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It has been shown that HSYA was able to significantly protect the liver from oxidative stress by increasing the activities of antioxidant enzymes, upregulating the expression of PPAR- and MMP-2, and downregulating the expression of TGF-1 and tissue inhibitor of metalloproteinases-1 (TIMP-1), and reducing -SMA level, which indicating that PPAR-TGF-1 would be a signal pathways for HSYA to reduce liver fibrosis induced by oxidative stress (Wang et al., 2013)

(C) TaC12-Cas9 expressing cells were analyzed by fluorescence-activated cell sorting (FACS) prior to cell sorting for BFP+/GFP-signal

61 Moreover, enhanced lipid uptake and peroxidation can result in high oxidative stress, which leads to CD8 + T cell dysfunction

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