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The current study was conducted to evaluate the ameliorative and protective potentials of Moringea oleifera leaves ethanolic extract (MOLE) against thioacetamide (TAA) toxicity. A total of 58 male albino rats were randomly assigned into six experimental groups. G1, rats received distilled water. G2, rats were injected with a single dose of TAA (200 mg/kg BW) i.p. G3, rats were given MOLE (300 mg/kg BW) orally for 26 days. G4, rats were injected TAA as in G2 and treated with MOLE as G3. G5, rats were kept for 26 days without treatment then on day 27 injected with TAA as in G2. G6, rats were given MOLE for 26 days then on day 27 injected with TAA. Phytochemical analysis of MOLE indicated the presence of kaempferol, kaempferol malonylglucoside, kaempferol hexoside, kaempferol -3- O -glucoside, kaempferol-3- O -acetyl-glucoside, cyanidin -3-O-hexoside, ellagic acid, quercetin, quercetin-3- O -glucoside, and apigenin glucoside. Intoxication of rats with TAA significantly elevated activities of serum AST, ALT, and ALP; concentrations of malondialdehyde, nitric oxide, and hepatic tissue protein expression of caspase 3 and COX2 with alteration of the histological structures of hepatic tissues, while it decreased serum levels of total protein, albumin, and hepatic tissue contents of reduced glutathione. Also, TAA intoxication resulted in 62.5% mortality in rats of G5. Treatment of TAA intoxicated rats (G4) with MOLE ameliorated the toxic effects of TAA on hepatic tissue structure and function. It decreased serum activities of AST, ALT, and ALP; enhanced hepatic GSH concentration; reduced pathological alterations and lipid peroxidation; and downregulated caspase 3 and COX2 proteins expression in hepatic tissue. In addition, MOLE protected rats of G6 from TAA-induced hepatic tissues injury and dysfunction, and increased survival rate of rats. In conclusion, MOLE had both ameliorating and protecting potentials against TAA-induced rats liver damage through regulation of antioxidant, anti-apoptotic, and inflammatory biomarkers. Graphical abstract

The current study investigated the protective potential of Azolla pinnate ethanolic extract (APE) against lead-induced hepatotoxicity in rats. Sixty male Wistar albino rats were randomly allocated into six groups (n = 10). The control group was orally administrated with saline. The second group received lead acetate (100 mg/kg body weight (BW) orally for 60 days). The third group was fed with APE (10 mg/kg BW orally for 60 days). The fourth group was administrated with lead acetate like the second group and APE like the third group, concomitantly, for 60 days. The fifth group was administrated with APE like the third group for 30 days, then orally administrated with the lead acetate like the second group for another 30 days. The sixth group was administrated with lead acetate like the second group for 30 days, then with APE like the third group for a further 30 days. Phytochemical analysis of APE indicated the presence of peonidin 3-O-glucoside cation, vitexin, rutin, thiamine, choline, tamarixetin, hyperoside, astragalin, and quercetin. The latter has been elucidated using one- and two-dimensional nuclear magnetic resonance (1D and 2D NMR) and liquid chromatography–mass spectrometry (LC–MS-MS). Lead acetate increased the serum levels of alanine and aspartate aminotransferases and that of urea, creatinine, tumor necrosis factor alpha, and interleukin 1β, hepatic tissue malondialdehyde contents, and caspase 3 protein expression, as well as altering the hepatic tissue architecture. However, it decreased the serum levels of interleukin 10 and glutathione (GSH) contents, and the activities of catalase and superoxide dismutase in hepatic tissue. In contrast, the administration of APE ameliorated the lead-induced alterations in liver function and structure, exemplifying the benefits of Azolla’s phytochemical contents. Collectively, A. pinnate extract is a protective and curative agent against lead-induced hepatotoxicity via its antioxidant, anti-inflammatory, and anti-apoptotic impacts.

