Abstract
Malaria is a dangerous disease spread across several countries. Recent studies have focused on medicinal plants to discover alternative agents to the currently used drugs for malaria treatment. Here, we investigated the potential role of Indigofera oblongifolia leaf extract (IE) on hepatic inflammation in mice with Plasmodium chabaudi-infected erythrocytes. Female C57BL/6 mice were divided into three groups. The first group served as a control noninfected group, while the second and third groups were intraperitoneally injected with 106 erythrocytes parasitized by P. chabaudi. Mice from the third group were treated daily with a dose of 100 mg/kg of IE for 7 days. IE significantly reduced the number of leukocytes and apoptotic cells. The numbers of CD68-positive cells decreased in the livers of mice from the treatment group. Moreover, IE raised the hepatic antioxidant levels (glutathione and catalase) and reduced the levels of hepatic oxidative stress markers (malondialdehyde, nitric oxide, and reactive oxygen species). IE regulated some functions of the genes related to immune responses, including apoptotic genes (B-cell lymphoma-2, Bax, and caspase-3) and cytokine genes (interleukin-1β (IL-1β), IL-6, interferon-γ, and tumor necrosis factor-α). Therefore, IE exerts significant effects against malaria and protects the liver from injury caused by P. chabaudi via antioxidant and anti-inflammatory ways.
Highlights
Malaria is a dangerous disease spread across the world, especially in the developing and underdeveloped countries
We demonstrate the role of Indigofera oblongifolia leaf extract (IE) in the modulation of cytokine expression and apoptosis in mouse liver infected with blood-stage malaria
The infection induced by P. chabaudi in female C57L/B6 mice causes an increase in leucocyte count; 10 IL-1훽
Summary
Malaria is a dangerous disease spread across the world, especially in the developing and underdeveloped countries. According to the World Health Organization, more efforts have been directed to reduce malaria-induced death by 60% as well as to eliminate malaria from many countries since 2000 [1]. The liver is the first site of sporozoite development before infection of erythrocytes [2]. Sporozoites cross the sinusoidal cell layer to infect hepatocytes and grow and develop into erythrocyte-invasive forms [3]. Several studies have investigated the effector role of the liver during blood-stage malaria [4,5,6]. Malaria infection is associated with both acquired immune [7, 8] and innate immune [9] responses, characterized with early and intense proinflammatory cytokine-mediated effector mechanisms that kill or remove parasite-infected cells [10]
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