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Furthermore, N-chloramines from HOCl-modified LDL have been reported to inactivate lecithin-cholesterol acyltransferase (LCAT), an enzyme involved in the maturation of the antiatherogenic high-density lipoprotein (HDL), thus providing another mechanism by which HOCl promotes atherogenesis [329]

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In addition to the major CSF1R pathway, microglial survival is regulated by several other signaling cascades

From these results, it can be assumed that the glutathione redox cycle has not yet been enhanced in proline group relative to control group at 3 h