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Silverman, DC, DACBN, DCBCN, MS, CCN, CNS, CSCS, CIISN, CKTP, CES, HKC, SASTM Dr

Supplementary material The Supplementary Material for this article can be found online at: Glossary Akt Protein kinase B ALP alkaline phosphatase ALT alanine aminotransferase AMPK Adenosine 5-monophosphate-activated protein kinase Apaf-1 Apoptotic protease activating factor 1 ARE Antioxidant response element AST aspartate aminotransferase Bax BCL2-associated X protein Bcl-2 B-cell lymphoma 2 CCND1 Cyclin D1 CI confidence interval COX-2 Cyclooxygenase-2 CYP2E1 Cytochrome P450 proteins EGFR Epidermal growth factor receptor ERK Extracellular signal-regulated protein kinase FoxO1 Forkhead box protein O1 GalN D-galactosamine GCLM Glutamate-cysteine Ligase GSH glutathione HepG2 Human hepatoma cell line HO-1 Heme oxygenase-1 IL-1 Interleukin-1 beta IL-6 Interleukin-6 IL-17 Interleukin-17 IL-18 Interleukin-18 iNOS Inducible nitric oxide synthase Keap1 Kelch-like ECH-associated protein 1 LC3-II Microtubule-associated protein 1A/1B-light chain 3-II LPS Lipopolysaccharide MDA malondialdehyde mTOR Mammalian target of rapamycin MyD88 Myeloid differentiation primary response 88 NF-B nuclear factor-B NQO1 NAD(P)H quinone dehydrogenase 1 Nrf2 nuclear factor erythroid-2-related factor 2 PCNA Proliferating cell nuclear antigen PI3K Phosphatidylinositol 3-Kinase PRISMA Preferred Reporting Items for Systematic Reviews and Meta-Analysis p-GSK3 Phospho-Glycogen synthase kinase 3 beta PXR pregnane X receptor ROS Reactive oxygen species SCF Schisandra chinensis Fructus SD standard deviation SEM standard error of the mean SMD standardized mean difference SOD superoxide dismutase SYRCLE Systematic Review Centre for Laboratory animal Experimentation TG Triglyceride TLR4 Toll-like receptor 4 TNF- Tumor necrosis factor-alpha References 1 AnY.WangY.XuL.FanH.ShenN.ZhaoL.et al (2014)

It is suggested that the divergent clade ShHTLs lost the ability to bind to KAR due to bulky residue 219, and they developed a highly sensitive subgroup (ShHTL4, ShHTL5, and ShHTL7) for SL binding likely via the evolution of F150 and other pocket-composing residues (e.g., residue 194)

Atherosclerosis 173 , 321328 (2004)