{'fraction_non_alphanumeric': 0.02812939521800281, 'fraction_numerical': 0.0035161744022503515, 'mean_word_length': 5.352678571428571, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The protective role of vitamin c and l-arginine on ischemic-reperfusion injury in the renal cortex of adult albino rats: histological and immunohistochemical study

Introduction Ischemia/reperfusion injury (IR) is defined as alterations due to deprivation and re-establishment of the oxygen supply to tissues and organs. It is a complex phenomenon, which not only involves intracellular effects but also involves an inflammatory response to the injury [1]. Renal injury caused by IR occurs inevitably in surgical procedures in which the kidneys remain without blood supply for some time – for example, during kidney transplantation and in partial nephrectomy. In kidney transplantation, graft dysfunction, acute rejection, and chronic disease correlate with the degree of ischemic injury [2]. The pathogenesis of IR is not completely understood. There is evidence, which relates it with the decrease in mitochondrial ATP production, loss of the selective permeability of the cell membranes, and an increase in intracellular sodium and calcium leading the renal cell to injury or death [1]. The reperfusion of ischemic tissue leads to a more severe damage compared with the ischemic injury itself [3]. IR injury leads to the production of excess reactive oxygen species (ROS) and reactive nitrogen species [4]. Reperfusion injury Department of Anatomy and Embryology, Faculty of Medicine, Ain Shams University, Cairo, Egypt