Therapeutic evaluation of Lithium Chloride against Malaria: Antiparasitic, Antioxidant, and Hepatoprotective Properties
DOI:
https://doi.org/10.30442/Keywords:
Antimalarial, Antioxidant, Hepatoprotection, Lithium chloride, Malaria, Plasmodium-bergheiAbstract
Background: Malaria remains a major cause of morbidity and mortality in tropical and subtropical regions, with drug resistance hindering eradication efforts. Lithium chloride (LiCl), an inhibitor of glycogen synthase kinase-3β, has shown therapeutic potential in several disease models and is being investigated as an antimalarial agent.
Objective: To evaluate the antimalarial, antioxidant, and hepatoprotective effects of LiCl in Plasmodium berghei-infected mice.
Methods: Fifty BALB/c mice were assigned to five groups: uninfected control, infected control, LiCl-treated (15 or 30 mg/kg), and chloroquine-treated (10 mg/kg). Treatments were given orally for three consecutive days beginning 72 hours after infection. Parasitemia, packed cell volume (PCV), mean survival time (MST), liver enzyme activities, antioxidant markers, and liver histology were assessed.
Results: LiCl significantly suppressed parasitemia from day 5 post-treatment, with 30 mg/kg producing effects comparable to chloroquine. Treated mice showed prolonged survival, with an MST of 30.3 days versus 31.6 days for chloroquine, and improved PCV values, indicating reduced malaria-associated anemia. LiCl also increased superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) levels while decreasing alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). Histological findings demonstrated reduced hepatic necrosis and evidence of liver regeneration in LiCl-treated groups.
Conclusion: LiCl exhibits potent antimalarial, antioxidant, and hepatoprotective activities in P. berghei-infected mice, supporting its potential as a therapeutic candidate for malaria and justifying further mechanistic studies.
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