In vivo stimulatory effect of multi-component herbal remedy PADMA 28 on mitogen-induced proliferation of mice splenic lymphocytes and their chemokinetic activity.

UNLABELLED: PADMA 28, a natural herbal multi-compound remedy originates from traditional Tibetan medicine and possesses a variety of beneficial effects on experimental and clinical models of inflammation and atherosclerosis, as well as angioprotecive, antioxidative and wound-healing properties. The aim of the present study was to evaluate the in vivo influence of this remedy on the in vitro mitogen-induced proliferation of murine splenic lymphocytes and their chemokinetic activity in cell culture.The study was performed on 6-8 weeks old inbred Balb/c mice. PADMA28 was administered to mice per os in daily doses 5.8 mg (calculated from the highest dose recommended for human) or 0.085 mg (dose from the range of active doses of other herbal extracts containing polyphenolic substances used previously by us in experiments with mice), for 7 days. Control groups received water. RESULTS: No substantial differences were observed between groups of mice fed with low and high PADMA doses. In both of them, response of splenic lymphocztes to mitogen PHA (p < 0.001) and their in vitro chemokinetic activity (p < 0.001 for low dose and p < 0.01 for high dose) were highly significantly increased as compared to the controls. CONCLUSION: The results of our investigations suggest that PADMA 28 can stimulate cell-mediated immunity in mice and might be used for this purpose in the wide spectrum of doses.

Influence of N-acetylcysteine on ICAM-1 expression and IL-8 release from endothelial and epithelial cells.

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. The initial step in the inflammatory process is overexpression of adhesion molecules, which leads to excessive transmigration of neutrophils. One of these adhesion molecules is ICAM-1 which is elevated in COPD patients. In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines. The methodology used consisted of immunochemistry for the assessment of surface ICAM-1 and ELISA method for that of soluble ICAM-1 and IL-8. NAC inhibited the TNF-alpha/IL-1 beta-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner. The most effective concentrations were 30 mM and 20 mM (99 and 90% inhibition respectively, P<0.01). We conclude that NAC is an effective inhibitor of TNF-alpha/IL-1 beta- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells. This fact highlights the anti-inflammatory potential of NAC in COPD.