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Biogeneration of Volatile Organic Compounds in Microalgae-Based Systems
Published in Gokare A. Ravishankar, Ranga Rao Ambati, Handbook of Algal Technologies and Phytochemicals, 2019
Pricila Nass Pinheiro, Karem Rodrigues Vieira, Andriéli Borges Santos, Eduardo Jacob-Lopes, Leila Queiroz Zepka
Many of the compounds detected in microalgae originate from the terpenoid pathways. β-ionone is produced by double-bond cleavage enzymes between carbons 9 and 10 of β-carotene. In addition, β-cyclocitral can be formed from the enzymatic cleavage of the double bond between carbons 7 and 8 of the same carotenoid, catalyzed by β-carotene- oxygenases bound to the cell membrane (Chang et al. 2011; Santos et al. 2016b).
Pharmacological Strategies for Uterine Relaxation
Published in Robert E. Garfield, Thomas N. Tabb, Control of Uterine Contractility, 2019
Michael Hollingsworth, Sandra J. Downing, Josephine M. S. Cheuk, Ian T. Piper, Sarah J. Hughes
Drugs acting as inhibitors of the production and/or release of spasmogens could have a major impact in reducing uterine contractility if they inhibit an early stage in a biochemical cascade that results in the production of many myometrial spasmogens. The cyclo-oxygenase inhibitors reduce the formation of many prostanoids, for example. However, such a mechanism has disadvantages. First, the inhibitor may also reduce the formation of prostanoid products that are uterine relaxants (see Subsection IV.B). Second, for an inhibitor to have a major impact on uterine contractions in vivo and parturition it is necessary that the spasmogens have a primary role in the causation of uterine contractions. Third, such inhibitors will lack selectively if the spasmogens are produced in many tissues and have many physiological or pathophysiological roles. Clearly the latter is the case with cyclo-oxygenase inhibitors.
Micronutrients in the Prevention and Improvement of the Standard Therapy for Alzheimer’s Disease
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
A review showed that markers of oxidative stress, such as protein nitrotyrosine, carbonyls in proteins, lipid oxidation products, and oxidized DNA bases were elevated in the autopsied brain tissue of patients with AD.5 A number of observations substantiate the presence of high levels of oxidative stress in patients with AD. For example, (a) higher expression of heme oxygenase-1 is found in the brains of AD patients161; (b) increased consumption of oxygen is found in AD patients162; (c) increased activity of glucose-6-phosphate dehydrogenase is found in the AD brain3; and (d) activation of calcium-dependent neural proteinase (calpain) is found in AD brains,163 which may trigger events leading to the formation of free radicals.164
Role of curcumin and its nanoformulations in the treatment of neurological diseases through the effects on stem cells
Published in Journal of Drug Targeting, 2023
Nasim Sabouni, Hadi Zare Marzouni, Sepideh Palizban, Sepideh Meidaninikjeh, Prashant Kesharwani, Tannaz Jamialahmadi, Amirhossein Sahebkar
Regarding the effects of curcumin on mesenchymal stem cells, curcumin has a protective role against H2O2-mediated apoptosis through an HO-1-dependent mechanism that was demonstrated by Wagener et al. Haem oxygenase is an enzyme that catalyses the degradation of haem and generates molecules including biliverdin/bilirubin, carbon monoxide (CO) and ferrous iron. It can mediate anti-oxidative, anti-inflammatory, and anti-apoptotic effects and causes cytoprotective effects likely via CO production. Since MSCs efficacy is damaged by oxidative stress in injured tissue, it was suggested in the mentioned study that curcumin can induce HO-1 to increase ADSC survival after administration to promote their therapeutic properties during the cell therapy process [187]. A recent in vitro work in 2019 reported the immunoregulatory, proliferative, and anti-oxidant effects of nanocurcumin on adipose-derived mesenchymal stem cells. Low doses of curcumin were shown to increase the survival and proliferation of ADSCs and decrease their apoptosis, inflammatory cytokines, and SOD activity [44]. Meanwhile, the proliferative effect of curcumin at low concentrations on adipose tissue-derived MSCs has been indicated in another study by Pirmoradi et al. They reported that curcumin increased the lifespan TERT gene expression level of rADCSs to reduce ageing in these cells [188]. In a study by Jiri Ruzicka1 et al. Co-treatment with MSCs and curcumin as an anti-inflammatory compound was demonstrated synergic effects in the rat model of spinal cord injury (SCI) recovery [189].
Corynoline ameliorates dextran sulfate sodium-induced colitis in mice by modulating Nrf2/NF-κB pathway
Published in Immunopharmacology and Immunotoxicology, 2023
Haihua Zhang, Wuying Lang, Sufen Li, Chao Xu, Xiumin Wang, Yunyu Li, Zhiqiang Zhang, Tonglei Wu, Minshan Feng
Immune inflammatory responses have been reported as important factors in the pathogenesis of UC [6]. The immune response in UC leads to the production of some cytokines interleukin-1 (IL)-1β, IL-6 and tumor necrosis factor Alpha (TNF-α), which exert a pro-inflammatory effect in the intestine and act as mediators of mucosal damage [7]. During intestinal inflammation, excessive reactive oxygen species (ROS) production at the site of inflammation leads to tissue injury [8]. Some studies have identified that the nuclear factor E2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway plays a critical role in the development of UC [9–11]. A study found that crocin alleviated AA-induced inflammatory response and oxidative stress in UC rats through the activation of Nrf2/HO-1 pathway [9]. Besides, the Nrf2/HO-1 activation by the maggot extracts efficiently suppressed inflammation and oxidative stress in UC [11]. Saber et al. found that olmesartan exerted protective effects in UC by regulating the nuclear factor kappa-B (NF-κB) and Nrf2 signaling [12]. Additionally, the existing evidence demonstrated that activation of Nrf2 negatively regulated expression of NF-κB [13]. Therefore, the Nrf2/NF-κB signaling may be a potential therapeutic strategy in treating UC.
Inhibition of Gap Junction–Mediated Intercellular Communication by Poly(I:C) in Cultured Human Corneal Fibroblasts
Published in Current Eye Research, 2020
Hui Zheng, Ye Liu, Dan Xu, Pingping Liu, Xiuxia Yang, Bing Li, Zimu Cao, Yang Liu, Xiaoshuo Zheng
Oxidative stress is caused by overproduction of reactive oxygen species and can result in lipid peroxidation, DNA damage, and cell death. It has been implicated in corneal inflammation,37 and it is an important factor in the pathogenesis of ocular diseases such as infectious keratitis, Fuchs endothelial corneal dystrophy, cataract, and age-related macular degeneration.38,39 The increased expression of oxygenases and reduced production of antioxidant enzymes both contribute to oxidative damage.40 Malondialdehyde is a toxic aldehyde formed as a result of membrane lipid peroxidation, whereas SOD is one of the most effective antioxidant enzymes.41 In the present study, poly(I:C) increased the amount of malondialdehyde and down-regulated the activity of SOD in HCFs, and these effects were inhibited by NAC, a scavenger of reactive oxygen species, suggesting that poly(I:C) induces oxidative stress in corneal fibroblasts. Furthermore, the poly(I:C)-induced inhibition of both Cx43 expression and GJIC activity in HCFs was attenuated by NAC, suggesting that the loss of gap junction function elicited by poly(I:C) is mediated, at least in part, by an increase in oxidative stress and that it may contribute to corneal inflammation and the disruption of corneal stromal homeostasis during corneal viral infection.