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In the same way, UVB radiation induces phosphorylation of p38 that modulates NF-B activation, triggered by an elevation of reactive oxygen species (ROS) [16]
Trx-(SH)2 and GSH then supply reducing equivalents for a number of different reactions, including those that are glutaredoxin (Grx)-dependent
In addition, astrocyte mitochondrial dysfunction triggers a pro-inflammatory response, whereas normal mitochondria inhibit microglia activation and the release of pro-inflammatory factors, such as TNF- and IL-6, indirectly protecting neurons from inflammation-related apoptosis [54]
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