In Vivo Ameliorative Effects of Vitamin E Supplements against Hydralazine Induced Systemic Lupus Erythematosus
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Date
2024-03
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Kenyatta University
Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease where the
immune system attacks body cells and tissues causing inflammation. The drug
therapy in SLE states that organ threatening disease should be managed
aggressively by high to low doses of corticosteroids often followed by institution
of steroid sparing measures in the form of immunosuppressive. Long term use
of these drugs have life threatening side effects. Toxic oxygen radicals such as
hydrogen peroxide have been associated with the development of SLE. The aim
of this project was to evaluate the potential of an anti-oxidant, Vitamin E to
eliminate the hydrogen peroxide levels in hydralazine induced lupus, a disease
model that closely resembles SLE. The experiment involved forty Bagg Albino
(BALB) c mice aged three to four weeks comprising of twenty females and
twenty males that were randomized into six different groups. Each group
contained three males and three females. To mimic the pathogenesis of SLE,
hydralazine hydrochloride 25mg/kg bdw was used to induce a lupus-like
condition in mice from groups B to F. The mice from group A received 1.0ml of
sterile water and served as the normal control. An anti-nuclear antibody test was
carried out every seven days to monitor the development of autoantibodies,
which are considered a hallmark of lupus. By the 35th day post hydralazine
administration, ANA antibodies were confirmed in all treated groups. Drug
treatments were initiated in all lupus-induced mice at the same time, daily for a
period of another 35 days with the exception of group B that served as the
negative control of lupus induced mice with no drug treatment. Group C received
prednisolone 25 mg/kg bdw, Group D received methotrexate 25 mg/kg bdw,
Group E received Vitamin E 25 mg/kg bdw, and Group F received Vitamin E 50
mg/kg bdw. Only the higher dose of Vitamin E significantly eliminated the levels
of lymphocyte hydrogen peroxide associated with the pathogenesis of
hydralazine induced lupus. Both doses of Vitamin E protected lupus-induced
mice from alterations in all blood cells. Mice from the methotrexate treatment
groups recorded significantly low levels of all blood cells. However, the
prednisolone group recorded significantly low lymphocyte count with eosinophil
and neutrophil counts significantly high. Notably, the prednisolone treated mice
had significantly increased platelet count. Both doses of Vitamin E protected the
mice from changes in liver biomarkers while prednisolone and methotrexate
treatment groups showed significantly high levels of liver enzymes. Both doses
of Vitamin E protected from alterations in the lipid profile. Prednisolone and
methotrexate treatment groups had high ANA titer concentrations, Mice treated
with Vitamin E had significantly low ANA titers. Vitamin E also was found to
prevent injury to the kidney, liver, spleen, heart and brain. Prednisolone group
had significantly elevated bodyweight compared to the normal control group. In
conclusion, this study found Vitamin E supplementation was able to counter
oxidative stress associated with the pathogenesis of lupus. Based on these
findings, Vitamin E supplementation may be beneficial for improving the
condition of SLE patients. Further research is recommended to explore other
relevant free radicals in SLE and determine the optimal dosage of Vitamin E to
effectively eliminate free radicals associated with SLE.
Description
A Thesis Submitted in Partial Fulfillment of the Requirements for the Award of the Degree of Masters of Science (Biotechnology) in the School of Pure and Applied Sciences, Kenyatta University March, 2024