Mesenchymal stem cells ameliorate oxidative stress, inflammation, and hepatic fibrosis via Nrf2/HO-1 signaling pathway in rats
| Autor: | Hanaa M. Mohamed, Ayman M. Mahmoud, Sally M. Khadrawy |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
medicine.medical_specialty
Cirrhosis Health Toxicology and Mutagenesis Inflammation 010501 environmental sciences medicine.disease_cause digestive system 01 natural sciences Proinflammatory cytokine chemistry.chemical_compound stomatognathic system Fibrosis Internal medicine medicine Environmental Chemistry 0105 earth and related environmental sciences business.industry General Medicine Malondialdehyde medicine.disease Pollution Endocrinology chemistry Liver function medicine.symptom Hepatic fibrosis business Oxidative stress |
| Zdroj: | Environmental Science and Pollution Research. 28:2019-2030 |
| ISSN: | 1614-7499 0944-1344 |
| Popis: | Liver fibrosis occurs in most types of chronic liver diseases and can develop into cirrhosis and liver failure. Bone marrow-derived mesenchymal stem cells (BMSCs) showed promising effects in the treatment of fibrosis. This study evaluated the possible role of Nrf2/HO-1 signaling in the ameliorative effect of BMSCs against carbon tetrachloride (CCl4)-induced liver fibrosis, oxidative stress, and inflammation in rats. Hepatic fibrosis was induced by subcutaneous injection of CCl4 twice per week for 6 consecutive weeks and rat BMSCs were administered intravenously. After 4 weeks, the rats were sacrificed, and samples were collected for analysis. CCl4-intoxicated rats showed elevated serum transaminases, ALP, γGT, bilirubin and pro-inflammatory cytokines, and decreased albumin. Hepatic NF-κB p65 and malondialdehyde (MDA) were significantly increased, and cellular antioxidants were decreased in CCl4-intoxicated rats. BMSCs ameliorated liver function markers, suppressed MDA, NF-κB p65, and inflammatory cytokines, and enhanced antioxidants in the liver of CCl4-intoxicated rats. BMSCs were engrafted within the liver tissue and prevented histological alterations and collagen accumulation induced by CCl4. In addition, BMSCs upregulated hepatic Nrf2 and HO-1 expression in CCl4-intoxicated rats. In conclusion, this study provides evidence that BMSCs suppress oxidative stress, inflammation, and liver fibrosis through a mechanism involving activation of the Nrf2/HO-1 signaling. |
| Databáze: | OpenAIRE |
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