Esam M. Al-Shaebi

Protective effect of berberine chloride on Plasmodium chabaudi-induced hepatic tissue injury in mice.

The present study aimed to investigate the protective role of berberine (BER) against Plasmodium chabaudi-induced infection in mice. Animals were divided into three groups. Group I served as a vehicle control. Group II and group III were infected with 1000 P. chabaudi infected erythrocytes. Group III was gavaged with 100 μl of 10 mg/kg berberine chloride for 10 days. All mice were sacrificed at day 10 post-infection. The percentage of parasitemia was significantly reduced more than 30%, after treatment of mice with BER. Infection caused marked hepatic injuries as indicated by histopathological alterations as evidenced by the presence of hepatic lobular inflammatory cellular infiltrations, dilated sinusoids, vacuolated hepatocytes, increased number of Kupffer cells and the malaria pigment, hemozoin. These changes in livers led to the increased histological score. Also, infection induced a significant increase in liver alanine aminotransferase and aspartate aminotransferase and a significant increase in the total leucocytic count. Moreover, mice became anemic as proved by the significant decrease in erythrocyte number and haemoglobin content. BER showed a significant protective potential by improving the above mentioned parameters. Based on these results, it is concluded that berberine could offer protection against hepatic tissue damage.

In vitro effectiveness of Curcuma longa and Zingiber officinale extracts on Echinococcus protoscoleces

Hydatid disease is an important economic and human public health problem with a wide geographical distribution. Surgical excision remains the primary treatment and the only hope for complete cure of hydatosis. The most important complications arising from surgical excision, however, is recurrence, which is due to dissemination of protoscolices during the surgery. Pre-surgical inactivation of the contents of the hydatid cyst by injection of scolicidal agent into the cyst has been used as adjunct to surgery in order to overcome the risk of recurrence. In the present study, ethanolic extracts of turmeric (Curcuma longa) and ginger (Zingiber officinale) were tested as scolicidal agent for Echinococcus protoscoleces. Protoscoleces were collected aseptically from sheep livers containing hydatid cysts. Three concentrations (10, 30 and 50 mg/ml) of each extract were investigated and viability of the protoscoleces was tested by 0.1% eosin staining. Ginger extract showed the strongest scolicidal effect (100%) after 20 min at a concentration of 30 mg/ml and 10 min at 50 mg/ml. The maximum scolicidal effect of turmeric was 93.2% after 30 min at a concentration of 50 mg/ml. It is concluded that turmeric and ginger extracts have high scolicidal activity and could be used as effective scolicidal agents against Echinococcus protoscoleces.

The antiplasmodial and spleen protective role of crude Indigofera oblongifolia leaf extract traditionally used in the treatment of malaria in Saudi Arabia.

Malaria is one of the most serious natural hazards faced by human society. Although plant leaves of Indigofera oblongifolia have been used for the treatment of malaria in Saudi Arabian society, there is no laboratory-based evidence for the effectiveness and safety of the plant. This study therefore was designed to investigate the antimalarial and spleen protective activity of I. oblongifolia leaf extract (IOLE) in mice. Three doses (100, 200 and 300 mg/kg) of IOLE were used to treat mice infected with Plasmodium chabaudi-parasitized erythrocytes. The suppressive effect produced by the 100 mg/kg dose on parasitemia was highly significant compared to the infected nontreated group. This dose was also able to repair the change in the thickness of the mice spleen and significantly lower the number of apoptotic cells in the spleen. Moreover, I. oblongifolia also altered gene expression in the infected spleen. On day 7 postinfection, the mRNA expression of six genes – with immune response functions – was upregulated by more than twofold, while that of 24 other genes was downregulated. Among the differentially up- and downregulated genes under the effect of IOLE, we quantified the expression of Ccl8, Saa3, Cd209a, and Cd209b mRNAs. The expression data, determined by microarrays, were largely consistent with the expression analyses we performed with several arbitrarily selected genes using quantitative polymerase chain reaction (PCR). Based on our results, I. oblongifolia exhibits antimalarial activity and could protect the spleen from P. chabaudi-induced injury.

Indigofera oblongifolia leaf extract regulates spleen macrophage response during Plasmodium chabaudi infection

Malaria is a major health problem that still affects numerous countries. The current study aimed to identify the role of Indigofera oblongifolia leaf extract in regulating mouse spleen macrophages during the progression of Plasmodium chabaudi infection. Three doses of the leaf extract (100, 200, and 300 mg/kg) were administered to mice inoculated with P. chabaudi infected erythrocytes. The weight of the infected mice improved after the treatment with I. oblongifolia. The infection causes disorganization of macrophage distribution in the spleen. After the mice had been treated with the leaf extract, the macrophages appeared to be reorganized in the white and red pulp areas. In addition, the I. oblongifolia leaf extract (IOLE) significantly increased the total antioxidant capacity of the mice spleens infected with P. chabaudi. The phagocytic activity of spleen macrophages was increased in the infected group as indicated by the significant decrease in the number of fluorescent particles in the spleen sections. This number increased in the mice spleens after treatment with IOLE. Based on these results, it is suggested that IOLE regulate macrophage response of the spleen during the blood stage of malaria in mice.

