Immunomodulatory Effects of Bio-Clean II on Some Inflammatory Cytokines in Rats Exposed to Purified Bacterial Lipopolysaccharide

Abstract

Bacterial inflammatory diseases have continued to be a major threat to public health. The aim of this study is to determine the effects of Bio-Clean II on serum levels of some selected cytokines in rats exposed to purified bacterial lipopolysaccharide (LPS). A total of 36 male Wistar rats weighing 150g±50g (mean±SD) were purchased and randomly assigned to six (6) groups of 6 rats each. Group 1, 2, 3, 5 and 6 were induced with a single dose of 5mg/Kg of purified LPS® (E.coli 0127:B8, Sigma-Aldrich, St. Louis, USA), administered through intraperitoneal route using 1ml sterile needle and syringe, except for group 4 which served as the zero control (given water and feed only throughout the experiment). Group 1 served as the inflammation control. Group 2 which served as the positive control received 50 mg diclofenac/kg [bid] and 500 mg ciprofloxacin/kg [bid] (positive control) in place of the Bio-Clean. Group 3 which served as the negative control received sterile phosphate buffer saline (PBS). While rats in group 5 and group 6 were treated orally with the herbal remedy “Bio-Clean II” for 7 days and 14 days, respectively. After which, the rats were sacrificed and a cardiac blood specimen was taken from each rat by terminal bleeding from the heart. The serum levels of Interleukin-6 (IL-6), Interleukin-10 (IL-10), Interferon-Gamma (IFN-γ), and Tissue Necrosis Factor-Alpha (TNF-α) were determined using ELISA technique. The outcome of this investigation shows that treatment with the Bio-Clean II resulted in a significant decrease (p=0.000*) in the serum level of IL-6, IFN-γ and TNF-α, but a significant (p=0.000*) increase in the serum level of IL-10 (in a duration-dependent manner) in rats exposed to LPS when compared to the inflammation control group. The outcome of this study suggests that Bio-Clean could find some use in the future for the alleviation of bacterial inflammatory diseases through modulations of host inflammatory responses to pathogens.