Document Type : Original research articles
Authors
1
Histology and Cell Biology Department, Faculty of Medicine, South Valley University, Qena, 83523, Egypt.
2
Histology and Cell Biology Department, Faculty of Medicine, Assuit University, Assuit,71515.Egypt. & Histology and Cell Biology Department, Faculty of Medicine, Sphinx University, New Assuit City, 10, Assuit, Egypt.
3
Histology and Cell Biology Department, Faculty of Medicine, Assuit University, Assuit,71515.Egypt. & Department of Restorative Dentistry and Basic Medical Sciencies, Faculty of Dentistry,University of Petra, Amman, 11196, Jordan.
4
Department of Biochemistry , Sphinx University, New Assuit City, 10, Assiut, Egypt. & Department of Medical Biochemistry , Faculty of Medicine, Assuit University, Assiut,71515, Egypt.
Abstract
Background: Chronic kidney disease (CKD) is a major worldwide public health concern. A hallmark that is shared by all progressive chronic kidney diseases is tubulointerstitial fibrosis. Prolonged exposure to high amounts of carbon tetrachloride (CCL4), especially in vapor form, can cause kidney injury. Autophagy played a major role in stress adaptation and organ homeostasis maintenance. Impaired autophagy has frequently been associated with renal damage and fibrosis.
Objectives: The aim of this work is to assess the kidneys' histopathological response to CCl4 and the potential involvement of autophagy in this disease.
Materials and Methods: Twenty adult male albino rats were randomly divided into two equal groups (10 rats, each); Group 1: Control group. Group 2: The CCl4 group, rats were received CCl4, 1.5 mg/kg twice weekly subcutaneously (S.C) for 12 weeks. After sacrifice, kidneys were taken from all animal groups and processed for light microscopy, Immunological studies, Biochemical tests and statistical analysis were done.
Results: When CCL4 was administered, the kidney tissue underwent histological alterations, including areas of tissue breakdown, inflammatory cell infiltration, congestion and fibrosis.
Conclusion: Renal adverse effects, including inflammation, degeneration, and subsequently fibrosis, were brought on by CCl4 treatment for a duration of 12 weeks. One of the key processes via which CCl4 damages tissue is autophagy suppression.
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