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Therapeutic Role of Thymoquinone on mitochondrial biogenesis in a Thioacetamide-Induced Hepatic Encephalopathy Rat Model
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Seyedeh Parisa Navabi   , Somayeh Hajipour , Alireza Sarkaki , Mohammad Amin Dehghani , Masoud Mahdavinia |
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Abstract: (255 Views) |
Introduction: The present study was designed to investigate the role of impaired mitochondrial functions and cerebral energy metabolism in the development of hepatic encephalopathy (HE) induced by thioacetamide (TAA). It is hypothesized by the authors that thymoquinone (TQ) improves HE complication in rats by preserving mitochondrial function via SIRT3/p53 signaling pathway.
Methods and Materials: Forty-five male Wistar rats were randomly divided into three groups: sham group, HE group, and HE+TQ (20 mg/kg, IP, vehicle: DMSO 5 %, once daily for at least seven consecutive days from 24 h after the last injection of TAA) treatment group. At the end of the experiment, mitochondrial membrane potential and oxidative stress assessments, western blot analysis of the proteins (SIRT3-P53) were carried out.
Result: TQ treatment significantly decreased the potential collapse of mitochondrial membrane and oxidative stress, and significantly improved the SIRT3 pathway in comparison to the sham group. TQ also significantly decreased the expression of apoptotic protein P53 after HE induction.
Conclusion: However, the data suggests that as a potential protective agent with a therapeutic capability against HE complication and its underlying mechanisms, TQ may be associated with modulation of SIRT3-P53 signaling pathway.
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| Keywords: Hepatic Encephalopathy, SIRT3/p53, mitochondrial oxidative stress |
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Full-Text [PDF 261 kb]
(36 Downloads)
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Type of Study: Research |
Subject:
General
Received: 2024/01/19 | Accepted: 2023/08/23 | Published: 2023/08/23
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