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Abstract
To investigate the role of mitochondria in the protective effects of ginsenoside Rb1 on cellular apoptosis caused by oxygen-glucose deprivation, in this study, MTT assay, TUNEL staining, flow cytometry, immunocytochemistry and western blotting were used to examine the cellular viability, apoptosis, ROS level, mitochondrial membrane potential, and the distribution of apoptosis inducing factor, cytochrome c, Bax and Bcl-2 in nucleus, mitochondria and cytoplasm. We found that pretreatment with GRb1 improved the cellular viability damaged by OGD. Moreover, GRb1 inhibited apoptosis in SH-SY5Y cells induced by OGD. Further studies showed that the elevation of cellular reactive oxygen species levels and the reduction of mitochondrial membrane potential caused by OGD were both counteracted by GRb1. Additionally, GRb1 not only suppressed the translocation of apoptosis inducing factor into nucleus and cytochrome c into cytoplasm, but also inhibited the increase of Bax within mitochondria and alleviated the decrease of mitochondrial Bcl-2. Our study indicates that the protection of GRb1 on OGD-induced apoptosis in SH-SY5Y cells is associated with its protection on mitochondrial function and inhibition of release of AIF and cytochrome c.
Highlights
Ischemic stroke due to lack of cerebral blood supply is one of the most common causes leading to death or disability in adults worldwide [1]
In order to investigate the protective effects of ginsenoside Rb1 (GRb1) on cell death caused by Oxygen-glucose deprivation (OGD), MTT assay was used to assess cellular viability in SH-SY5Y cells
100 μmol/L GRb1 did not show any protection on cellular viability when compared with that in the OGD group; we think this might because a higher concentration of GRb1 might produce toxic effects on SH-SY5Y
Summary
Ischemic stroke due to lack of cerebral blood supply is one of the most common causes leading to death or disability in adults worldwide [1] Both animal studies and clinical finding revealed that reperfusion following ischemia results in delayed neuronal injury or death [2,3]. It is found that the protective effects of ischemic postconditioning and preconditioning on neuronal death induced by ischemia and reperfusion are associated with inhibition of apoptosis [10]. These previous studies show that apoptosis plays an important role in neuronal death caused by various pathological stresses, and indicate that anti-apoptosis might be a strategy to prevent or alleviate neuronal damage induced by ischemia and reperfusion. The present study aimed to determine whether ginsenoside Rb1 protects against SH-SY5Y apoptosis caused by OGD via maintaining mitochondrial function
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