽

10.3390/molecules26020361 ◽

2021 ◽

Vol 26 (2) ◽

pp. 361

Author(s):

Gabriel Gonzalez ◽

Jiří Grúz ◽

Cosimo Walter D’Acunto ◽

Petr Kaňovský ◽

Miroslav Strnad

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cell Death ◽

Neuronal Cell Death ◽

Disease Model ◽

Neuronal Cell ◽

Zeatin Riboside ◽

Neuroprotective Activity ◽

Protective Activity

Cytokinins are adenine-based phytohormones that regulate key processes in plants, such as cell division and differentiation, root and shoot growth, apical dominance, branching, and seed germination. In preliminary studies, they have also shown protective activities against human neurodegenerative diseases. To extend knowledge of the protection (protective activity) they offer, we investigated activities of natural cytokinins against salsolinol (SAL)-induced toxicity (a Parkinson’s disease model) and glutamate (Glu)-induced death of neuron-like dopaminergic SH-SY5Y cells. We found that kinetin-3-glucoside, cis-zeatin riboside, and N6-isopentenyladenosine were active in the SAL-induced PD model. In addition, trans-, cis-zeatin, and kinetin along with the iron chelator deferoxamine (DFO) and the necroptosis inhibitor necrostatin 1 (NEC-1) significantly reduced cell death rates in the Glu-induced model. Lactate dehydrogenase assays revealed that the cytokinins provided lower neuroprotective activity than DFO and NEC-1. Moreover, they reduced apoptotic caspase-3/7 activities less strongly than DFO. However, the cytokinins had very similar effects to DFO and NEC-1 on superoxide radical production. Overall, they showed protective activity in the SAL-induced model of parkinsonian neuronal cell death and Glu-induced model of oxidative damage mainly by reduction of oxidative stress.

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Nitric Oxide-induced Activation of the Type 1 Ryanodine Receptor Is Critical for Epileptic Seizure-induced Neuronal Cell Death

EBioMedicine ◽

10.1016/j.ebiom.2016.08.020 ◽

2016 ◽

Vol 11 ◽

pp. 253-261 ◽

Cited By ~ 19

Author(s):

Yoshinori Mikami ◽

Kazunori Kanemaru ◽

Yohei Okubo ◽

Takuya Nakaune ◽

Junji Suzuki ◽

...

Keyword(s):

Nitric Oxide ◽

Cell Death ◽

Ryanodine Receptor ◽

Epileptic Seizure ◽

Neuronal Cell Death ◽

Neuronal Cell

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Effects of Periodic Body Acceleration on the In Vivo Vasoactive Response to N-w-nitro–L-arginine and the In Vitro Nitric Oxide Production

Annals of Biomedical Engineering ◽

10.1114/1.1623486 ◽

2003 ◽

Vol 31 (11) ◽

pp. 1337-1346 ◽

Cited By ~ 28

Author(s):

Jose A. Adams ◽

James E. Moore, Jr. ◽

Michael R. Moreno ◽

Jaqueline Coelho ◽

Jorge Bassuk ◽

...

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Production ◽

Body Acceleration ◽

Oxide Production

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Mesenchymal Stem Cells (MSCs) Coculture Protects [Ca2+]i Orchestrated Oxidant Mediated Damage in Differentiated Neurons In Vitro

Cells ◽

10.3390/cells7120250 ◽

2018 ◽

Vol 7 (12) ◽

pp. 250 ◽

Cited By ~ 9

Author(s):

Adel Alhazzani ◽

Prasanna Rajagopalan ◽

Zaher Albarqi ◽

Anantharam Devaraj ◽

Mohamed Hessian Mohamed ◽

...

Keyword(s):

Cell Death ◽

Transforming Growth Factor ◽

Neuronal Cells ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Apoptotic Cells ◽

Sequence Of Events ◽

Cox 2 ◽

Anti Inflammatory

Cell-therapy modalities using mesenchymal stem (MSCs) in experimental strokes are being investigated due to the role of MSCs in neuroprotection and regeneration. It is necessary to know the sequence of events that occur during stress and how MSCs complement the rescue of neuronal cell death mediated by [Ca2+]i and reactive oxygen species (ROS). In the current study, SH-SY5Y-differentiated neuronal cells were subjected to in vitro cerebral ischemia-like stress and were experimentally rescued from cell death using an MSCs/neuronal cell coculture model. Neuronal cell death was characterized by the induction of proinflammatory tumor necrosis factor (TNF)-α, interleukin (IL)-1β and -12, up to 35-fold with corresponding downregulation of anti-inflammatory cytokine transforming growth factor (TGF)-β, IL-6 and -10 by approximately 1 to 7 fold. Increased intracellular calcium [Ca2+]i and ROS clearly reaffirmed oxidative stress-mediated apoptosis, while upregulation of nuclear factor NF-B and cyclo-oxygenase (COX)-2 expressions, along with ~41% accumulation of early and late phase apoptotic cells, confirmed ischemic stress-mediated cell death. Stressed neuronal cells were rescued from death when cocultured with MSCs via increased expression of anti-inflammatory cytokines (TGF-β, 17%; IL-6, 4%; and IL-10, 13%), significantly downregulated NF-B and proinflammatory COX-2 expression. Further accumulation of early and late apoptotic cells was diminished to 23%, while corresponding cell death decreased from 40% to 17%. Low superoxide dismutase 1 (SOD1) expression at the mRNA level was rescued by MSCs coculture, while no significant changes were observed with catalase (CAT) and glutathione peroxidase (GPx). Interestingly, increased serotonin release into the culture supernatant was proportionate to the elevated [Ca2+]i and corresponding ROS, which were later rescued by the MSCs coculture to near normalcy. Taken together, all of these results primarily support MSCs-mediated modulation of stressed neuronal cell survival in vitro.

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