Effects of Green Tea Catechin on Polymorphonuclear Leukocyte 5′-Lipoxygenase Activity, Leukotriene B4 Synthesis, and Renal Damage in Diabetic Rats

Abstract

The purpose of this study was to investigate the effects of green tea catechin on polymorphonuclear leukocyte 5′-lipoxygenase activity, leukotriene B₄ synthesis, and renal damage in diabetic rats. Male Sprague-Dawley rats weighing 100 ± 10 g were randomly assigned to 1 normal group and 3 diabetic groups given a catechin-free diet (DM-0C group), 0.25% catechin diet (DM-0.25C group), or 0.5% catechin diet (DM-0.5C group), respectively. 5′-Lipoxygenase activity in the polymorphonuclear leukocytes significantly increased by 54% in the DM-0C group compared to the normal group, while the level in the DM-0.5C group remained the same as in the normal group. The leukotriene B₄ content in the polymorphonuclear leukocytes increased 55% in the DM-0C group compared to the normal group, whereas the DM-0.25C and DM-0.5C groups exhibited the same level as the normal group. The superoxide radical content in the kidney microsomes increased 116% in the DM-0C group when compared to the normal group, yet decreased 29% in the DM-0.25C group and 50% in the DM-0.5C group compared to DM-0C group. The lipofuscin content was 197 and 136% higher in the DM-0C and DM-025C groups, respectively, than in the normal group, whereas the DM-0.5C group exhibited the same content as in the normal group. The carbonyl value increased 118% in the DM-0C group compared to the normal group, and the DM-0.25C and DM-0.5C groups were not significantly different from the DM-0C group. Accordingly, these results indicate that dietary catechin inhibited the generation of superoxide radicals, oxidized protein, and lipid peroxide in the kidney of streptozotocin-induced diabetic rats. Furthermore, green tea catechin supplementation in diabetic rats also appeared to inhibit the production of leukotriene B₄ based on regulating the activity of 5′-lipoxygenase, thereby potentially reducing renal oxidative damage and inflammatory reactions.