Corvitin restores metallothionein and glial fibrillary acidic protein levels in rat brain affected by pituitrin-izadrin

Abstract

In this research, we investigated the effect of pituitrin-izadrin induced injury on the levels of metallothionein (MT) and soluble and filament forms of glial fibrillary acidic protein (GFAP) in the hippocampusA strocytes are amongst the earliest and prominent to express changes under attacks [1]. They are the most numerous nonneuronal cell types in the central nervous system (CNS) and make up about 50% of the volume of the human brain [1,2]. Their functions are known to be critical, such as scavenge transmitters released during synaptic activity, control ion and water homeostasis, release neurotrophic factors, shuttle metabolite, and waste products, and to participate in the formation of the blood-brain-barrier [3,4]. Failure of any of these supportive functions of astrocytes will constitute a threat to neuronal survival. Astrocytes are home to a number of essential proteins of the CNS, including metallothionein and glial fibrillary acidic protein, which presumably carry out some astrocyte functions.Metallothioneins (MTs) are cysteine-rich, low molecular weight, heat stable proteins firstly described by Margoshes [5]. They are largely synthesized in the liver and the kidney in humans but are found at a number of other sites. In the CNS, MT-I and MT-II are conspicuously absent from neuronal populations, yet abundant in fibrous and protoplasmic astrocytes. MT is detectable in the extracellular fluid of the injured brain and astrocytes are capable of secreting MT in a regulatable manner [6].MTs have been implicated as regulatory molecules in gene expression, homeostatic control of cellular metabolism of metals, and cellular adaptation to stress. Thus, they fulfill a regulatory capacity and influence transcription, replication, protein synthesis, metabolism, as well as other zinc-dependent biological processes [7]. It has been shown that the ability of animals to recover from CNS injuries or degenerative diseases depends on the deficiency or excess availability of MT-I/-II [7][8][9][10][11]. MT has equally been demonstrated to be down-regulated in cases of induced intoxication [12] and infection [13] but its correlated effect to other astrocyte proteins has yet to be tested.GFAP is expressed in mature astrocytes in the CNS [14]. It is a member of the family of cytoskeletal proteins and is the primary intermediate filament with a size of 8-9 nm, highly specific to the CNS. However, it has been found outside the CNS in relatively low amounts [15]. It has two physicochemical GFAP forms: water-soluble (sGFAP) and filament (fGFAP) [16]. The sGFAP is unevenly distributed in various brain regions, with the maximum con-

The Cardio- and Neuroprotective Effects of Corvitin and 2-Oxoglutarate in Rats with Pituitrin-Isoproterenol-Induced Myocardial Damage

“…In our previous studies, an established regulatory action of Corvitin on the metallothionein (MT) and glial fibrillary acidic protein (GFAP) levels in various parts of the brain was shown. It is known that GFAP is responsible for the functional activity of astrocytes and nutrition of neurons, while MT regulates gene expression and cell adaptation to the stress factors [ 60 ]. Behavioral activation of rats with PIMD after the treatment by 2-OG is the definitive result of its multifactor impact on brain metabolism.…”

Low doses of imidacloprid induce disruption of intercellular adhesion and initiate proinflammatory changes in Caco-2 cells

“…On the other hand, oxidative stress can interact with individual signalling pathways, which may be more closely related to the detrimental effect and specificity of outer stimuli. In the nervous system, for example, the glial fibrillary acidic protein (GFAP) is known as a neurotoxicity biomarker (Shiyntum et al, 2017;Abdel Salam, 2021) which is obviously connected with the ROS production (Gasso et al, 2020a;Fernandes & Özcelik, 2021). On the other hand, the inflammation is an important part of innate defence against infectious agents as well as xenobiotic toxicity.…”

Low doses of imidacloprid induce neurotoxic effects in adult marsh frogs: GFAP, NfL, and angiostatin as biomarkers

“…After 7 days of the experiment, a decrease in GFAP in frog brain astrocytes was observed, which might indicate impaired astrocyte development (Flaskos, 2014). Given that GFAP is a classical biomarker of astrocyte disorders (Eliasson et al, 1999;Tykhomyrov et al, 2016;Shiyntum et al, 2017), a decrease in GFAP levels may indicate a dysfunction of brain nervous tissue (Müller et al, 2012). According to Markiewicz et al (2006), a decrease in GFAP was observed in the brain of rats after administration of low doses of the pyrethroid cypermethrin after 2 and 21 days of the experiment.…”