solaiman, A., Sawires, S. (2022). The Ameliorative Potential of Alda-1 on Experimentally Induced Liver Fibrosis in Adult Male Mice. A Histological, Immunohistochemical and Biochemical Study. Egyptian Journal of Histology, 45(3), 949-968. doi: 10.21608/ejh.2022.133870.1674
amany solaiman; silvia Kamil Seddik Sawires. "The Ameliorative Potential of Alda-1 on Experimentally Induced Liver Fibrosis in Adult Male Mice. A Histological, Immunohistochemical and Biochemical Study". Egyptian Journal of Histology, 45, 3, 2022, 949-968. doi: 10.21608/ejh.2022.133870.1674
solaiman, A., Sawires, S. (2022). 'The Ameliorative Potential of Alda-1 on Experimentally Induced Liver Fibrosis in Adult Male Mice. A Histological, Immunohistochemical and Biochemical Study', Egyptian Journal of Histology, 45(3), pp. 949-968. doi: 10.21608/ejh.2022.133870.1674
solaiman, A., Sawires, S. The Ameliorative Potential of Alda-1 on Experimentally Induced Liver Fibrosis in Adult Male Mice. A Histological, Immunohistochemical and Biochemical Study. Egyptian Journal of Histology, 2022; 45(3): 949-968. doi: 10.21608/ejh.2022.133870.1674
The Ameliorative Potential of Alda-1 on Experimentally Induced Liver Fibrosis in Adult Male Mice. A Histological, Immunohistochemical and Biochemical Study
2histology and cell biology, alexandria university, Egypt
Abstract
Introduction: Because of its complex pathogenesis, liver fibrosis remains one of the diseases with no standard treatment. Alda-1 is considered as a promising drug in ameliorating such fibrosis. Aim of the Work: To evaluate the potential effect of Alda-1 after thioacetamide (TAA)-induced liver fibrosis in male mice. Materials and Methods: Twenty-five adult male mice (25–27 gm aged 2-3 months) were allocated into five equal groups. Group I (control group), group II (Alda-1 group): each mouse was given Alda-1 [5 mg/kg, intraperitoneally (ip)] twice weekly for four weeks. Group III (TAA group): each animal received TAA (200 mg/kg, ip) twice weekly for seven weeks. Group IV (TAA +Alda-1 group): each mouse was given TAA as group III. After stoppage of TAA administration, Alda-1 was given at a dose as group II and continued for four weeks. Group V (recovery group) each animal received TAA treatment as group III and left without any treatment for an extra four weeks. The histological changes were identified by the light (H&E and Masson’s trichrome stains) and electron microscopies, immunohistochemical and morphometric analysis. Blood samples were taken to evaluate the liver's function. Results: TAA caused marked histological and biochemical attenuation of hepatocytes structure and function with significant increase in collagen deposition. In addition, TAA caused significant elevation of liver enzymes. In Alda-1treated In Alda-1treated group (IV), hepatocytes revealed nearly normal structure, significantly decreased the elevated liver enzymes and significant increase in reduced glutathione and decrease in malondialdehyde in liver homogenate. Alda-1 decreased the elevated transforming growth factor, collagen-1 gene expression and the area percentage of collagen. In addition, alpha smooth muscle actin was significantly reduced. The anti-inflammatory effects were also detected by the decrease in the interleukin-6 and tumor necrosis factor-α. Conclusion: Alda-1 ameliorated TAA-induced liver fibrosis in mice. This might be due to its antioxidant, antifibrotic and anti-inflammatory effects.
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