Susceptibility of mice strains to oxidative stress and neurotransmitter activity induced by Plasmodium berghei

This study investigated the susceptibility of female C57Bl/6 and Swiss Albino mice to oxidative stress and neurotransmitters activity induced by Plasmodium berghei. On day 9 p.i. with P. berghei infected erythrocytes, the mice reduced in weight. This weight loss was markedly higher in SW mice and reached about −14%. Also, the infection was able to cause oxidative damage to the brain tissue. Catalase activity as well as glutathione, malondialdehyde and nitric oxide levels were different in the two mice strains. Moreover, the brain content of neurotransmitters, epinephrine, norepinephrine, dopamine and serotonin in mice brain was higher in SW mice than B6 mice. We concluded that, the strain of mice is one factor that could alter the response of mice to P. berghei infection.

Evaluation of nanoselenium and nanogold activities against murine intestinal schistosomiasis

Nanomedicine is one of the most important methods used to treat human diseases including parasitic diseases. Schistosomiasis is a major parasitic disease that affects human health in tropical regions. Whilst Praziquantel is the main classic antischistosomal drug, new drugs are required due to the poor effect of the drug on the parasite juveniles and immature worms, and the emergence of drug resistant strains of Schistosoma. The present study aimed to examine the curative roles of both gold and selenium nanoparticles on jejunal tissues of mice infected with Schistosoma mansoni. Transmission electron microscopy was used for characterization of nanoparticles. Gold nanoparticles of 1 mg/kg mice body weight and selenium nanoparticles 0.5 mg/kg body weight were inoculated separately into mice infected with S. mansoni. The parasite induced a significant decrease in glutathione levels; however, the levels of nitric oxide and malondialdehyde were significantly increased. Additionally, the parasite introduced deteriorations in histological architecture of the jejunal tissue. Treatment of mice with metal nanoparticles reduced the levels of body weight changes, oxidative stress and histological impairment in the jejunal tissue significantly. Therefore, our results revealed the protective role of both selenium and gold nanoparticles against jejunal injury in mice infected with S. mansoni.

Vitamin D receptor regulates intestinal inflammatory response in mice infected with blood stage malaria

Malaria is a harmful disease affecting both tropical and subtropical countries and causing sometimes fatal complications. The effects of malaria-related complications on the intestine have been relatively neglected, and the reasons for the intestinal damage caused by malaria infection are not yet clear. The present study aims to evaluate the influence of intestinal vitamin D receptor on host-pathogen interactions during malaria induced in mice by Plasmodium chabaudi. To induce the infection, animals were infected with 106P. chabaudi-parasitized erythrocytes. Mice were sacrificed on day 8 post-infection. The infected mice experienced a significant body weight loss and parasitaemia affecting about 46% of RBCs. Infection caused marked pathological changes in the intestinal tissue indicated by shortening of the intestine and villi. Moreover, the phagocytic activity of macrophages increased significantly (P < 0.01) in the infected villi compared to the non-infected ones. Infection by the parasite also induced marked upregulation of nuclear factor-kappa B, inducible nitric oxide synthase, Vitamin D Receptor, interleukin-1β, tumour necrosis factor alpha and interferon gamma-mRNA. It can be implied from this that vitamin D receptor has a role in regulating malarial infection.

Gene expression of the liver of vaccination-protected mice in response to early patent infections of Plasmodium chabaudi blood-stage malaria

BackgroundThe role of the liver for survival of blood-stage malaria is only poorly understood. In experimental blood-stage malaria with Plasmodium chabaudi, protective vaccination induces healing and, thus, survival of otherwise lethal infections. This model is appropriate to study the role of the liver in vaccination-induced survival of blood-stage malaria.MethodsFemale Balb/c mice were vaccinated with a non-infectious vaccine consisting of plasma membranes isolated in the form of erythrocyte ghosts from P. chabaudi-infected erythrocytes at week 3 and week 1 before infection with P. chabaudi blood-stage malaria. Gene expression microarrays and quantitative real-time PCR were used to investigate the response of the liver, in terms of expression of mRNA and long intergenic non-coding (linc)RNA, to vaccination-induced healing infections and lethal P. chabaudi malaria at early patency on day 4 post infection, when parasitized erythrocytes begin to appear in peripheral blood.ResultsIn vaccination-induced healing infections, 23 genes were identified to be induced in the liver by > tenfold at p < 0.01. More than one-third were genes known to be involved in erythropoiesis, such as Kel, Rhag, Ahsp, Ermap, Slc4a1, Cldn13 Gata1, and Gfi1b. Another group of > tenfold expressed genes include genes involved in natural cytotoxicity, such as those encoding killer cell lectin-like receptors Klrb1a, Klrc3, Klrd1, the natural cytotoxicity-triggering receptor 1 Ncr1, as well as the granzyme B encoding Gzmb. Additionally, a series of genes involved in the control of cell cycle and mitosis were identified: Ccnb1, Cdc25c, Ckap2l were expressed > tenfold only in vaccination-protected mice, and the expression of 22 genes was at least 100% higher in vaccination-protected mice than in non-vaccinated mice. Furthermore, distinct lincRNA species were changed by > threefold in livers of vaccination-protected mice, whereas lethal malaria induced different lincRNAs.ConclusionThe present data suggest that protective vaccination accelerates the malaria-induced occurrence of extramedullary erythropoiesis, generation of liver-resident cytotoxic cells, and regeneration from malaria-induced injury in the liver at early patency, which may be critical for final survival of otherwise lethal blood-stage malaria of P. chabaudi.