The Effect of Mesedin on the Content of Oxidative Stress Biomarkers in the Brain Tissue in Ischemia

Tananyan, Armen; Balasanyan, M. G.; Baykov, A. V.; Hovsepyan, L.; Ghazaryan, Gayane

doi:10.1134/s1819712419010173

Cited by 1 publication

(2 citation statements)

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“…Extrapolating this result to the progression of liver injury, it can be assumed that mesedin may exert its antifibrotic properties through IL-10, which is known to possess strong protective features in hepatocytes and to induce the senescence of activated HSCs [41,42]. By acknowledging the antihypoxic properties of mesedin in the central nervous system in vitro and in vivo [9][10][11], future investigations of mesedin's effects on parenchymal and nonparenchymal liver cells exposed to hypoxia can provide additional mechanistic insight into the function of hepatic α2-AR and the feasibility of its blockade in the treatment of chronic liver injury.…”

Section: Discussionmentioning

confidence: 99%

“…Mesedin has been previously shown to possess neuroprotective features in vivo and in vitro. In a model of focal ischemia, mesedin improved memory and anxiety symptoms and decreased oxidative stress markers in brain tissue [9,10]. In astroglial primary culture of normal and Alzheimer's mouse model (3xTg-AD) brains, the increased survival of neurons, upregulated neurogenesis markers, and anti-inflammatory cytokines have been observed upon treatment with mesedin [11].…”

Section: Introductionmentioning

confidence: 99%

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α2-Adrenergic Receptor in Liver Fibrosis: Implications for the Adrenoblocker Mesedin

Schwinghammer

Melkonyan

Hunanyan

et al. 2020

Cells

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The noradrenergic system is proposed to play a prominent role in the pathogenesis of liver fibrosis. While α1- and β-adrenergic receptors (ARs) are suggested to be involved in a multitude of profibrogenic actions, little is known about α2-AR-mediated effects and their expression pattern during liver fibrosis and cirrhosis. We explored the expression of α2-AR in two models of experimental liver fibrosis. We further evaluated the capacity of the α2-AR blocker mesedin to deactivate hepatic stellate cells (HSCs) and to increase the permeability of human liver sinusoidal endothelial cells (hLSECs). The mRNA of α2a-, α2b-, and α2c-AR subtypes was uniformly upregulated in carbon tetrachloride-treated mice vs the controls, while in bile duct-ligated mice, only α2b-AR increased in response to liver injury. In murine HSCs, mesedin led to a decrease in α-smooth muscle actin, transforming growth factor-β and α2a-AR expression, which was indicated by RT-qPCR, immunocytochemistry, and Western blot analyses. In a hLSEC line, an increased expression of endothelial nitric oxide synthase was detected along with downregulated transforming growth factor-β. In conclusion, we suggest that the α2-AR blockade alleviates the activation of HSCs and may increase the permeability of liver sinusoids during liver injury.

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