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Thyroid Hormones and Calcium Metabolism
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
Vitamin D (1,25-dihydroxycholecalciferol) increases both Ca++ and phosphate absorption in the small intestine. It induces the synthesis of calbindin D-28K, a vitamin-D-dependent cytosolic Ca++ binding protein which can bind four Ca++ ions. Ca++ diffuses down an electrochemical gradient at the luminal membrane into the enterocyte. Ca++ binds to calbindin D-28K within the cytoplasm and subsequently pumped across the basolateral membrane by Ca++-ATPase pump into the blood.
Preclinical Antidepressant-Like Effects of Terpenes, Polyphenolics, and Other Non-Flavonoid Phytochemicals
Published in Scott Mendelson, Herbal Treatment of Major Depression, 2019
Paeoniflorin has neuroprotective effects that might at least partially explain its antidepressant-like effect. For example, it protected cultured rat pheochromocytoma cells from the toxic effects of corticosterone. Paeoniflorin decreased levels of intracellular reactive oxygen species and malondialdehyde, and reversed the reductions in nerve growth factor in the corticosterone‐treated cells. Overall, it increased cell viability.152 It was further shown to protect rat pheochromocytoma cells from the toxic effects of NMDA. This was seen to be due to attenuation of NMDA-induced increases in intracellular calcium activation of Calbindin‐D28K.153
Normal and Abnormal Intestinal Absorption by Humans
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
David W. Hobson, Valerie L. Hobson Balldin
The rate limiting step in transcellular calcium absorption is transport across the epithelial cell, which is greatly enhanced by the carrier protein calbindin, the synthesis of which is totally dependent on vitamin D [40–47].
Autophagy precedes apoptosis among at risk cerebellar Purkinje cells in the shaker mutant rat: an ultrastructural study
Published in Ultrastructural Pathology, 2018
Calbindin is a calcium-binding protein that is unique to the PCs in the cerebellum.2 Immunohistochemistry was performed using a previously described protocol.5,25–27 Briefly, three 5-week-old shaker mutant rats were transcardially perfused, and their cerebella were subsequently dissected and immediately stored in 30% sucrose in 0.1 M phosphate buffer (pH 7.4) overnight at 4–8°C. Serial 5-µm-thick sagittal sections were made using a freezing sliding microtome. Immunohistochemistry was performed using a mouse anti-calbindin antibody (1:5000; Sigma, Aldrich Inc, MO), which was recognized using biotinylated secondary anti-mouse antibodies (1:200; Vector) and visualized using 3,30-diamobenzidine-hydrogen peroxide (Sigma, Aldrich Inc, MO). Negative control slides were immunoprocessed without primary antibodies.
Ketogenic diet: overview, types, and possible anti-seizure mechanisms
Published in Nutritional Neuroscience, 2021
Mohammad Barzegar, Mohammadreza Afghan, Vahid Tarmahi, Meysam Behtari, Soroor Rahimi Khamaneh, Sina Raeisi
As mentioned above, it seems that excitotoxicity and apoptosis are the main mechanisms involved in seizure-induced neuronal damage and death. It has been suggested that the adverse consequences of these pathologic processes can be ameliorated by KD [89]. It has been revealed that KD can upregulate calbindin which has neuroprotective potential through its capability to buffer intracellular calcium [90]. Other neuroprotective effects of KD may be mediated by inhibition of the pro-apoptotic factors such as caspase-3 [87,88,90,91]. Moreover, the opening of the mitochondrial permeability transition pore can also be inhibited by KD [87].
Neuroprotective effects of quercetin on the cerebellum of zinc oxide nanoparticles (ZnoNps)-exposed rats
Published in Tissue Barriers, 2023
Shaimaa A. Abdelrahman, Amal S. El-Shal, Abeer A. Abdelrahman, Ebtehal Zaid Hassen Saleh, Abeer A. Mahmoud
Calbindin D28k (CB) is a calcium-binding protein that helps to maintain calcium balance. It inhibits various pro-apoptotic pathways so, prevents neuronal death.81 CB is an antioxidant that protects against oxidative stress and harmful substances.82 Its levels drop dramatically in degenerative neuronal disorders.83 In our investigation, exposure to ZnONPs reduced the strength of CB immunoexpression in Purkinje cells. The buffering ability of neurons is reduced when CB is depleted, resulting in an increase in intracellular and intranuclear calcium.84