Vitamin B12 blocked Trypanosoma brucei rhodesiense-driven disruption of the blood brain barrier,and normalized nitric oxide and malondialdehyde levels in a mouse model |
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| Institution: | 1. Department of Biomedical Science & Technology, Technical University of Kenya, P. O. Box 52428, 00200 Nairobi, Kenya;2. Department of Pharmaceutical Sciences and Technology, Technical University of Kenya, P. O. Box 52428, 00200 Nairobi, Kenya;3. Department of Biochemistry and Biotechnology, Technical University of Kenya, P. O. Box 52428, 00200 Nairobi, Kenya;1. Institute of Pathogens and Vectors, Yunnan Provincial Key Laboratory for Zoonosis Control and Prevention, Dali University, 22 Wanhua St, Dali 671000, China;2. Jilin Provincial Key Laboratory of Animal Resource Conservation and Utilization, Northeast Normal University, 5268 Renmin St, Changchun 130000, China;1. The Laboratory of Aquatic Parasitology and Microbial Bioresources, School of Marine Science and Engineering, Qingdao Agricultural University, Qingdao 266109, China;2. Laboratory of Parasitology, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi 1677-1, Japan;3. Laboratory for Marine Biology and Biotechnology, Pilot National Laboratory for Marine Science and Technology (Qingdao), Qingdao, Shandong Province 266237, China;1. College of Veterinary and Animal Husbandry, Abdul Wali Khan University Mardan, Pakistan;2. Department of Zoology, Abdul Wali Khan University, Mardan 2320, Pakistan;3. Department of Microbiology, Shaheed Benazir Women University Peshawar, Pakistan;4. Department of Zoology, Bacha Khan University, Charsadda, Pakistan;6. Department of Basic Sciences, Higher Institute of Biotechnology of Sidi Thabet, University of Manouba, Manouba 2010, Tunisia;7. Laboratory of Microbiology, National School of Veterinary Medicine of Sidi Thabet, University of Manouba, Manouba 2010, Tunisia |
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| Abstract: | Infection with Trypanosoma brucei rhodesiense (T.b.r) causes acute Human African Trypanosomiasis (HAT) in Africa. This study determined the effect of vitamin B12 on T.b.r -driven pathological events in a mouse model. Mice were randomly assigned into four groups; group one was the control. Group two was infected with T.b.r; group three was supplemented with 8 mg/kg vitamin B12 for two weeks; before infection with T.b.r. For group four, administration of vitamin B12 was started from the 4th days post-infection with T.b.r. At 40 days post-infection, the mice were sacrificed to obtain blood, tissues, and organs for various analyses. The results showed that vitamin B12 administration enhanced the survival rate of T.b.r infected mice, and prevented T.b.r-induced disruption of the blood-brain barrier and decline in neurological performance. Notably, T.b.r-induced hematological alteration leading to anaemia, leukocytosis and dyslipidemia was alleviated by vitamin B12. T.b.r-induced elevation of the liver alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and total bilirubin as well as the kidney damage markers urea, uric acid and creatinine were attenuated by vitamin B12. Vitamin B12 blocked T.b.r-driven rise in TNF-α and IFN-γ, nitric oxide and malondialdehyde. T.b.r-induced depletion of GSH levels were attenuated in the presence of vitamin B12 in the brain, spleen and liver tissues; a clear indication of the antioxidant activity of vitamin B12. In conclusion, treatment with vitamin B12 potentially protects against various pathological events associated with severe late-stage HAT and presents a great opportunity for further scrutiny to develop an adjunct therapy for severe late-stage HAT. |
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