Immunomodulatory Role ofOcimum gratissimumand Ascorbic Acid against Nicotine-Induced Murine Peritoneal MacrophagesIn Vitro
Author(s) -
Santanu Kar Mahapatra,
Subhankari Prasad Chakraborty,
Somenath Roy
Publication year - 2011
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2011/734319
Subject(s) - ascorbic acid , immune system , nicotine , pharmacology , proinflammatory cytokine , phagocytosis , macrophage , chemistry , in vitro , immunology , biology , inflammation , biochemistry , medicine , food science
The aim of this present study was to evaluate the immune functions and immune responses in nicotine-induced (10 mM) macrophages and concurrently establish the immunomodulatory role of aqueous extract of Ocimum gratissimum (Ae-Og) and ascorbic acid. In this study, nitrite generations and some phenotype functions by macrophages were studied. Beside that, release of Th1 cytokines (TNF- α , IL-12) and Th2 cytokines (IL-10, TGF- β ) was measured by ELISA, and the expression of these cytokines at mRNA level was analyzed by real-time PCR. Ae-Og, at a dose of 10 μ g/mL, significantly reduced the nicotine-induced NO generation and iNOSII expression. Similar kinds of response were observed with supplementation of ascorbic acid (0.01 mM). The administration of Ae-Og and ascorbic acid increased the decreased adherence, chemotaxis, phagocytosis, and intracellular killing of bacteria in nicotine-treated macrophages. Ae-Og and ascorbic acid were found to protect the murine peritoneal macrophages through downregulation of Th1 cytokines in nicotine-treated macrophages with concurrent activation of Th2 responses. These findings strongly enhanced our understanding of the molecular mechanism leading to nicotine-induced suppression of immune functions and provide additional rationale for application of anti-inflammatory therapeutic approaches by O. gratissimum and ascorbic acid for different inflammatory disease prevention and treatment during nicotine toxicity.
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