Abstract

The present study was aimed efficiency to evaluate the unsaturated fatty acid omega-3 in reducing the side effects that resulted from the administration of cyclosporine drug in white rabbits. (60) white males' rabbits were used in this study, divided into four groups contain (15) rabbits per group and its subdivision into three groups (5) rabbits per group. The first group is orally administered with normal saline, the second group was administered cyclosporine (25mg/kg) only. Third groups were administered cyclosporine on the first day and omega-3 (500mg/kg) on the second day, while Fourth groups were administered cyclosporine on the first day and omega-3 (1000mg/kg) on the second day for periods (21,30,60) days respectively. After ending study periods, the animals were sacrificed and the blood was collected and the results were shown the following: Administration with cyclosporine (25mg/kg)only and for periods were led to a significant increase(P<0.05) in total cholesterol, triglycerides and low-density lipoprotein(LDL) and a significant decrease(P<0.05) in high-density lipoprotein(HDL).whereas interaction with (500&1000mg/kg) of omega-3 and to all periods showed a significant decrease (p<0.05) in the total cholesterol, triglycerides and low-density lipoprotein(LDL) and significant decrease(p<0.05) in high-density lipoprotein(HDL), while the non-significant difference in high-density lipoprotein(HDL). This study concluded that omega-3 has an important role in reducing biochemistry side effects that result from the administration of cyclosporine drugs in white rabbits.

Highlights

  • IntroductionCyclosporine targets the T cells by binding to cytoplasmic receptors in T cells called (Cyclophilin), the cyclophilin, makes to inhibit a substance called (Calcineurin) responsible for stimulating the nuclear factor to activate lymphocytes to produce cytokines (Crespo-Leiro, 2005)

  • The drug makes to suppress the immune system by inhibiting the receptors of T-lymphocytes, this effect prevents the binding of cytokines, which are the natural stimuli for the immune response (Borel, 1989).Cyclosporine targets the T cells by binding to cytoplasmic receptors in T cells called (Cyclophilin), the cyclophilin, makes to inhibit a substance called (Calcineurin) responsible for stimulating the nuclear factor to activate lymphocytes to produce cytokines (Crespo-Leiro, 2005)

  • The current study found a significant increase in the concentration of total cholesterol and triglycerides after treatment with cyclosporine

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Summary

Introduction

Cyclosporine targets the T cells by binding to cytoplasmic receptors in T cells called (Cyclophilin), the cyclophilin, makes to inhibit a substance called (Calcineurin) responsible for stimulating the nuclear factor to activate lymphocytes to produce cytokines (Crespo-Leiro, 2005). Several studies have indicated that the effect of cyclosporine is through the activation of the enzyme Thyronin Phosphatase as it makes to remove a phosphate group from the cytoplasmic component of the NF-ATc, and it is transferred to the nucleus and is called (NF-ATn) and is linked to the Promotor dependent to the responsible gene On the encoding of interleukin-2 (IL-2), which leads to its non-production and non-stimulation of lymphocytes, and as a result the effect on the performance of the function, reproduction and functioning of lymphocytes (Kelly & Kahan, 2002). Almost all of the cyclosporine is excreted by hepatic metabolism by two methods: bile and about 6% in urine, and 1% of the antagonist is excreted unchanged (without metabolism), i.e. crude during urination and bile (Bistrup et al, 2001)

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