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 JTR  Vol.5 No.1 , March 2017
TNF-α (Tumor Necrosis Factor Alpha) and iNOS (Inducible Nitric Oxide Synthase) Expression in Rat Brain Infected by Mycobacterium tuberculosis Strain H37RV
Abstract: Tuberculosis is an infectious disease caused by the Mycobacterium tuberculosis. Mycobacterium tuberculosis will form the primary focus or Ghon focus in the lungs of infected people. The primary focus can break and get into the bloodstream and/or lymph to the entire body, including the central nervous system, especially the brain. Tuberculosis infection in the brain can cause microglia secrete inflammatory factors such as TNF-α and IL-1β is emerging as the body’s immune response. The factors that can trigger microglia to secrete iNOS (Inducible Nitric Oxide Synthase) in order to protect the brain from attacking bacteria. iNOS is shown to have an important role in tuberculosis infection in the brain. TNF-α is a pro-inflammatory cytokine which is mostly produced by macrophages/microglia through several mechanisms. Therefore, to investigate how the expression of TNF-α and iNOS in the brain tissue of the mice is not infected with tuberculosis, tuberculosis infection with an incubation period of 8 weeks and 16 weeks. This study is a semiquantitative study by comparing the amount of expression of TNF-α and iNOS and all three groups of samples with treatment as has been mentioned. The expressions observation of TNF-α and iNOS in brain cell tissue of mice was conducted using immunohistochemical staining, and was seen in a microscope with a magnification of ×100. Brain cells that express TNF-α and iNOS are brown core, cytoplasm and cell walls. The results were obtained by the longer exposure to infection of the higher expression of TNF-α (r > 0688) and the expression of iNOS decreased (0.993).
Cite this paper: Hidayati, D. , Sujuti, H. , Wulandari, L. , Saputra, A. and Santoso, G. (2017) TNF-α (Tumor Necrosis Factor Alpha) and iNOS (Inducible Nitric Oxide Synthase) Expression in Rat Brain Infected by Mycobacterium tuberculosis Strain H37RV. Journal of Tuberculosis Research, 5, 58-68. doi: 10.4236/jtr.2017.51006.
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