LPS induces mediators of neuroinflammation, cell proliferation, and GFAP expression in human astrocytoma cells U373MG: the anti-inflammatory and anti-proliferative effect of guggulipid

• Published in: Neurological sciences 2014-03, Vol.35 (3), p.409-414
• Main Authors: Niranjan, Rituraj, Nagarajan, Rajasekar, Hanif, Kashif, Nath, Chandishwar, Shukla, Rakesh
• Format: Article
• Language: English
• Subjects: Astrocytoma - pathology; Astrocytoma cells; Cell Line, Tumor; Cell Proliferation - drug effects; Cell Survival - drug effects; Cyclooxygenase 2 - metabolism; Cytokines - metabolism; Dose-Response Relationship, Drug; Drug Interactions; Gene Expression Regulation, Neoplastic - drug effects; Glial Fibrillary Acidic Protein - metabolism; Humans; Lipopolysaccharides - pharmacology; Medicine; Medicine & Public Health; Neurology; Neuroradiology; Neurosciences; Neurosurgery; NF-kappa B - metabolism; Nitrites - metabolism; Original Article; Plant Extracts - pharmacology; Plant Gums - pharmacology; Protein Transport - drug effects; Psychiatry
• ISSN: 1590-1874; 1590-3478
• DOI: 10.1007/s10072-013-1530-6

Neuroinflammation has been considered to be an integrated part of human neurodegenerative diseases. In this study, we examined the effect of guggulipid on cell proliferation, nitrite release, interleukin IL-6 and IL-1 beta release, and expression of COX-2 and glial fibrillary acidic protein (GFAP) in LPS-stimulated U373MG cells. LPS significantly stimulated human astrocytoma cells U373MG by up-regulating these neuroinflammatory mediators. Guggulipid alone had no effect on the cell proliferation of U373MG cells. The up regulation in nitrite release, cell proliferation, and release of IL-6 and IL-1 beta in LPS stimulated human astrocytoma cells were dose-dependently inhibited by co-treatment with guggulipid. The expression level of COX-2 and GFAP proteins was up regulated by LPS but the increased level of COX-2 and GFAP was significantly down regulated by treatment with guggulipid. These data indicate that guggulipid has a modulatory effect on all these parameters, which might explain its beneficial effect in the treatment of neuroinflammation-associated disorders directly relating to human aspects.