title: The chloroform fraction of Solanum nigrum suppresses nitric oxide and tumor necrosis factor-α in LPS-stimulated mouse peritoneal macrophages through inhibition of p38, JNK and ERK1/2.
abstract: Solanum nigrum L., commonly known as black nightshade, is used worldwide for the treatment of skin and mucosal ulcers, liver cirrhosis and edema. We aimed to determine the anti-inflammatory active fraction of S. nigrum by serial extractions. S. nigrum was first extracted with methanol, then fractionated with chloroform and water. The effects of S. nigrum fractions, diosgenin and α-solanine on LPS/interferon-gamma-induced nitric oxide (NO) and inducible NO synthase (iNOS), or LPS-induced tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, in mouse peritoneal macrophages were determined. Western blotting analysis was used to detect LPS-induced phosphorylation of p38, JNK and ERK1/2. The chloroform fraction of S. nigrum was cytotoxic in a time and concentration dependent manner; however, the methanol and water fractions were not. The chloroform fraction reduced NO through inhibition of iNOS synthesis and inhibited TNF-α and IL-6 at the level of protein secretion; the methanol and water fractions showed a weak or no effect. The chloroform fraction also suppressed p38, JNK and ERK1/2. Diosgenin and α-solanine were cytotoxic at a high concentration. In particular, diosgenin was able to inhibit TNF-α and IL-6, but both compounds did not affect LPS-induced iNOS expression. These results indicate that the anti-inflammatory compounds of S. nigrum exist preferentially in the nonpolar fraction, ruling out the possibility that diosgenin and α-solanine are the likely candidates. The inhibition of iNOS, TNF-α and IL-6 by the chloroform fraction may be partly due to the suppression of p38, JNK and ERK1/2. Further study is required to identify the active compounds of S. nigrum.
authors.affiliation: Department of East-West Medical Science, Graduate School of East-West Medical Science, Kyung Hee University, Yongin-si, Gyeonggi-do, South Korea.
authors.forename: Hee
authors.initials: H
authors.lastname: Kang
authors.forename: Ha-Deok
authors.initials: HD
authors.lastname: Jeong
authors.forename: Ho-Young
authors.initials: HY
authors.lastname: Choi
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002478:Cells, Cultured; D015536:Down-Regulation / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000276:immunology; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000276:immunology; D009569:Nitric Oxide / Q000276:immunology*; D010936:Plant Extracts / Q000494:pharmacology*; D032324:Solanum nigrum / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D020928:Mitogen-Activated Protein Kinases