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

Activation of cell mediated immune response and apoptosis towards malignant cells with turmeric treatment in murine model

23-29The effect of ethanolic turmeric extract (ETE) on murine lymphocytes vis-à-vis tumor cells was studied, in terms of its ability to activate lymphocytes and to induce apoptosis in tumor cells. Degree of activation and proliferation of lymphocytes treated with ETE was analyzed in terms of blastogenesis, DNA synthesis through ³H-thymidine incorporation and cell cycle analysis by flourescence activated cell sorter (FACS). FACS analysis was also carried out to observe the proliferation as well as apoptosis of tumor cells. Morphological condition of both the cell types in presence of ETE was examined by scanning electron microscopy (SEM). Cytotoxic capability of ETE-treated effector T lymphocytes towards tumor cells was judged in vitro by ⁵¹Cr-release assay and the growth of tumor in situ. ETE stimulated murine lymphocytes towards blastogenesis and synthesis of DNA, as revealed by increased incorporation of ³H-thymidine. FACS indicated that the lymphocytes were driven towards mitotic cycle by activating G₂-M transition. In the same count, the tumor cells mostly remained accumulated in the G₂-M phase, and thus mitotically arrested. Scanning electron photomicrographs revealed the blastoid transformation of lymphocytes and ETE-induced apoptotic condition of tumor cells. Furthermore, ETE-treated T cells were cytotoxic towards tumor cells in vitro, as shown by ⁵¹Cr- release assay. ETE administered intravenously or orally could delay the onset and growth of tumor, and thus prolonged the life span of the tumor-bearing host. The present investigation suggests potential of turmeric both to destroy the malignant cells directly and via activation of the host’s cellular immunit