Combined intake of blueberry juice and probiotics ameliorate mitochondrial dysfunction by activating SIRT1 in alcoholic fatty liver disease
| Autor: | Tingting Ren, Yanyan Shen, Lili Zhu, Houmin Fan, Qiuju Mou, Tao Lin, Ya Ren |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
RC620-627
Endocrinology Diabetes and Metabolism Medicine (miscellaneous) Mitochondrion Pharmacology Alcoholic fatty liver disease Blueberry Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound Liver disease 0302 clinical medicine SIRT1 medicine TX341-641 Nutritional diseases. Deficiency diseases 030304 developmental biology chemistry.chemical_classification 0303 health sciences Reactive oxygen species Nutrition and Dietetics biology Nutrition. Foods and food supply Research Probiotics Malondialdehyde medicine.disease medicine.anatomical_structure chemistry 030220 oncology & carcinogenesis Hepatocyte biology.protein Alcoholic fatty liver Liver function Mitochondrial dysfunction |
| Zdroj: | Nutrition & Metabolism, Vol 18, Iss 1, Pp 1-11 (2021) Nutrition & Metabolism |
| ISSN: | 1743-7075 |
| Popis: | Background Mitochondrial dysfunction has been implicated as a significant factor in the liver disease process. Blueberry juice and probiotics (BP) synergistically improve liver function in alcoholic fatty liver disease (AFLD), although the mechanism for this effect was unclear. This study aims to investigate the effect and specific mechanisms of BP on AFLD. Methods C57/BL6 mice were randomly divided into seven groups: CG (control), MG (AFLD model), BJ (MG mice treated with blueberry), BJB (MG mice treated with BP), SI (AFLD mice treated with SIRT1 siRNA), BJSI (SI mice treated with blueberry), and BJBSI (SI mice treated with BP). The mice were fed an alcohol liquid diet for 10 days to establish the AFLD model, and subjected to BP and SIRT1 siRNA intervention for 10 days. Liver pathology was performed on day 11, and biochemical and molecular analyses of liver mitochondria were employed on day 12. Results BP significantly ameliorated hepatic mitochondrial injury, mitochondrial swelling, and hepatic necrosis in AFLD. BP alleviated hepatic mitochondrial dysfunction by increasing the expression of succinate dehydrogenase and cytochrome c oxidase, increasing respiratory control rate and the ADP/O ratio, and facilitating the synthesis of energy-related molecules. Besides, BP increased the expression of glutathione and superoxide dismutase, and inhibited malondialdehyde expression and reactive oxygen species activity. BP-induced sirtuin 1 (SIRT1), which activates peroxisome proliferator-activated receptor-gamma coactivator-1α, both of which mediate mitochondrial homeostasis. SIRT1 silencing suppressed the BP-induced changes in liver mitochondria, blunting its efficacy. Conclusions The ingredients of BP ameliorate hepatocyte mitochondrial dysfunction in AFLD mice. |
| Databáze: | OpenAIRE |
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