scholarly journals Neuromodulatory effects of aqueous extract of Coriandrum sativum seeds against acrylamide induced toxicity in Drosophila melanogaster#

2019 ◽  
Vol 10 (2) ◽  
pp. 1127-1135
Author(s):  
Sathya N Prasad ◽  
Muralidhara
Keyword(s):  
Aqueous Extract ◽  
Neuronal Damage ◽  
Thioredoxin Reductase ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Glutathione S Transferase ◽  
Oxidative Stress Parameter ◽  
Ameliorative Effect ◽  
Significant Attenuation ◽  
Primary Focus

Acrylamide (ACR) exposure leads to neuronal damage in both experimental animals and humans and has been established as a neurotoxin. The primary focus of this study was to assess the potential ameliorative effect of aqueous extract of coriander seeds against ACR-induced neurotoxicity in a Drosophila model. In this co-exposure study, adult male flies (8–10 days) were exposed (7 days) to ACR (5 mM) with or without aqueous extract of coriander seeds (0.005% and 0.01%) in the medium. The incidence of mortality among flies fed with ACR and extract was significantly reduced (40-60%). The ACR fed flies showed improvement in negative geotaxis assay when co-exposed with coriander extract (50-60%). Further, a significant attenuation in the ACR induced oxidative stress parameter such as Reactive Oxygen Species (ROS), and malondialdehyde (MDA) was evident. Although the effect of ACR with or without extract showed a differential effect on the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione –S – transferase (GST), the reduced levels of Thioredoxin Reductase (TRR) activity was robustly enhanced with extract supplement. Further, the cholinergic and dopaminergic function was assessed among all flies. While ACR induced elevation of acetylcholine esterase (AChE) activity remained unaltered with coriander supplement, a significant improvement was evident in the ACR induced reduction of dopamine levels.  While the underlying mechanism of action needs further investigation, the protective effects may be at least in part related to the antioxidant capacity of the phytoconstituents of coriander.

scholarly journals Sildenafil (Viagra) Protective Effects on Neuroinflammation: The Role of iNOS/NO System in an Inflammatory Demyelination Model

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Catarina Raposo ◽  
Ana Karolina de Santana Nunes ◽  
Rayana Leal de Almeida Luna ◽  
Shyrlene Meiry da Rocha Araújo ◽  
Maria Alice da Cruz-Höfling ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Wild Type ◽  
Glutathione S Transferase ◽  
Cox 2 ◽  
Inflammatory Regulation ◽  
Inos Inhibition ◽  
Inflammatory Effect

We recently demonstrated that sildenafil reduces the expression of cytokines, COX-2, and GFAP in a demyelinating model induced in wild-type (WT) mice. Herein, the understandings of the neuroprotective effect of sildenafil and the mediation of iNOS/NO system on inflammatory demyelination induced by cuprizone were investigated. The cerebella of iNOS−/−mice were examined after four weeks of treatment with cuprizone alone or combined with sildenafil. Cuprizone increased GFAP, Iba-1, TNF-α, COX-2, IL-1β, and IFN-γexpression, decreased expression of glutathione S-transferase pi (GSTpi), and damaged myelin in iNOS−/−mice. Sildenafil reduced Iba-1, IFN-γ, and IL-1βlevels but had no effect on the expression of GFAP, TNF-α, and COX-2 compared to the cuprizone group. Sildenafil elevated GSTpi levels and improved the myelin structure/ultrastructure. iNOS−/−mice suffered from severe inflammation following treatment with cuprizone, while WT mice had milder inflammation, as found in the previous study. It is possible that inflammatory regulation through iNOS-feedback is absent in iNOS−/−mice, making them more susceptible to inflammation. Sildenafil has at least a partial anti-inflammatory effect through iNOS inhibition, as its effect on iNOS−/−mice was limited. Further studies are required to explain the underlying mechanism of the sildenafil effects.

Vitexin regulates EPAC and NLRP3 and ameliorates chronic cerebral hypoperfusion injury

2021 ◽  
Author(s):  
Qilong Zhang ◽  
Zhijia Fan ◽  
wei xue ◽  
Fanfan Sun ◽  
Huaqing Zhu ◽  
...  
Keyword(s):  
Neuronal Damage ◽  
Critical Factor ◽  
Underlying Mechanism ◽  
Cerebrovascular Diseases ◽  
Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Protective Effects ◽  
Ht22 Cells

Chronic cerebral hypoperfusion (CCH), as a critical factor of chronic cerebrovascular diseases, has greatly influenced the health of patients with vascular dementia (VD). The putative protective effects of vitexin on the CCH need further investigations. In the current study, the role of vitexin and its underlying mechanism were investigated with permanent bilateral common carotid artery occlusion (2VO) in rats as well as HT22 cells with OGD/R injury model. The results demonstrated that vitexin improved cognitive dysfunction as well as alleviated pathological neuronal damage in HE and TUNEL results. The decreased levels of Epac1, Epac2, Rap1 and p-ERK were reversed by vitexin in rats with CCH. Furthermore, this study indicated that vitexin alleviated CCH-induced inflammation injuries by reducing the expression of NLRP3, Caspase-1, IL-1β, IL-6, and cleaved Caspase-3. In vitro, vitexin increased the expression of Epac1 and Epac2, decreased the activation of the NLRP3-mediated inflammation, and improved cell viability. Taken together, our findings suggest that vitexin can reduce the degree of the progressing pathological damage in the cortex and hippocampus and inhibit further deterioration of cognitive function in rats with CCH. Epac and NLRP3 can be regulated by vitexin, which provides enlightenment for the protection of CCH injury.

scholarly journals Artemisinin protects against sepsis-associated encephalopathy by activating the AMPK axis in the microglia

