Protective effect of gallic acid against thioacetamide-induced metabolic dysfunction of lipids in hepatic and renal toxicity
Gallic acid (GA) has significant antioxidant bioactivity and can prevent diet-induced hypertriglyceridemia by reducing adipocytes. GA was also observed to enhance cell glucose uptake. The current study looked at the effect of gallic acid (GA) (100 mg, 200 mg/kg orally) on liver and kidney damage cau...
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| Published in | Journal of King Saud University. Science Vol. 35; no. 3; p. 102531 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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Elsevier B.V
01.04.2023
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| Abstract | Gallic acid (GA) has significant antioxidant bioactivity and can prevent diet-induced hypertriglyceridemia by reducing adipocytes. GA was also observed to enhance cell glucose uptake.
The current study looked at the effect of gallic acid (GA) (100 mg, 200 mg/kg orally) on liver and kidney damage caused by thioacetamide (TAA; 100 mg/Kg via intraperitoneal route). TAA was treated thrice weekly for eight weeks, whereas gallic acid was administered daily.
GA alleviated the thioacetamide-induced decreases in hepatic or renal reduced glutathione (GSH) or increases in malondialdehyde (MDA, an indication of lipid peroxidation). TAA treatment significantly increased plasma inflammatory markers, tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP), liver enzymes, Gamma-glutamyltransferase (GGT), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), alkaline phosphatase (ALP), and kidney function parameters (creatinine and urea) and uric acid. However, these values decreased after GA treatment in a dose-dependent manner. Furthermore, GA mitigated the considerable decrease in plasma protein caused by TAA. GA also reduced hepatic fibrosis or histological abnormalities in the liver and kidney.
Our results suggest that GA may attenuate TAA-induced liver and kidney toxicity via suppression of oxidative stress and inflammatory markers. Moreover, the hypolipidemic effect of GA may be considered another route for protection. |
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| AbstractList | Background: Gallic acid (GA) has significant antioxidant bioactivity and can prevent diet-induced hypertriglyceridemia by reducing adipocytes. GA was also observed to enhance cell glucose uptake. Methods: The current study looked at the effect of gallic acid (GA) (100 mg, 200 mg/kg orally) on liver and kidney damage caused by thioacetamide (TAA; 100 mg/Kg via intraperitoneal route). TAA was treated thrice weekly for eight weeks, whereas gallic acid was administered daily. Results: GA alleviated the thioacetamide-induced decreases in hepatic or renal reduced glutathione (GSH) or increases in malondialdehyde (MDA, an indication of lipid peroxidation). TAA treatment significantly increased plasma inflammatory markers, tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP), liver enzymes, Gamma-glutamyltransferase (GGT), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), alkaline phosphatase (ALP), and kidney function parameters (creatinine and urea) and uric acid. However, these values decreased after GA treatment in a dose-dependent manner. Furthermore, GA mitigated the considerable decrease in plasma protein caused by TAA. GA also reduced hepatic fibrosis or histological abnormalities in the liver and kidney. Conclusion: Our results suggest that GA may attenuate TAA-induced liver and kidney toxicity via suppression of oxidative stress and inflammatory markers. Moreover, the hypolipidemic effect of GA may be considered another route for protection. Gallic acid (GA) has significant antioxidant bioactivity and can prevent diet-induced hypertriglyceridemia by reducing adipocytes. GA was also observed to enhance cell glucose uptake. The current study looked at the effect of gallic acid (GA) (100 mg, 200 mg/kg orally) on liver and kidney damage caused by thioacetamide (TAA; 100 mg/Kg via intraperitoneal route). TAA was treated thrice weekly for eight weeks, whereas gallic acid was administered daily. GA alleviated the thioacetamide-induced decreases in hepatic or renal reduced glutathione (GSH) or increases in malondialdehyde (MDA, an indication of lipid peroxidation). TAA treatment significantly increased plasma inflammatory markers, tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP), liver enzymes, Gamma-glutamyltransferase (GGT), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), alkaline phosphatase (ALP), and kidney function parameters (creatinine and urea) and uric acid. However, these values decreased after GA treatment in a dose-dependent manner. Furthermore, GA mitigated the considerable decrease in plasma protein caused by TAA. GA also reduced hepatic fibrosis or histological abnormalities in the liver and kidney. Our results suggest that GA may attenuate TAA-induced liver and kidney toxicity via suppression of oxidative stress and inflammatory markers. Moreover, the hypolipidemic effect of GA may be considered another route for protection. |
| ArticleNumber | 102531 |
| Author | Ebaid, Hossam Morsy, Fatma A. Al-Tamimi, Jameel Alhazza, Ibrahim M. Hassan, Iftekhar Bashandy, Samir A.E. |
| Author_xml | – sequence: 1 givenname: Hossam surname: Ebaid fullname: Ebaid, Hossam organization: Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia – sequence: 2 givenname: Samir A.E. surname: Bashandy fullname: Bashandy, Samir A.E. organization: Department of Pharmacology, Medical Division, National Research Centre, 33 EL Bohouth st., Dokki, Giza, P.O.12622, Egypt – sequence: 3 givenname: Fatma A. surname: Morsy fullname: Morsy, Fatma A. organization: Department of Pathology, Medical Division, National Research Centre, 33 EL Bohouth st., Dokki, Giza, P.O.12622, Egypt – sequence: 4 givenname: Jameel surname: Al-Tamimi fullname: Al-Tamimi, Jameel organization: Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia – sequence: 5 givenname: Iftekhar surname: Hassan fullname: Hassan, Iftekhar email: iftekharhassan2002@gmail.com, ihassan@ksu.edu.sa organization: Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia – sequence: 6 givenname: Ibrahim M. surname: Alhazza fullname: Alhazza, Ibrahim M. organization: Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia |
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| CitedBy_id | crossref_primary_10_3390_foods12173178 crossref_primary_10_1186_s12906_023_04067_9 crossref_primary_10_1186_s12906_023_04250_y crossref_primary_10_13005_bpj_2941 |
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| Issue | 3 |
| Keywords | Oxidative stress Thioacetamide hepatic injury Inflammatory markers Gallic acid Kidney injury |
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| Title | Protective effect of gallic acid against thioacetamide-induced metabolic dysfunction of lipids in hepatic and renal toxicity |
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