The Probable Protective Role of Vitamin C against Cyclosporine an Induced Pulmonary Changes in Mice

Abstract

Cyclosporine A (Cs-A) is a frequently used immunosuppressive agent in transplant medicine to prevent rejection and in the treatment of autoimmune diseases. Vitamin c is a potent antioxidant that has the ability to scavenge factors causing free radical formation in animals receiving Cs-A. It play a major role in disease prevention. Cs-A induced histological and ultrastructural alterations in the pulmonary tissue. These included congestion and hemorrhage of most blood capillaries, increased number of lymphocytes within the thickened interalveolar septa and destruction of the inner border of the respiratory bronchioles and increase of collagen fibers. Changes were seen in type I& II alveolar cells in the form of vacuolation, increase in the number of lysosomes, shortening of the apical microvilli and irregularity and swollen of the nuclei. Also, an increase in number of macrophages and fragmentation of the rough endoplasmic reticulum. Most of the main cell types in the alveolar tissue had restored their normal histological and ultrastructural appearance by VC. Conclusion: Antioxidant nutrients (VC) can improve lung histological and ultrastructural damage produced by Cs-A administration.

Histopathological Study of Cyclosporine Pulmonary Toxicity in Rats

“…Our results revealed that the third group which received 40 mg/kg/day of cyclosporine induced marked pulmonary histopathological abnormalities such as a pyknotic nucleus of pneumocyte type II, degeneration of alveoli with its microvilli, and emphysema with inflammatory cellular infiltration and pulmonary vessels congestion in consistency with Yousef and ALRajhi [ 16 ] while the second group which received 25 mg/kg/day of cyclosporine showed mild pulmonary ultrastructures and histopathological changes such as a shrinkage nucleus of pneumocyte type II, degenerated microvilli on the alveolar surface, thickened wall of bronchiole with moderately congested blood capillaries and macrophages infiltration in the alveolar spaces, and nearly normal architecture of alveoli with thickened interalveolar septa. Furthermore, the overall lung lesion severity scores were differed significantly between the second and third groups indicating that the severity of cyclosporine induced pulmonary histological changes depending on its dose.…”

The Potential Protective Effect and Underlying Mechanisms of Physiological Unconjugated Hyperbilirubinemia Mediated by UGT1A1 Antisense Oligonucleotide Therapy in a Mouse Model of Cyclosporine A-Induced Chronic Kidney Disease

“…The effects of CsA therapy on nephrotoxicity, kidney lesions, and creatinine levels have been previously reported [ 9 ]. CsA causes an increase in reactive oxygen species (ROS) and lipid peroxidation products, both of which have been linked to its toxicity [ 10 ]. CsA causes kidney damage, accompanied by an increase in inflammatory and oxidative stress markers [ 11 ].…”