2019 ◽  
Author(s):  
Shao-Peng Lin ◽  
Jue-Xian Wei ◽  
Shan Ye ◽  
Jiasong Hu ◽  
Jingyi Bu ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Neuronal Damage ◽  
Immunohistochemical Analysis ◽  
Adenosine Monophosphate ◽  
Underlying Mechanism ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Bv2 Cells ◽  
Anti Inflammatory

Abstract Background and purpose: Artemisinin has been in use as an anti-malarial drug for almost half a century in the world. There is growing evidence that artemisinin also possesses potent anti-inflammatory and immunoregulatory properties. However, the efficacy of artemisinin treatment in sepsis-associated encephalopathy (SAE) remains unknown. Here, we evaluate the possible protective effects and explore the underlying mechanism of action of artemisinin on SAE. Methods: Male C57BL/6mice were pretreated with either vehicle or artemisinin, and then injected with LPS to establish an animal model of SAE. The cognitive function was then assessed using the Morris water maze. Neuronal damage and neuroinflammation in the hippocampus were evaluated by immunohistochemical analysis. Additionally, the protective mechanism of artemisinin was determined in vitro. Results: The results showed that artemisinin preconditioning attenuated LPS-induced cognitive impairment, neural damage, and microglial activation in the mouse brain. Luminex liquid chip revealed that artemisinin could inhibit the pro-inflammatory cytokines and chemokines induced by LPS in the BV2 microglia cells. Meanwhile, artemisinin suppressed the migratory ability of BV2 cells. Western blot demonstrated that artemisinin promoted adenosine monophosphate-activated protein kinaseα1 (AMPKα1) expression and suppressed nuclear translocation of NF-κB. Furthermore, knock-down of AMPKα1 markedly abolished the anti-inflammatory effects of artemisinin when exposed to LPS. Conclusion: Artemisinin is a potential therapeutic agent for SAE, and its effect was probably mediated by the activation of AMPKα1signalling pathway in microglia.

scholarly journals UVB protective effects of Sargassum horneri through the regulation of Nrf2 mediated antioxidant mechanism

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eui Jeong Han ◽  
Seo-Young Kim ◽  
Hee-Jin Han ◽  
Hyun-Soo Kim ◽  
Kil-Nam Kim ◽  
...  
Keyword(s):  
Skin Barrier ◽  
Human Keratinocytes ◽  
Underlying Mechanism ◽  
Ultraviolet B ◽  
Sargassum Horneri ◽  
Cellular Damage ◽  
Protective Effects ◽  
Skin Damage ◽  
Antioxidant Mechanism ◽  
Induced Apoptosis

AbstractThe present study aimed to evaluate the protective effect of a methanol extract of Sargassum horneri (SHM), which contains 6-hydroxy-4,4,7a-trimethyl-5,6,7,7a-tetrahydrobenzofuran-2(4H)-one (HTT) and apo-9′-fucoxanthinone, against ultraviolet B (UVB)-induced cellular damage in human keratinocytes and its underlying mechanism. SHM significantly improved cell viability of UVB-exposed human keratinocytes by reducing the generation of intracellular reactive oxygen species (ROS). Moreover, SHM inhibited UVB exposure-induced apoptosis by reducing the formation of apoptotic bodies and the populations of the sub-G1 hypodiploid cells and the early apoptotic cells by modulating the expression of the anti- and pro-apoptotic molecules, Bcl-2 and Bax, respectively. Furthermore, SHM inhibited NF-κB p65 activation by inducing the activation of Nrf2/HO-1 signaling. The cytoprotective and antiapoptotic activities of SHM are abolished by the inhibition of HO-1 signaling. In further study, SHM restored the skin dryness and skin barrier disruption in UVB-exposed human keratinocytes. Based to these results, our study suggests that SHM protects the cells against UVB-induced cellular damages through the Nrf2/HO-1/NF-κB p65 signaling pathway and may be potentially useful for the prevention of UVB-induced skin damage.

scholarly journals Effects of Propentofylline on Hypoxia—Hypoglycemia-Induced Calcium Accumulation in Gerbil Hippocampal Slices

1992 ◽  
Vol 12 (2) ◽  
pp. 301-305 ◽  
Author(s):  
Fumito Kadoya ◽  
Akira Mitani ◽  
Tatsuru Arai ◽  
Kiyoshi Kataoka
Keyword(s):  
Cerebral Ischemia ◽  
Intracellular Calcium ◽  
Neuronal Damage ◽  
Hippocampal Slices ◽  
Dependent Manner ◽  
Protective Effects ◽  
Calcium Accumulation ◽  
Xanthine Derivative ◽  
Acute Increase ◽  
Dose Dependent

The xanthine derivative propentofylline (HWA 285) has been reported to show protective effects against neuronal damage induced by cerebral ischemia. In the present study, microfluorometry was used to investigate the effect of propentofylline on the hypoxia–hypoglycemia-induced intracellular calcium accumulation in gerbil hippocampal slices. When slices were superfused with hypoxic–hypoglycemic medium that did not contain propentofylline, an acute increase in calcium accumulation was detected 75–200 s (mean latency of 123 s) after the beginning of hypoxia–hypoglycemia. When slices were superfused with hypoxic–hypoglycemic mediums that contained 10 μ M, 100 μ M, and 1 m M propentofylline, the latency of the acute increase in calcium accumulation was prolonged in all subregions of the hippocampus in a dose-dependent manner: mean latencies in field CA1 were 146, 168, and 197 s after hypoxia–hypoglycemia, respectively. This retardation in calcium accumulation may be involved in the mechanisms by which propentofylline diminishes ischemic injury.

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