title: Ginsenoside Rb1 eliminates HIV-1 (D3)-transduced cytoprotective human macrophages by inhibiting the AKT pathway.
abstract: Abstract Acquired immunodeficiency syndrome patients treated with red ginseng, which contains protopanxadiol and protopanaxatriol ginsenosides as its main constituents, have been reported to remain healthy for >20 years in the absence of highly active antiretroviral therapy. Of these ginsenosides, ginsenoside Rh1, a protopanaxatriol ginsenoside, is known to eliminate cytoprotective HIV-1-infected macrophages by inhibiting pyruvate dehydrogenase lipoamide kinase isozyme 1 (PDK-1) phosphorylation. In this study, we investigated the capacity of ginsenoside Rb1, a protopanaxadiol ginsenoside, to eliminate cytoprotective primary human macrophages. We found that ginsenoside Rb1 could also eliminate cytoprotective primary human macrophages infected with HIV-1 D3. Ginsenoside Rb1 inhibited lipopolysaccharide/cycloheximide-induced AKT and glycogen synthase kinase-3β phosphorylation in the D3-transduced macrophages, but not the phosphorylation of PDK-1 and phosphoinositide-3-kinase (PI3K). Furthermore, we also observed that a combined treatment with ginsenoside Rb1 and miltefosine synergistically abolished the cytoprotective CHME5 cells expressing HIV-1 tat. Based on these findings, we can conclude that ginsenoside Rb1 can eliminate cytoprotective macrophages infected with HIV-1 by inhibiting the AKT pathway.
authors.affiliation: 1 Department of Life and Nanopharmaceutical Sciences, Kyung Hee University , Seoul, South Korea .
authors.forename: Jin-Ju
authors.initials: JJ
authors.lastname: Jeong
authors.forename: Baek
authors.initials: B
authors.lastname: Kim
authors.forename: Dong-Hyun
authors.initials: DH
authors.lastname: Kim
mesh_terms: D000328:Adult; D002460:Cell Line; D002478:Cells, Cultured; D036145:Ginsenosides / Q000494:pharmacology*; D015658:HIV Infections / Q000188:drug therapy / Q000378:metabolism* / Q000821:virology; D015497:HIV-1 / Q000187:drug effects / Q000235:genetics* / Q000502:physiology; D006801:Humans; D008264:Macrophages / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000821:virology; D008297:Male; D005894:Panax / Q000737:chemistry*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D000081382:Pyruvate Dehydrogenase Acetyl-Transferring Kinase; D015398:Signal Transduction / Q000187:drug effects; D014161:Transduction, Genetic; D055815:Young Adult
chemical_list: D036145:Ginsenosides; D019869:Phosphatidylinositol 3-Kinases; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt; D000081382:Pyruvate Dehydrogenase Acetyl-Transferring Kinase; C000631429:PDK1 protein, human; C442759:ginsenoside Rb1
keywords: antiviral activity; ginseng; ginsenosides