Human babesiosis is caused by the apicomplexan parasite Babesia microti, which is of major public health concern in the United States and elsewhere, resulting in malaise and fatigue, followed by a fever and hemolytic anemia. In this paper we focus on the characterization of a novel B. microti thrombospondin domain (TSP1)-containing protein (BmP53) from the new annotation of the B. microti genome (locus 'BmR1_04g09041'). This novel protein (BmP53) had a single TSP1 and a transmembrane domain, with a short cytoplasmic tail containing a sub-terminal glutamine residue, but no signal peptide and Von Willebrand factor type A domains (VWA), which are found in classical thrombospondin-related adhesive proteins (TRAP). Co-localization assays of BmP53 and Babesia microti secreted antigen 1 (BmSA1) suggested that BmP53 might be a non-secretory membranous protein. Molecular mimicry between the TSP1 domain from BmP53 and host platelets molecules was indicated through different measures of sequence homology, phylogenetic analysis, 3D structure and shared epitopes. Indeed, hamster isolated platelets cross-reacted with mouse anti-BmP53-TSP1. Molecular mimicry are used to help parasites to escape immune defenses, resulting in immune evasion or autoimmunity. Furthermore, specific host reactivity was also detected against the TSP1-free part of BmP53 in infected hamster sera. In conclusion, the TSP1 domain mimicry might help in studying the mechanisms of parasite-induced thrombocytopenia, with the TSP1-free truncate of the protein representing a potential safe candidate for future vaccine studies.

Mohamad Alaa Terkawi is not affiliated with #1 but with #2 National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido, Japan.Yoshifumi Nishikawa is not affiliated with #3 but with #2 National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido, Japan.Xuenan Xuan is not affiliated with #3 but with #2 National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido, Japan. 1.Indication of a molecular mimicry between thrombospondin domains from a novel Babesia microti BmP53 protein and host platelets molecules.

The present study aimed to investigate the protective effect of argan oil (AO) against nephrotoxic effects following overdose and long-term administration of betamethasone (BM). The phytochemical compositions of AO were assessed using GC/MS. Forty eight male Wister albino rats were divided into six groups and treated for 3 successive weeks. The control group was orally administrated distilled water daily, the BM group received BM (1 mg/kg, IM, day after day), AO/0.5 and AO/1 groups received AO (0.5 mL/kg, 1 mL/kg, orally, daily, respectively), BM + AO/0.5 group and BM + AO/1 group. The results revealed that BM induced hematological changes, including reduction of red blood cells with leukocytosis, neutrophilia, monocytosis, lymphocytopenia, and thrombocytopenia. Moreover, BM caused a significant increase of serum urea and creatinine levels, and renal malondialdehyde and nitric oxide contents with significant decrease of reduced glutathione content. BM also caused vascular, degenerative, and inflammatory histopathological alterations in kidney, along with an increase in the Bax/Bcl-2 ratio, activation of caspase-3, and decrease of proliferating cell nuclear antigen expression. Conversely, the concomitant administration of AO (0.5, 1 mL/kg) with BM ameliorated the aforementioned hematological, biochemical, pathological, and histochemical BM adverse effects. In conclusion, AO has protective effects against BM-induced renal damage, possibly via its antioxidant, anti-apoptotic, and proliferative properties.

A heterologous prime-boost vaccination regime with DNA and recombinant vaccinia virus (rvv) vectors expressing relevant antigens has been shown to induce effective immune responses against several infectious pathogens. In this study, we describe the effectiveness of the prime-boost strategy by immunizing dogs with a recombinant plasmid followed by vaccinia virus, both of which expressed the glutamic acid-rich protein (BgGARP) of Babesia gibsoni . The dogs immunized with the prime-boost regime developed a significantly high level of specific antibodies against BgGARP when compared with the control groups. The antibody level was strongly increased after a booster immunization with a recombinant vaccinia virus. Two weeks after the booster immunization with a recombinant vaccinia virus expressing BgGARP, the dogs were challenged with B. gibsoni parasite. The dogs immunized with the prime-boost regime showed partial protection, manifested as a significantly low level of parasitemia. These results indicated that this type of DNA/rvv prime-boost immunization approach may have use against B. gibsoni infection in dogs.