Introduction: Cyclosporine A (CsA) used frequently in fields of organ transplantation and autoimmune diseases for its effect as immunosuppressive. However, CsA-induced cytotoxicity represents a main clinical problem, oxidative stress has been concerned as a conceivable responsible mechanism. Fucidan (FU) is a potent polysaccharides matter, extracted from brown algae, it has an important antioxidant and anti-inflammatory effects.

Objective of study: The present study evaluated the protective and therapeutic impact of fucoidan against CsA-induced lymph nodes degeneration.

Materials and Methods: Wistar albino male rats were randomly divided into five groups (G). The control group (G1) received normal saline and olive oil (vehicles), G2  and G3 were for the protective effect and received low doses in which G2 received CsA alone and the G3 received CsA associated with FU. However, G4 and G5 were for the therapeutic effect and received the high dose in which G4 received CsA and allowed to recover for another 10 days, whereas G5 was treated with CsA, followed by FU for another 10 days. After the treatment period, lymph nodes specimens were taken and prepared for the pathological examination under the light and the electronic microscope. The immunehistochemistry technic was applied for CD3+ T cells density determination.

Results: Treatment of rats with CsA alone induced a degenerated histological changes, most of them were in the plasma cells, lymphocytes and reticular cells. Most degeneration were the apoptotic bodies, shrunken and condensed chromatin nuclei and lysing organelles with rarefied cytoplasm. Concurrent FU administration with CsA improved cells morphological, mostly became resemble those in control. After recovery without FU treatment, many degenerated and vacuolated cells with karyolysis and cytolysis were observed. However, most cells were improved after recovery with FU treatment. Immunohistochemistry study revealed a low condensed of CD3+ T lymphocytes by CsA treatment, whereas FU treatment caused a high condensed of this  cell type.

Conclusion: These results indicate that FU produces a protective and therapeutic mechanism against lymph node cytotoxicity induced by CsA.

  Keywords: Lymph nodes, Cyclosporine, Fucoidan, Degeneration, Plasma cells