Cutaneous leishmaniasis is one form of leishmaniasis that chiefly infected the poor sections of the society. The prototypical therapeutic interventions in vogue are handicapped due to toxicity and an alarming increase in drug resistance. Furthermore, the absence of vaccines has raised the quest for alternative therapies. So, the aim of our study was to assess the anti-leishmanial activity of Euphorbia cactus Ehrenb, Euphorbia ammak Forssk, Euphorbia inarticulate Schweinf, and Pergularia tomentosa L. The extracts of plants were prepared by maceration method and by Soxhlet extractor. The extracts were dried and re-dissolved in 2% dimethyl sulfoxide (DMSO) 1% solvent. Leishmania spp. cells were then tested with serial concentrations (15.6 μgml-1 to 500 μg ml-1 ) of the extracts, using the 3-(4,5-dimethylthazolk-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. All experiments were performed in triplicate and analyzed by ANOVA test. The optical density values as measured by Enzyme-Linked Immunosorbent Assay (ELISA) were used to calculate the IC50 values. The results indicated that the methanolic latex extract of Euphorbia cactus Ehrenb, Euphorbia ammak Forssk had potent anti-leishmanial activity against the promastigotes of Leishmania spp. based on a dose-dependent response analysis. The IC50 values for Euphorbia cactus Ehrenb and Euphorbia ammak Forssk after 24h incubation against Leishmania spp. promastigotes were less than <15.6 μgml-1. Furthermore, the phytochemical analysis of methanolic extracts showed the presence of alkaloids, phytosterols, phenols, saponins, and flavonoids in which these components have been proven previously to be the active compounds against Leishmania parasite. In conclusion, the present study reveals that latex extract of Euphorbia cactus Ehrenb and Euphorbia ammak Forssk contain active compounds that have anti-leishmanial activity, which could serve as an alternative agent in the treatment of Cutaneous leishmaniasis, but further studies would, therefore, be needed to assess the activity of these materials of this plants in vivo clinical response and study their toxicity on cell lines.
ObjectiveThe present study aimed to investigate the ameliorative effect of melittin, a major polypeptide in the venom of honeybee (Apis mellifera) on isoniazid (INH) and rifampicin (RIF) induced hepatotoxicity in male albino rats. Method: The rats (140-200g) were divided into five groups (n=6): normal control (NC); toxic (T) group treated with INH+RIF (100 mg/kg, p.o.); melittin-treated (Mel15, Mel30) group (15 or 30 µg/kg s.c); and normal recovery (NR) group. Blood and liver samples were collected for biochemical, hematological and histopathological studies respectively.ResultsThe administration of melittin was found to prevent the antitubercular drug-induced alterations in the diagnostic markers; reduced glutathione (GSH), direct bilirubin (DB), total bilirubin (TB), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and total serum protein (TSP). Besides, hematological alterations were significantly high (P<0.0001) in Mel-treated groups when compared to the toxic control. The NR group exhibited lower levels of DB, TB, ALP, LDH and TSP. In addition, treatment with melittin offered protection in the NR group with respect to MDA levels.ConclusionEvidence from this study indicate that melittin is beneficial for the prevention of acute hepatic failure in antitubercular drug-induced hepatoxicity.
Background: Cyclosporine A (CsA) is an immunosuppression agent used frequently in fields of organs transplantation and autoimmune diseases. However, CsA-induced kidney injury is a major clinical problem associated with CsA therapy in which the conceivable accountable mechanism is oxidative stress (OS). The present study evaluated the protective and ameliorated effects of fucoidan (FU) as an antioxidant and an anti-inflammatory agent against CsA-induced kidney injury. Methods: Male rats were randomly divided into three groups. The first group was served as a control group that administered olive oil orally and normal saline subcutaneously, the second group (CA) was treated with CsA orally, and the third group (CA + FU) was treated with CsA orally in concomitant with FU subcutaneously. Experimental animals were sacrificed 20 days following the treatment period and serum samples were analyzed for creatinine test. The homogenate of renal tissues was prepared for OS assessment. Light and ultrastructure microscopic kidney sections were prepared for histopathological examination. Results: Treatment of rats with CsA alone produced a significant increase in the levels of creatinine, nitric oxide (NO), and malondialdehyde (MDA), as well as the activities of superoxide dismutase (SOD), catalase (CAT), and glucose 6 phosphate dehydrogenase (G6PD), whereas the level of glutathione reduced (GSH) was decreased. Some histopathological changes of the kidney tissue including tubular epithelial hypertrophy, vacuolizations, necrotic glomerulus cell, capillaries network shrinking, vascular congestion, interstitial infiltration, loss of apical microvilli, and deteriorated mitochondria were observed in CA group. Concomitant FU administration with CsA enhanced renal function, as indicated by the low level of creatinine. Moreover, FU ameliorated the oxidative status in kidney tissue as well as it provided histological protection against CsA-induced kidney injury. Conclusion: FU can develop a protective mechanism against kidney injury induced by CsA that mediated by OS.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.