Abstract
Asthma is a serious global health risk characterized by chronic airway inflammation of lungs with infiltration of inflammatory cells, enhanced mucus secretion and narrowing of airways that leads to poor respiratory functions. The clinical symptoms of asthma includes recurrent episodes of cough, shortness of breath, wheezing and chest tightness. One of the pathophysiology of asthma was mediated by overproduction of pro-inflammatory asthmatic leukotrienes through arachidonic acid pathway catalyzed phospholipase A2 (PLA2 ) and 5-lipoxygenase (5-LOX) enzymes. The available conventional therapies to treat asthma may induce severe side effects on health and high cost. To overcome the disadvantages to treat asthma and to improve the current therapeutic strategy, we used natural products as an alternative therapy. Finger millet (Eleusine coracana) has been used by folk and traditional medicinal practitioners to treat various inflammatory conditions. Previously, we have found the promising anti-inflammatory phytochemicals in finger millet bran (Fmb). Hence, aim of the present study was to identify and characterize anti-asthmatic phytochemicals from Fmb and the objective was to test its anti-inflammatory activity in ovalbumin induced asthma mouse model. Phytochemical analysis of Fmb revealed the presence of phenolics, saponins and anthraquinone. Among all the extracted fractions, finger millet bran methanol extract (FbMe) possessed strong in vitro anti-inflammatory activity by inhibiting pro-inflammatory PLA2 and 5-LOX enzymes activity. Further, in vivo anti-inflammatory activity of FbMe was evaluated in an ovalbumin induced asthma mouse model. FbMe (50 mg/kg) significantly reduced the infiltration of inflammatory cells, lung fibrosis by reducing the deposition of collagen in the tissue. It also inhibited the PLA2 as well as 5-LOX enzymes activity in collected BAL fluid. This finding concludes the presence of strong anti-inflammatory and anti-fibrotic phenolic compounds in the FbMe, which attenuates the lung inflammation and fibrosis probably via inhibition of PLA2 and 5-LOX enzymes activity.
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