The Effect of Ascorbic Acid on Interleukin-10 and Tumor Necrosis Factor-α Cytokines in Rattus norvegicus with Endometritis

2021 
BACKGROUND: Endometritis is a gynecological disease characterized by inflammation of the endometrial glands and stroma. Inflammatory stimuli or tissue injury induce inflammatory pain through the release of cytokines. Ascorbic acid (AA) is a water-soluble Vitamin that plays a role in inhibiting the production of proinflammatory cytokines and increases the expression of anti-inflammatory cytokines. AIM: The purpose of this study was to find out the association between administration of AA and inflammatory cytokines in experimental animals Rattus norvegicus with endometritis. METHODS: The research was conducted using virgin female R. norvegicus laboratory mice weighing 250–300 g and aged 11–12 weeks with an estrus cycle of 5–6 days. Mice with regular oestrous cycles were randomly divided into three groups: group 1 was given 200 L of water orally without Escherichia coli inoculation and represented a negative control. Groups 2 and 3 were inoculated (50 L/rat) E. coli intravaginally, 106 colony-forming unit/mL, Group 2 was not given AA and the other side Group 3 was assigned AA. The interleukin (IL)-10 and tumor necrosis factor (TNF)-α _cytokines examination was carried out by histopathological examination through a biopsy of the endometrial tissue. Hypothesis testing on the data was analyzed by the Kruskal Wallis test using Statistical Package for Social Sciences. RESULTS: Data from the current study revealed that the highest mean value of IL-10 was found in the negative control group (2.5) and the lowest value in the positive control group (1.3). Regarding TNF-α _the highest mean value (2.8) was found in the treatment group and the lowest mean value (2.1) was found in the treatment group. Using the Kruskal Wallis test, IL-10 and TNF-α _showed insignificant results (p = value 0.304 and 0.145 respectively). CONCLUSIONS: The administration of AA did not affect the decrease in TNF-α _or the upregulation of IL-10 as anti-inflammatory cytokines.
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