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Mulberry leaves extract ameliorates alcohol-induced liver damages through reduction of acetaldehyde toxicity and inhibition of apoptosis caused by oxidative stress signals.
- Source :
-
International journal of medical sciences [Int J Med Sci] 2021 Jan 01; Vol. 18 (1), pp. 53-64. Date of Electronic Publication: 2021 Jan 01 (Print Publication: 2021). - Publication Year :
- 2021
-
Abstract
- Mulberry leaves (Morus alba L.), which are traditional Chinese herbs, exert several biological functions, such as antioxidant, anti-inflammation, antidiabetic, and antitumor. Alcohol intake increases inflammation and oxidative stress, and this increase causes liver injury and leads to liver steatosis, cirrhosis, and hepatocellular carcinoma, which are major health problems worldwide. Previous report indicated that mulberry leaf extract (MLE) exited hepatoprotection effects against chronic alcohol-induced liver damages. In this present study, we investigated the effects of MLE on acute alcohol and liver injury induced by its metabolized compound called acetaldehyde (ACE) by using in vivo and in vitro models. Administration of MLE reversed acute alcohol-induced liver damages, increased acetaldehyde (ACE) level, and decreased aldehyde dehydrogenase activity in a dose-dependent manner. Acute alcohol exposure-induced leukocyte infiltration and pro-inflammation factors, including cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), were blocked by MLE in proportion to MLE concentration. MLE prevented alcohol-induced liver apoptosis via enhanced caveolin-1 expression and attenuated EGFR/STAT3/iNOS pathway using immunohistochemical analysis. ACE induced proteins, such as iNOS, COX-2, TNF-α, and IL-6, and inhibited superoxide dismutase expression, whereas co-treated with MLE reversed these proteins expression. MLE also recovered alcohol-induced apoptosis in cultured Hep G2 cells. Overall, our findings indicated that MLE ameliorated acute alcohol-induced liver damages by reducing ACE toxicity and inhibiting apoptosis caused by oxidative stress signals. Our results implied that MLE might be a potential agent for treating alcohol liver disease.<br />Competing Interests: Competing Interests: The authors have declared that no competing interest exists.<br /> (© The author(s).)
- Subjects :
- Acetaldehyde metabolism
Aldehyde Dehydrogenase antagonists & inhibitors
Aldehyde Dehydrogenase metabolism
Animals
Antioxidants isolation & purification
Apoptosis drug effects
Disease Models, Animal
Enzyme Assays
Ethanol administration & dosage
Ethanol adverse effects
Ethanol metabolism
Hep G2 Cells
Humans
Liver drug effects
Liver enzymology
Liver pathology
Liver Diseases, Alcoholic etiology
Liver Diseases, Alcoholic pathology
Mice
Mice, Inbred ICR
Oxidative Stress drug effects
Plant Extracts isolation & purification
Plant Leaves chemistry
Reactive Oxygen Species metabolism
Acetaldehyde toxicity
Antioxidants administration & dosage
Liver Diseases, Alcoholic drug therapy
Morus chemistry
Plant Extracts administration & dosage
Subjects
Details
- Language :
- English
- ISSN :
- 1449-1907
- Volume :
- 18
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- International journal of medical sciences
- Publication Type :
- Academic Journal
- Accession number :
- 33390773
- Full Text :
- https://doi.org/10.7150/ijms.50174