FIGURE 1 Inflammation Neuroinflammation is a key pathophysiological mechanism of secondary injury, as it can produce neurotoxic effects on neurons through oxidative stress, apoptosis, and excitotoxicity (Kumar and Loane, 2012), inducing a progressive cycle of chronic inflammation (Sulhan et al., 2020)
Acetaminophen Toxicity Acetaminophen has some safe metabolic pathways to form non-toxic products
Sudakov views DSIP as one of the 4 main substances, responsible for the stress-resistance of the organism, another 3 being substance P, prolactin and beta-endorphin
After the model was expanded to include GS-H 2 Q adduct formation as a function of its reduction potential, it was then combined with the Reed glutathione model 21 in order to simulate how the quinone redox-metabolism of doxorubicin influenced the glutathione metabolism
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Next, we identified DEGs between the control group and the WT group, the (-)-Vestitol group and the control group, the Salviolone group and the control group, and the combination group and the control group