Abstract. The aim of the present study was to investigate the protective effects of camel milk on hepatic pathogenicity induced by experimental infection with Escherichia (E. coli) and Staphylococcus aureus (S. aureus) in Wistar rats. The rats were divided into six groups: The control and camel milk groups received water and camel milk, respectively; two groups received camel milk for 2 weeks prior to intraperitoneal injection of either E. coli or S. aureus; and two groups were injected intraperitoneally with E. coli and S. aureus, respectively. All animals were maintained under observation for 7 days prior to biochemical and gene expression analyses. The rats treated with camel milk alone exhibited no changes in expression levels of glutamic-pyruvate transaminase (GPT) or glutamic-oxaloacetic transaminase (GOT), compared with the water-treated group. The E. coli-and S. aureus-injected rats exhibited a significant increase in oxidative stress, and prior treatment with camel milk normalized the observed changes in the expression levels of GPT, GOT and malondialdehyde (MDA). Treatment with camel milk decreased the total bacterial count in liver tissue samples obtained from the rats injected with E. coli and S. aureus. Camel milk administration increased the expression levels of glutathione-S-transferase and superoxide dismutase, which were downregulated following E. coli and S. aureus injection. In addition, camel milk downregulated the increased expression of interleukin-6 and apoptosis-associated genes. Of note, administration of camel milk alone increased the expression levels of the B cell lymphoma 2-associated X protein and survivin anti-apoptotic genes, and supplementation prior to the injection of E. coli and S. aureus induced further upregulation, In conclusion, camel milk exerted protective effects against E. coli and S. aureus pathogenicity, by modulating the extent of lipid peroxidation, together with the antioxidant defense system, immune cytokines, apoptosis and the expression of anti-apoptotic genes in the liver of Wistar rats.
A new series of nucleosides, moieties, and Schiff bases were synthesized from sulfadimidine. Infrared (IR), 1HNMR, 13C NMR, and mass spectrometry techniques and elemental analysis were employed to elucidate the synthesized compounds. The prepared analogues were purified by different chromatographic techniques (preparative TLC and column chromatography). Molecular docking studies of synthesized compounds 3a, 4b, 6a, and 6e demonstrated the binding mode involved in the active site of DNA gyrase. Finally, all synthesized compounds were tested against selected bacterial strains. The most effective synthesized compounds against S. aureus were 3a, 4d, 4b, 3b, 3c, 4c, and 6f, which exhibited inhibition zones of inhibition of 24.33 ± 1.528, 24.67 ± 0.577, 23.67 ± 0.577, 22.33 ± 1.528, 18.67 ± 1.528 and 19.33 ± 0.577, respectively. Notably, the smallest zones were observed for 4a, 6d, 6e and 6g (6.33 ± 1.528, 11.33 ± 1.528, 11.67 ± 1.528 and 14.66 ± 1.155, respectively). Finally, 6b and 6c gave negative zone values. K. pneumoniae was treated with the same compounds and the following results were obtained. The most effective compounds were 4d, 4c, 4b and 3c, which showed inhibition zones of 29.67 ± 1.528, 24.67 ± 0.577, 23.67 ± 1.155 and 19.33 ± 1.528, respectively, followed by 4a and 3d (15.33 ± 1.528 for both), while moderate results (13.67 ± 1.155 and 11.33 ± 1.528) were obtained for 6f and 6g, respectively. Finally, 6a, 6b, 6c, 3a, and 3b did not show any inhibition. The most effective compounds observed for the treatment of E. coli were 4d, 4b, 4c, 3d, 6e and 6f (inhibition zones of 26.33 ± 0.577, 21.67 ± 1.528, 21.67 ± 1.528, 19.67 ± 1.528, 17.67 ± 1.155 and 16.67 ± 1.155, respectively). Compounds 3b, 3c, 6a, 6c, and 6g gave moderate results (13.67 ± 1.528, 12.67 ± 1.528, 11.33 ± 0.577, 15.33 ± 1.528 and 12.67 ± 1.528, respectively), while 6b showed no effect. The MIC values against S. aureus ranged from 50 to 3.125 mg, while those against E. coli and K. pneumoniae ranged from 50 to 1562 mg. In vitro, the antibacterial effects were promising. Further research is required to study the in vivo antibacterial effects of these compounds and determine therapeutic doses.
Background: Heavy metals that normally cause problems are mercury (HgCl 2 ) and lead acetate (LA). Chelating and inhibitor agents are the target to treat and overcome metal toxicity. The current study has been carried out to evaluate the protective effects of N-acetyl cysteine (NAC) and meso 2,3 dimercaptosuccinic acid (DMSA) against HgCl 2 and LA toxicity. Materials and Methods: Ninety male Wistar rats were divided into nine equal groups. The groups were administered NAC and/or DMSA in presence or absence of LA (LA; 0.2% in drinking water) or HgCl 2 (2 mg/kg BW) for 2 consecutive months. Serum and organs were collected for biochemical, genetic and histopathological changes. Results: Biochemical results revealed that LA and HgCl 2 significantly increased the levels of liver and kidney biomarkers. Administration of NAC and DMSA considerably improved these altered changes. LA and HgCl 2 decreased serum levels of antioxidants and were ameliorated in NAC and DMSA administered rats. LA and HgCl 2 administration upregulated expression of IL-1β and IL-8 that were normalized by NAC and DMSA. Kidneys of LA and HgCl 2 groups showed intraluminal hyaline casts. Kidneys of DMSA-administrated rats showed mild hydropic degeneration of renal tubular epithelium in LA and HgCl 2 groups. Kidneys of NAC administrated rats showed atrophy of capillary tufts. Kidneys of LA and HgCl 2 administered rats which received DMSA and NAC showed normal glomerular structure. Liver histopathology showed sever changes that were ameliorated by NAC and DMSA. Conclusion: Taken together, usage of NAC and DMSA provide significant protection against LA and HgCl 2 -induced hepatotoxicity and nephrotoxicity in male Wistar rats.
The resistance of methicillin-resistant staphylococcus aureus (MRSA) to antimicrobials drugs is due to expression of the mecA gene. Current study was conducted on 33 MRSA clinical samples (Cefotaxime and Oxacillin positive). All MRSA isolates were examined using Antibiogram, Minimum Inhibitory concentration (MIC) and PCR to clarify the expression of SCCmec genes and to detect the differences on repeats of coagulase gene (Coa). Results showed that all isolates were 100% resistant against Amoxycillin-clavulanate, Ampicillin and Cefotaxime, 45.5% were resistant against Ciprofloxacin and erythromycin. mecA gene is expressed in all examined isolates (100%). The expression of SCCmec genes showed that 11.11% expressed type I, 45.45% contained type II, 45.45% contained type III, 63.63% were type IV and 5.55% were typeV. All examined isolates harbored and expressed coagulase gene repeats. Coagulase repeats were 27.27% with 5 repeats (81pb), and 72.72% with 4 repeats. In conclusion, the virulence of MRSA strains is increased and gave different antibiogram activities from different global regions and the repeats of Coa gene give no detectable differences among MRSA strains.
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