Protective Role of Taurine Against Morphine-Induced Neurotoxicity in C6 Cells via Inhibition of Oxidative Stress

Abstract

This study was carried out to investigate the protective role of taurine (2-aminoethanesulphonicacid) against morphine-induced neurotoxicity in C6 cells. It was found that taurine significantly increased the viability of C6 cells treated by morphine, showing the neuroprotective role against morphine-induced neurotoxicity. However, such neuroprotective effect of taurine could not be blocked by bicuculline, an antagonist of gamma-amino butyrate (GABA) receptor. To determine the oxidative damage induced by morphine, the superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured in C6 cells. The decreased activities of SOD, CAT, and GPx in C6 cells were observed after morphine treatment for 48 h. However, taurine administration effectively ameliorated morphine-induced oxidative insult. To estimate anti-apoptosis effect of taurine, flow cytometry analysis as well as detection for caspase-3 and Bcl-2 expressions was performed after morphine exposure for 48 h. It was found that Bcl-2 expression was down regulated by morphine, whereas taurine could reverse morphine-induced decrease in Bcl-2 expression. Taurine showed no effect on caspase-3 expression. Collectively, the results show that taurine possesses the capability to ameliorate morphine-induced oxidative insult and apoptosis in C6 cells, probably due to its antioxidant activity rather than activation of GABA receptors.

Therapeutic concentration of morphine reduces oxidative stress in glioma cell line

“…Studies indicating a pro-oxidant activity of morphine used high doses and/or evaluated oxidative stress as a mechanism associated with tolerance and/or dependence on the opioid (7,9,11-13). Exposure to increased concentrations of morphine (as high as 6 mM) has already been used as a model of neuronal damage by oxidative stress in both in vivo and in vitro studies (including the C6 cell line) (7,11-13).…”

Neuroprotective effects of Kukoamine B against hydrogen peroxide-induced apoptosis and potential mechanisms in SH-SY5Y cells

“…After these treatments, the supernatant was used to determine the protein concentrations using the BCA protein assay kit (Beyotime, Nanjing, China). And the supernatant was also used in the assays of GSH-Px, SOD, CAT activities and MDA level according to the manufacturer's instructions (Tian et al, 2014;Zhou et al, 2011). GSH-Px activities were determined at 340 nm by the ability to oxidize GSH, using cumene hydroperoxide (Cum-OOH) as a substrate, coupled to the reduction rate of triphosphopyridine nucleotide (NADPH) by glutathione reductase (GR).…”

Effect of taurine on the proliferation and apoptosis of human hepatocellular carcinoma HepG2 cells

“…Firstly, Tau has been hypothesized to enhance antioxidation in the body through the removal of strong oxidizing agents, which subsequently protects normal cells from oxidative damage and induces tumor cell apoptosis (9,20,21). For example, Tau can reverse the morphine-induced downregulation of Bcl-2 and effectively control morphine-induced oxidative damage, thus preventing nerve cell toxicity (22). In B16F10 mouse melanoma cells, Tau functions by upregulating superoxide dismutase genes, glutathione peroxidase and catalase, while inhibiting cell growth by decreasing the concentration of reactive oxygen species in a dose-dependent manner (23).…”