Abstract
Nyctanthes arbor-tristis L. contains various phytochemicals with tremendous potential to fight against different infections. However, the effect of these phytochemicals on Mycobacterium tuberculosis is yet unknown. Treatment of multi-drug resistance (MDR) and extensively drug-resistant (XDR) strains of the tuberculosis bacterium are still challenging. Therefore, there is an urgent need to overcome this problem. The present review focuses on the potential action of the hypolipidemic phytochemicals obtained from N. arbor-tristis on the growth and survival of M. tuberculosis in the human host. The extracts from different parts of this plant are hypolipidemic by various established mechanisms. Phytochemicals like iridoids and flavonoids from plant origin exhibit a high capacity to regulate cholesterol and fatty acid biosynthesis in vivo. The hypolipidemic properties of N. arbor-tristis-derived extracts are probably due to the presence of phytochemicals such as iridoids, flavonoids, etc. It may regulate fatty acid biosynthesis in M. tuberculosis by targeting bacterial fatty acid synthase enzyme. Additionally, these phytochemicals also inhibit cholesterol biosynthesis in the host by interrupting the function of HMG-CoA reductase. M. tuberculosis is an intracellular pathogen. It is also established fact as on date that entry of tuberculosis bacterium in the macrophage is macrophage membrane cholesterol-dependent. Host cholesterol is also otherwise necessary by multiple mechanisms for the pathogenesis of tuberculosis. Based on the above facts, we believe that N. arbor-tristis derived phytochemicals can act both on the tuberculosis bacterium and on the host for prevention and cure of tuberculosis.
Highlights
The management of tuberculosis has become far more complex due to the emergence of drug-resistant strains of Mycobacterium tuberculosis
The current treatment of tuberculosis mainly relies on the drugs such as isoniazid, rifampin, ethambutol, pyrazinamide (Yew et al, 2010; McIlleron et al, 2006)
The present review indicates a specific and targetbased approach against the pathogenesis of M. tuberculosis
Summary
The management of tuberculosis has become far more complex due to the emergence of drug-resistant strains of Mycobacterium tuberculosis. Cholesterol helps to arrange TACO proteins around the phagosome and prevents phagolysosome complex formation This mechanism subsequently facilitates the survival and persistence of M. tuberculosis inside the macrophage.N. arbor-tristis phytochemicals may inhibit the function of HMG-CoA reductase, which interrupts the bacterial survival and persistence. We feel that iridoids like arbortristoside A, B, C, and 6βhydroxyloganin (or some other iridoids) present in N. arbor-tristis may reduce the growth of M. tuberculosis by interrupting fatty acid synthase activity acting through FabI inhibition. It is logical to think that iridoid glycosides, extracted from N. arbor-tristis, may decrease the survival of M. tuberculosis by reducing cholesterol biosynthesis through inhibition of HMG-CoA reductase. We consider that such a review of basic biology and ethnopharmacological relevance related to the context is necessary for novel drug discovery to prevent and cure tuberculosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
