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Diversity Analysis of Indian Mangrove Organisms to Explore Their Potential in Novel and Value-Added Biomolecules
Published in Jayanta Kumar Patra, Gitishree Das, Sanjeet Kumar, Hrudayanath Thatoi, Ethnopharmacology and Biodiversity of Medicinal Plants, 2019
Angana Sarkar, Sushant Prajapati, Amulya Sai Bakshi, Asma Khatoon, Raghavarapu Swathi, Siddharth Kumar, Arpita Behera, Rahul Pradhan
Mangrove organisms such as sponge have many useful compounds such as cytarabine (Ara C), Vidarabine (Ara-A), Eribulin Mesylate (E7389) which are all FDA approved and targets dangerous diseases such as cancer (Mayer et al., 2016; Newman and Cragg, 2016) (Table 2.3). Other mangrove organisms such as Tunicate, Mollusca, Nudibranch also targets the disease, cancer. The omega 3 fatty acid ethyl esters from fish can be used for the treatment of Hypertriglyceridemia. Some important compounds such as Brentuximab Vedotin (SGN-35) Elisidesin, Glembatumumab Vedotin (CDX 011), SGN-75, ASG-5ME can be obtained from Mollusca majorly found in Baratang and Krishna Godavari mangroves. The bacterium Bryozoa gives Bryostatin, which can treat cancer and Alzheimer’s disease. The soft Coral produces pseudopterosins whose molecular target is Eicosanoid Metabolism and helps in wound healing. The compound Trabectedin (ET 743), which belongs to the alkaloid class targets the minor, grooves of DNA and helps in the treatment of cancer. The compound, Eribulin Mesylate (E7389) obtained from the sponge targets the microtubules for the treatment of cancer. Zincoside, obtained from cone nail is used as an analgesic drug. The compound DMXBA (GTS-21) obtained from worm targets the alpha-7 Nicotinic Acetylcholine Receptor and helps in the treatment of cognition schizophrenia (Table 2.3). Mangrove pharmaceuticals can be used as cytostatic drugs, antiviral drugs, analgetic drugs, antihyperlipidemic drugs and can also be used as diagnostic and experimental tools. The cosmetics industry is also stepping towards the sea, so as to find new ingredients (Fenical et al., 2009; Martins et al., 2014).
The effect of electronic cigarettes exposure on learning and memory functions: behavioral and molecular analysis
Published in Inhalation Toxicology, 2021
Karem H. Alzoubi, Rahaf M. Batran, Nour A. Al-Sawalha, Omar F. Khabour, Nareg Karaoghlanian, Alan Shihadeh, Thomas Eissenberg
The hippocampus plays an important role in the learning and memory. The dentate gyrus, and the Cornu ammonis 1 (CA1), Cornu ammonis 2 (CA2), and Cornu ammonis 3 (CA3) regions are among the involved hippocampal subregions. The corticohippocampal circuit, either in its classical or nonclassical pathways, participates in the process of memory formation (Basu and Siegelbaum 2015). Nicotinic acetylcholine receptors (nAChRs) are major type of receptors that are expressed in several areas of hippocampus. nAChRs regulate the release of several neurotransmitters in hippocampus and modulate synaptic plasticity and eventually mediates learning and memory (Placzek et al. 2009). The administration of nicotine enhanced learning and memory in aged rats (Arendash et al. 1995), and chronic stress and Alzheimer’s Disease animal models (Alkadhi 2011). Further, it has been shown that the administration of nAChRs agonists such as GTS-21 and lobeline resulted in enhanced learning and memory in animal models (Decker et al. 1993; Arendash et al. 1995). However, other studies revealed contradictory findings about the effect of nicotine. It has been shown that the administration of nicotine-induced learning and memory impairment by enhancing oxidative stress in the brain (Hritcu et al. 2009). Further, nicotine induced oxidative stress in the brain of young and old rats (Jain and Flora 2012).
The role of alpha7 nicotinic acetylcholine receptors in inflammatory bowel disease: involvement of different cellular pathways
Published in Expert Opinion on Therapeutic Targets, 2018
Mohammad Seyedabadi, Reza Rahimian, Jean-Eric Ghia
On the other hand, a recent randomized, double-blind, placebo-controlled study failed to show pro-cognitive effects for ABT-126, a potent α7nAChR agonist, in patients with mild-to-moderate Alzheimer’s disease who were on stable doses of AChE inhibitors [105]. Similarly, GTS-1 failed to improve cognitive impairment in a phase II clinical trial of patients suffering from schizophrenia. However, at higher doses, it did improve clinical ratings of negative symptoms [106]. Likewise, higher doses of GTS-21 correlated with lower levels of inflammatory cytokines, but the highest dose tested to be safe in human failed to produce a significant decrease in inflammatory mediators in septic shock [107]. It should be noted, however, that this agent may also target α4β2 nicotinic receptors [108]. Similarly, AstraZeneca decided to terminate a phase II clinical trial (NCT00669903) which aimed to assess pharmacodynamics, pharmacokinetics, safety, and tolerability of AZD0328, a selective α7nAChR agonist, in patients suffering from schizophrenia, because the drug was unlikely to meet the current target product profile [109]. Albeit, earlier reports demonstrated enhancement of cortical dopamine release and improvement of learning and attentional processes by this agent [110]. Moreover, the α7nAChR agonist, AQW051, failed to significantly improve levodopa-associated dyskinesia or the severity of Parkinson’s disease [111]. Eventually, a translational meta-analysis of rodent and human studies did not support α7nAChR agonists as a robust therapeutic option for cognitive dysfunction in schizophrenia or Alzheimer’s disease [112].
From nicotine to the cholinergic anti-inflammatory reflex – Can nicotine alleviate the dysregulated inflammation in COVID-19?
Published in Journal of Immunotoxicology, 2021
Alex G. Gauthier, Mosi Lin, Jiaqi Wu, Thomas P. Kennedy, Lee-Anne Daley, Charles R. Ashby, Lin L. Mantell
Recent epidemiological studies have reported that men and women have similar prevalence rates for COVID-19; however, men are more susceptible to developing severe COVID-19 symptoms and have higher mortality rates (Jin et al. 2020). In pulmonary arterial hypertension patients, men have higher mortality rates due to an increased level of pulmonary vascular necrosis and an increased amount of HMGB1 in the extracellular milieu (Rafikov et al. 2019; Zemskova et al. 2020). Thus, increased HMGB1 levels could explain why men with COVID-19 have a higher mortality rate compared to women. Therefore, the activation of the cholinergic anti-inflammatory pathway with α7nAChR agonists offers at least two hypothetical mechanisms for protection against SARS-CoV-2 infection: (1) attenuation of SARS-CoV-2-induced hyper-cytokinemia, particularly by decreasing the secretion of HMGB1; and (2) inhibition of endocytosis of HMGB1-SARS-CoV-2 RNA complexes, thus decreasing hyper-inflammatory responses. Furthermore, in silico-based investigations have reported a potential interaction between the α7nAChR and the SARS-CoV-2 glycoprotein spike protein (Farsalinos et al. 2020a). The interaction between α7nAChR and the spike protein was predicted to be similar to that of α-bungarotoxin, a molecule in the venom of the snake, Bungarus multicinctus multicinctus, that selectively antagonizes α7nAChR (Farsalinos et al. 2020b). This interaction may play a critical role in disrupting the cholinergic anti-inflammatory system in COVID-19 patients, resulting in lung inflammation and severe ARDS. α7nAChR agonists, such as nicotine or GTS-21, could also compete with the binding of the spike protein for α7nAChR, representing a third protective mechanism.