Abstract
Objective. To investigate the effect of tea polysaccharides (TPS) mediated by miR-375/SRXN1 axis on mice with cerebral ischemia-reperfusion injury and proliferation and apoptosis of astrocytes (AS) conducted with oxygen-glucose deprivation/reoxygenation (OGD/R). Methods. Mouse model of middle cerebral artery occlusion (MCAO) and OGD/R-induced AS injury model were established; brain obstruction volume was measured by TTC staining; dry/wet weight ratio was used for measuring brain water content; hydrogen peroxide (H2O2) content in brain tissue was measured by H2O2 assay kit; cell viability and apoptosis rate were detected by MTT assay and flow cytometry, respectively; the expression level of miR-375 in OGD/R-AS was detected using qPCR; dual-luciferase reporter assay was used to verify the targeting relationship between miR-375 and SRXN1; mRNA levels of miR-375, SRXN1, Bcl-2, Bax, and caspase-3 were measured by qPCR; the protein levels of SRXN1, Bcl-2, Bax, and caspase-3 were measured by Western blotting. Results. The volume of cerebral obstruction, brain water content and H2O2 content in mice decreased gradually with the increase of TPS concentration. TPS treatment in vitro could effectively improve OGD/R-AS viability and reduce the apoptotic rate; overexpression of miR-375 inhibited AS viability but increased the apoptotic rate; TPS treatment resulted in a decrease in the expression of miR-375 in OGD/R-AS; MiR-375 targeted SRXN1 in AS; inhibition of miR-375 expression significantly upregulated SRXN1 levels; TPS treatment with simultaneous overexpression of SRXN1 significantly increased OGD/R-AS activity and reduced apoptosis; however, TPS treatment with simultaneous overexpression of SRXN1 and miR-375 resulted in no significant difference in cell viability and apoptosis rate compared with the control group. Conclusion. TPS reduces astrocyte injury induced by cerebral ischemia-reperfusion in mice by regulating the miR-375/SRXN1 molecular axis.
Highlights
Ischemic stroke, one of the leading causes of interruption of cerebral blood flow, is an important factor of death and disability worldwide [1]
The H2O2 content in the brain tissues was measured, and it was found that the content gradually decreased as the concentration of tea polysaccharides (TPS) increased in the brain tissues with cerebral ischemia-reperfusion injury (Figure 1(c))
The effect of TPS on AS proliferation under oxygen-glucose deprivation/reoxygenation (OGD/R) treatment was examined using MTT assay, and the results revealed that AS cell viability was gradually enhanced with increasing TPS concentration, with the highest cell viability under 40 mg L−1 treatment (Figure 2(a))
Summary
One of the leading causes of interruption of cerebral blood flow, is an important factor of death and disability worldwide [1]. Restoration of blood supply to the brain following ischemic stroke may lead to reperfusion injury [2]. Reperfusion stimulates the overproduction of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2), which induces cell proliferation, growth arrest, and causes apoptosis and necrosis [3]. There is increasing evidence that apoptosis and death of nerve cells after ischemia-reperfusion are the main causes of exacerbated brain injury [5]. Sulfiredoxin-1 (SRXN1) is an endogenous antioxidant protein [6] that plays an important role in neuroprotection [7]. SRXN1 can resist cellular oxidative stress-induced ROS production [8, 9]. Zhou et al [10] reported the antioxidant function exerted by Advances in Polymer Technology
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