02384nas a2200217   4500008004100000022001400041245013500055210006900190260009900259300001200358490000600370520152100376653001201897653002301909653001501932100002001947700001901967700002401986700003102010856012502041       2013                        eng d  a1995-764500aIsolation, fractionation and evaluation of the antiplasmodial properties of Phyllanthus niruri resident in its chloroform fraction0 aIsolation fractionation and evaluation of the antiplasmodial pro  aTHE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLANDbELSEVIER SCI LTDcMAR  a169-1750 v63 a<p>Objective: To investigate the antiplasmodial activity of Phyllanthus niruri (P. niruri) methanol extract (ME) and its fractions in mice. Methods: P. niruri methanol extract and its chloroform, ethanol and aqueous portions were tested against chloroquine-sensitive Plasmodium berghei berghei. in early, established mid repository models of infection using Knight and Peter's 4-day suppressive model, Ryley and Peters curative model and Peters prophylactic model respectively. Results: Chemosuppression of parasitaemia (37.65%-50.53 %) was elicited by 100-400 mg/kg (b.w.) of ME. At doses of 100 mg/kg b.w., the chloroform fraction (F1) significantly (P&lt;0.01) suppressed parasitaemia by 85.29%, while ethanol and aqueous fractions (F2 and F3, respectively) elicited 67.06% and 51.18% chemosuppression. The most active fraction, F1 was selected for further antiplasmodial screening. In established infection, ME reduced parasitaemia (15.81%-62.96%) while F1 significantly (P&lt;0.01) reduced parasitaemia (44.36%-90.48%), with effects comparable to that of chloroquine (96.48%). The prophylactic antiplasmodial activity of ME (92.50% suppression) was also significant (P&lt;0.01) and was more effective than pyrimethamine (85.00%). Additionally, cell membrane integrity of non-parasitized erythrocytes incubated with 125-500 mg/mL F1 was maintained. Conclusions: These findings indicate the antiplasmodial efficacy of P. niruri methanol extract, and the localization of this effect in its chloroform fraction.</p>10amalaria10aPhyllanthus niruri10aPlasmodium1 aIfeoma, Obidike1 aSamuel, Okhale1 aItohan, Aboh, Mercy1 aAdeola, Salawu, Oluwakanyi  uhttps://library.ncl.res.in/content/isolation-fractionation-and-evaluation-antiplasmodial-properties-phyllanthus-niruri-002296nas a2200241   4500008004100000022001400041245011200055210006900167260000800236300001100244490000800255520148600263653001801749653002401767653001201791653001501803653001501818100002501833700001901858700002801877700001701905856013201922       2022                        eng d  a0166-685100aProfiling of metabolic alterations in mice infected with malaria parasites via high-resolution metabolomics0 aProfiling of metabolic alterations in mice infected with malaria  cNOV  a1115250 v2523 a<p>
	Background: Malaria infection can result in distinct clinical outcomes from asymptomatic to severe. The association between patho-physiological changes and molecular changes in the host, and their correlation with severity of malaria progression is not fully understood. Methods: In this study, we addressed mass spectrometry-based temporal profiling of serum metabolite levels from mice infected with Plasmodium berhgei (strain ANKA). Results: We show global perturbations and identify changes in specific metabolites in correlation with disease progression. While metabolome-wide changes were apparent in late-stage malaria, a subset of metabolites exhibited highly correlated changes with disease progression. These metabolites changed early on following infection and either continued or maintained the change as mice developed severe disease. Some of these have the potential to be sentinel metabolites for severe malaria. Moreover, glycolytic metabolites, purine nucleotide precursors, tryptophan and its bioactive derivatives were many fold decreased in late-stage disease. Interestingly, uric acid, a metabolic waste reported to be elevated in severe human malaria, increased with disease progression, and subsequently appears to be detoxified into allantoin. This detoxification mechanism is absent in humans as they lack the enzyme uricase. Conclusions: We have identified candidate marker metabolites that may be of relevance in the context of human malaria.</p>
10aHost response10aInfectious diseases10amalaria10ametabolite10aPlasmodium1 aChhibber-Goel, Jyoti1 aShukla, Anurag1 aShanmugam, Dhanasekaran1 aSharma, Amit  uhttps://library.ncl.res.in/content/profiling-metabolic-alterations-mice-infected-malaria-parasites-high-resolution-metabolomics