颅神经损伤
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Figure 1｜Taurine-mediated neuroprotection against glutamate-induced retinal cell death.
The prospects of the benefits of TAU as a neuroprotective agent are also supported by other investigations showing that several mechanisms may, in fact, collectively contribute to its neuroprotective effects (Figure 1). For example, the study of Chen et al. (2009) demonstrated that TAU protects RGCs against hypoxic damage in vivo by preventing mitochondrial dysfunction. Similarly, TAU has been shown to improve the viability of glucose deprived cells by attenuating mitochondrial and endoplasmic reticulum stress in a dose-dependent manner (Yang et al., 2013). Another study using rat osteogenic sarcoma line, UMR-106, showed that TAU reduced H2O2-induced oxidative stress and apoptosis in a dose-dependent manner (Lou et al. 2018). Another study provided evidence that neuroprotection by TAU is associated with its antioxidant function (Jafri et al., 2018; Arfuzir et al., 2018). In our studies, the effect of TAU on oxidative stress was evaluated in NMDA and ET-1 exposed retina and it was observed that TAU increased the retinal reduced glutathione (GSH) level, which was in accordance with a previous study (Pushpakiran et al., 2004). The effect of TAU on GSH levels may be due to its ability to act as a pH-stabilizing buffer in mitochondria which helps to establish the equilibrium between the NADH/NAD(+) redox pair and the redox buffer pair of reduced/oxidized glutathione (GSH/GSSG) (Hansen and Grunnet, 2013). Studies done by Jafri et al. (2018) and Arfuzir et al. (2018) have also shown that superoxide dismutase (SOD) activity was upregulated in the retina after treatment with TAU. SOD plays an important role in scavenging free radicals and its improved activity after TAU treatment has been attributed to reduced ER stress (Nonaka et al., 2001). The activity of another antioxidant enzyme, catalase, was also found to be increased in our studies after TAU treatment (Jafri et al., 2018), which was in accordance with a previous study (Yu and Kim, 2009). In the same studies by Jafri et al. (2018) and Arfuzir et al. (2018), it was observed that the malondialdehyde contents that indicate the extent of lipid peroxidation, in the retinas treated with TAU were significantly low compared to controls treated with NMDA/ET-1. This clearly shows the ability of TAU to efficiently scavenge reactive oxygen species and enhance antioxidant defenses. In a study done by Oliveira et al (2010), TAU exhibited a significant free radical scavenging potential against peroxyl radical, nitric oxide, and superoxide donors in a dose-dependent manner.