Anti-Inflammatory Potential of Ethanolic Leaf Extract of Eupatorium adenophorum Spreng. Through Alteration in Production of TNF-α, ROS and Expression of Certain Genes.

Search for a novel anti-inflammatory agent from a herbal source, such as Eupatorium adenophorum Spreng., a plant from the Eastern Himalayas, is of prime interest in the present investigation. Inflammation causes tissue destruction and development of diseases such as asthma, rheumatoid arthritis, and so forth. The ethanolic leaf extract of E. adenophorum (EEA) was administered intravenously and in other cases topically at the site of delayed type hypersensitivity (DTH) reaction in mouse foot paw induced with dinitrofluorobenzene. EEA can effectively inhibit DTH reaction and bring back normalcy to the paw much earlier than the controls. Efficacy of EEA on regulatory mechanisms for inflammation has also been considered. Intravenous administration of EEA increased the number of CD4(+) T cells in spleen and tumor necrosis factor (TNF)-α in serum of DTH mice. Initially it was difficult to reconcile with the anti-inflammatory role of EEA and simultaneous induction of TNF-α, an established pro-inflammatory cytokine. EEA induces higher expression of TNF-α gene and amount of the cytokine in serum. We discussed the other role of TNF-α, its involvement in repairing tissue damage incurred in course of inflammatory reaction. EEA also induces TGF-β encoding a cytokine involved in tissue repair mechanism. EEA inhibits expression of another pro-inflammatory cytokine gene IL-1β and downregulates cycloxygenase 2 (COX2) gene responsible for metabolism of inflammatory mediators like prostaglandins. Furthermore, anti-inflammatory role of EEA is also revealed through its inhibition of hydroxyl radical generation. Notably EEA does not necessarily affect the expression of other inflammation-related genes such as IL-6, IL-10 and IKK. The present study reports and analyzes for the first time the anti-inflammatory property of the leaf extract of E. adenophorum.