Abstract
Complete malarial therapy depends largely on the immunological and inflammatory response of the host to the invading potentials of malarial parasite. In this study, we evaluated the roles of betulinic acid on immunological response, anti-inflammatory potentials, cardiac and skeletal muscle tissue damage in mice infected with chloroquine susceptible (NK 65) and resistant (ANKA) strains of Plasmodium berghei. Serum Interleukins 1β and 6 (IL-1β, IL-6), tumour necrosis factor alpha (TNF-α), immunoglobulins G and M (IgG and IgM), C-reactive protein (CRP) and creatine kinase (CK) were determined using ELISA technique. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma glutammyl transferase (GGT) were determined using ELISA technique. The results showed that betulinic acid decreased the levels of IL-1β, IL-6, TNF-α and CRP relative to the infected control. The IgG and IgM levels significantly increased in both models while CK did not decrease significantly in both models although serum AST, ALT and GGT significantly decreased compared to the infected control. These results showed that betulinic acid possessed anti-inflammatory, immunomodulatory and remediating effects on tissue damage. Furthermore, the decrease in activity of CK brought about by betulinic acid is indicative of decrease in cardiac and skeletal muscle injury which is a major pathological concern in Plasmodium infection and treatment.
Highlights
The pathophysiology and lethal effect of human malarial infection has been adjudged to be a consequence of imbalance between the pro- and anti-inflammatory cytokines in the system
Interlukin IL-1β (IL)-1β levels in betulinic acid treated mice in both models significantly increased compared with the normal control including the standard drug in the susceptible model, 12.5mg/kg treatment in the susceptible model significantly decreased IL-1β levels to a level that is not statistically significant from the normal control (Fig. 1b)
This disease has been treated with some drugs and promising phytochemicals such as friedelan-3-one and betulinic acid have been used for the treatment of this deadly infectious disease. Cytokines such as tumour necrosis factor alpha (TNFα) and interlukins are essential mechanisms for systemic disease of which malaria is paramount (Clark et al 2006). Regulated release of these mediators have been linked with protective effects and inhibition of parasite growth, extensive release of inflammatory cytokines has been linked with pathological conditions in systemic diseases including malarial infection
Summary
The pathophysiology and lethal effect of human malarial infection has been adjudged to be a consequence of imbalance between the pro- and anti-inflammatory cytokines in the system. Malarial infection causes a systemic human disease with clinical and biomedical similarities to other infectious diseases such as bacterial and viral diseases Common symptoms such as loss of appetite, tiredness, aching joints and muscles, fever and sleepiness that patients experience in systemic infection is common to vivax and falciparum malaria. To protect the cellular contents of the host, malarial infection elicits immune response via the secretion of cytokines by the specific cells of immune system. They are signaling molecules that mediate and regulate inflammation. There are both pro-inflammatory and anti-inflammatory cytokines and some of them are pleiotrophic in functions (Zhang and An 2007). During infection, leucocytes, lymphocytes, monocytes and phagocytes are activated to secret inflammatory mediators that accelerate detectable parasite infection (Mavondo et al 2019)
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Schedule a callMore From: Journal of parasitic diseases : official organ of the Indian Society for Parasitology
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