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Marine Drugs: A Source of Medicines for Neuroinflammatory Disorders
Published in Rohit Dutt, Anil K. Sharma, Raj K. Keservani, Vandana Garg, Promising Drug Molecules of Natural Origin, 2020
Arunachalam Muthuraman, Narahari Rishitha, Nallapilai Paramakrishnan
The molecular mechanism of neuroinflammatory disorders varies based on the category of cells involved, level of mediator released, and duration of process ongoing for neuroinflammatory reaction (Agostinho et al., 2010). In the acute stage, PNS & CNS immune cells and endothelial cells based release of IL and TNF are involved in the neuroinflammatory reaction. In addition, local release of autocoids like prostaglandin, leukotriene, brady-kinins, histamine, and serotonin also contributes to the neuroinflammatory reaction, which leads to alters the ion and fluid exchange process leads to cause the potential neuroinflammation (Kasperska-Zajac et al., 2008). If acute neuroinflammation is prolonged conditions, it activates the multiple cytosolic cellular environments like generation ROS from mitochondrial; accumulation of calcium ion via the release of stored calcium and opening of stored operated calcium ion channels; induces the oxidative enzymatic system; alteration of the phospholipid layer of the membrane via peroxidative process; and modulation of DNA and post-translational proteins including misfolding of expressed proteins leads to cause the neurodegeneration (Rizzuto et al., 2012).
Pulmonary Circulation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The primary function of the pulmonary circulation is to bring systemic venous (mixed venous) blood into contact with the alveoli for gas exchange. Additionally, it has three secondary functions: (i) as blood filter, (ii) as blood reservoir and (iii) as a metabolic organ. The small pulmonary arterial vessels and capillaries trap emboli (gas, fat and blood clots) and prevent systemic embolization. It has a high capacitance and stores 450–500 mL of blood (150 mL in the arteries, 80 mL in the capillaries and 250 mL in the pulmonary veins). Another important activity is the metabolism of vasoactive autocoids/hormones. Angiotensin-converting enzyme, located on the surface of pulmonary capillary endothelial cells, converts angiotensin I to angiotensin II. Bradykinin, serotonin, noradrenaline and prostaglandins E and F are inactivated by pulmonary endothelial cells.
Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Lipid mediators are synthesized and released by a wide variety of cell types, including neutrophilic, eosinophilic, and basophilic polymorphonuclear leukocytes, monocytes, mast cells, macrophages, and platelets. These lipid mediators can be grouped into two classes; (1) mediators derived from the arachidonic acid metabolism and (2) acetylated alkyl phosphoglycerides. These mediators and related compounds are now classified as autacoids rather than as mediators. Autacoids represent highly potent pharmacological agents previously described as autopharmacological agents or local hormones.
Advances in the discovery of novel agents for the treatment of glaucoma
Published in Expert Opinion on Drug Discovery, 2021
Francesco Mincione, Alessio Nocentini, Claudiu T. Supuran
Among the many prostaglandins (PGs) known to date, PGD2, PGE2 and PGF2α are involved in ocular physiology [67]. Diverse PG receptors are expressed in various tissues including the eye, where they are involved in a host of physiological processes including chemotaxis, inflammation, immune response, etc [67]. PGD2 was demonstrated to decrease ocular aqueous flow in 1988 [68], but this autacoid is involved in immune responses and other essential processes, and it also provoked a strong reddening of the eye due to its pro-inflammatory action, and for such reasons, subsequent studies focused on PGF2, PGE2 and their agonists, which should not elicit immune responses and such strong adverse effects as PGD2 [67–70]. These autacoids exert their action through G-protein-coupled receptors (GPCR). There are four PGE2 receptors (EP1-EP4) and one PGF2α receptor (FP), which are widely expressed in various eye tissues, such as the cornea, conjunctiva, ciliary body, TM, iris and retina [69]. EP/FP receptor agonists constitute an interesting class of anti-glaucoma agents, as these compounds activate TM and ciliary muscle cells, increasing thus the aqueous outflow both by the non-conventional pathway [67,69,70]. Nowadays, at least four drugs belonging to the PG receptors agonists are in clinical use as anti-glaucoma agents: latanoprost 28 [71], bimatoprost 29 [72], travoprost 30 [73], and tafluprost 31 [74] (Figure 6).
Angina due to coronary artery spasm (variant angina): diagnosis and intervention strategies
Published in Expert Review of Cardiovascular Therapy, 2021
Thanh Ha Nguyen, Gao-Jing Ong, Olivia C Girolamo, Viviane De Menezes Caceres’, Armin Muminovic, Yuliy Y Chirkov, John D Horowitz
(d) What are the key stimuli for triggering CAS crises? There is substantial evidence that patients with CAS exhibit increased concentrations and effects of a number of inflammatory markers. However, the precise triggers for CAS crises have remained uncertain in the past. We have recently shown [28] that plasma concentrations of the mast cell enzyme tryptase increase during CAS crises, and that intravenous infusion of NAC, a sulphydryl-containing antioxidant, reverses biochemical anomalies associated with CAS. Furthermore, this pro-homeostatic effect of NAC depends on enzymatically mediated release of hydrogen sulfide (H2S), an endothelial autacoid that potentiates NO effects, partially by limiting release of superoxide anion and of hypochlorous acid from neutrophils and mast cells. Our findings are consistent with previous observations of CAS in Kounis syndrome, essentially a mast cell disorder, and for the reported finding of adventitial mast cell aggregates as stimuli for refractory CAS [80]. It therefore seems likely that NO and H2S usually act synergistically to stabilize mast cells: in their absence there is mast cell degranulation, with resultant inflammatory damage to both platelets and vasculature. Stabilization of mast cells probably accounts for the utility of both corticosteroids and of NAC during CAS crises, and may represent a novel form of prophylaxis for chronic symptoms.
Are We missing out the role of oxytocin in overactive bladder syndrome?
Published in The Aging Male, 2020
Prostaglandins (PGs) are hormones that are produced, released, and effective locally; such agents are called autocoids. One of the earliest recognized effects of PGs was the stimulation of myometrial contractions. Besides stimulating uterine myometrial contraction, OT causes the release of PGs from different organs including bladder [35]. PGs are locally synthesized in the bladder muscle and mucosa [36]. This synthesis is initiated by stretch of the detrusor muscle, bladder nerve stimulation, bladder mucosa damage, and inflammation mediators. PGs are released from the bladder into the general circulation in response to distension. In regard to PG related changes in the micturition reflex, it was envisaged that they might act directly on the afferent nerves to modulate firing and so, trigger micturition at lower bladder volumes [34].