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Fenugreek in Management of Neurological and Psychological Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Rohini Pujari, Prasad Thakurdesai
Many natural products, including fenugreek, were explored to develop the CNS specifically to prevent diabetes-linked neurological and cognitive disorders (Patel and Udayabanu 2017). Fenugreek seed powder reported antihyperglycemic and neuroprotective activities in alloxan monohydrate (15 mg/100 g body weight)-induced diabetic rats (Kumar et al. 2012). In this study, 21 day supplementation of 5% finely powdered fenugreek seeds in rat feed (5 g of powder + 95 g of powdered rat feed) showed reversal of the hyperglycemia-induced changes (membrane linked enzymes (Na+K+ATPase, Ca2+ATPase), anti-oxidant enzymes (SOD, glutathione S-transferase), calcium (Ca2+) levels, and neurolipofuscin accumulation levels) to normal levels in the diabetic rat brain (Kumar et al. 2012). These parameters, especially the plasma membrane Ca2+-ATPase pumps, play an essential role in maintaining precise levels of intracellular Ca2+ essential to the functioning of neurons (Zaidi 2010). A decrease in synaptosome membrane fluidity is reported to influence the activity of membrane-linked enzymes in diabetes (Kamboj, Chopra, and Sandhir 2009). Additional experiments on the fenugreek powder (5% in feed) in combination with sodium orthovanadate (SOV), a competitive inhibitor of ATPases, reported similar reversal of the alloxan-induced changes in synaptosome membrane fluidity and histochemical localization and distribution of neurolipofuscin along with levels of membrane-linked enzymes (Na+/K+-ATPase and Ca2+ATPase activities) (Kumar et al. 2015).
The Cell Membrane in the Steady State
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Similar to the Na+-K+ pump is the plasma membrane Ca2+-ATPase (PMCA) that helps maintain a low intracellular Ca2+ concentration in the resting state by pumping Ca2+ outward against a large electrochemical potential gradient. Ion pumps are an example of ion transporters, which transport ions across plasma membranes and membranes of cell organelles. Other types of ion transporters are uniporters and cotransporters that will be discussed in the following section.
Neurophysiology of Old Neurons and Synapses
Published in David R. Riddle, Brain Aging, 2007
The change in homeostasis, which shifts the cell away from Ca2+ influx through NMDA receptors, may be neuroprotective against Ca2+-mediated damage and thus act as compensation for increased vulnerability to neurotoxicity [140]. Alternatively, the shift in Ca2+ homeostasis could result from an age-related increase in oxidative stress [141–143]. Reactive oxygen species could induce a rise in intracellular Ca2+ through release of Ca2+ from Ca2+ binding proteins (i.e., decreased buffering), and oxidation of calcium regulatory proteins (calmodulin, SERCA, PMCA) would disrupt intracellular stores, and increase entry through Ca2+ channels [142, 144]. In the hippocampus, oxidative stress has effects that mimic aging: increasing Ca2+ influx through L-channels [145, 146], increasing the function of Ca2+-dependent K+ channels [23, 147], and decreasing NMDAR function [148]. Furthermore, oxygen radicals can influence the activity of Ca2+-dependent enzymes. The unstable superoxide (O·) or high levels of H2O2 (beyond the physiological range) inhibit calcineurin in tissue homogenates [149, 150]. However, in intact tissue, reactive oxygen species increase calcineurin activity, either through changes in the calcineurin inhibitory protein [151] or altered Ca2+ regulation involving increased Ca2+ from intracellular stores and VGCCs, leading to impaired induction of LTP [149]. Future research will be required to determine whether treatments designed to reduce oxidative stress can reverse senescent physiology or ameliorate cognitive decline (see Chapter 15).
Fisetin, a potential caloric restriction mimetic, modulates ionic homeostasis in senescence induced and naturally aged rats
Published in Archives of Physiology and Biochemistry, 2022
Sandeep Singh, Geetika Garg, Abhishek Kumar Singh, Shambhoo Sharan Tripathi, Syed Ibrahim Rizvi
NKA pump is one of the key transport systems associated with cytoplasmic viscosity via maintaining the osmotic balance across the cell membrane, and membrane potential in addition to regulation of Na+ gradient (Bor-Kucukatay et al.2003). The activity of NKA pump is impaired during the homeostatic imbalance basically mediated by oxidative stress (Mense, Stark, and Apell 1997, Pandey and Rizvi 2014). A decreased erythrocytes NKA pump activity has been implicated in the pathogenesis of age-associated neurological disorders and cardiovascular diseases (de Lores Arnaiz and Ordieres 2014, Yan and Shapiro 2016). Similarly, the PMCA pump plays an important role in the maintenance of precise level of intracellular calcium ion, essential to maintain the membrane integrity. The PMCA is very sensitive to oxidative stress and undergoes functional and structural changes when exposed to oxidants (Asha Devi et al.2011, Pandey and Rizvi 2014).
Melatonin exerts neuroprotection in a chronodisrupted rat model through reduction in oxidative stress and modulation of autophagy
Published in Chronobiology International, 2022
Avnish Kumar Verma, Sandeep Singh, Geetika Garg, Syed Ibrahim Rizvi
Figure 2 exhibits the brain synaptosomal activities of Na+/K+-ATPase (NKA) & plasma membrane Ca2+-ATPase (PMCA). A one-way ANOVA detected the significant effect of CLE, CDE and melatonin treatment [F (4, 25) = 47.81, 84.73 for NKA and PMCA respectively]. These transporters were significantly (p ≤ 0.05; q = 9.80 and 13.53) reduced in CLE exposed rats (25.50% & 30.73%) while significant (p ≤ 0.05; q = 8.90 and 7.93) upregulation in both transporters (23.16% & 18.03%, respectively) was observed in CDE rats when compared with control. After melatonin supplementation, a non-significant change was observed in the activity of NKA whereas significant (p ≤ 0.05; q = 7.74) enhanced (17.59%) activity of PMCA was found in Group II with respect to control. Melatonin administration in the CLE group further significantly (p ≤ 0.05; q = 8.34 and 7.54) increased (29.16% & 10.52%) both NKA & PMCA activities respectively as compared to the CLE rats (Figure 2a,b).
Kidney stone proteomics: an update and perspectives
Published in Expert Review of Proteomics, 2021
Paleerath Peerapen, Visith Thongboonkerd
Furthermore, plasma membrane Ca2+-ATPase (PMCA), a calmodulin-dependent calcium ATPase located at plasma membrane to regulate Ca2+ transport, has been identified as the COM crystal receptor from the large-scale proteomics study [89]. Immunofluorescence staining using a specific antibody against PMCA2 showed the fluorescence signal of PMCA2 protein on the COM crystal surface after incubation of the crystals with apical membrane proteins followed by vigorous washes [98]. Additionally, crystal-cell adhesion assay and crystal internalization assay demonstrated that blocking the surface PMCA2 by monoclonal anti-PMCA2 antibody led to the decrease in number of the adhered and internalized crystals [98]. These data strengthen the role of PMCA2 as the COM crystal receptor on renal tubular cell surface.