Effects of blueberry on hepatic fibrosis and transcription factor Nrf2 in rats
Wang YP, Cheng ML, Zhang BF, Mu M, Wu J
World journal of gastroenterology · 43 citas
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Animales
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- Guizhou Science and Technology Department
Según 1 financiador declarado.
Publicación
- Publicado
- 2010-01-01 · World J Gastroenterol · vol. 16 · número 21 · pág. 2657
- Editorial
- Baishideng Publishing Group
- Citado
- 56 citas · más que el 91% de estudios similares · 2.8× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 28 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY-NC
- Áreas de investigación
- Liver physiology and pathology · Liver Disease Diagnosis and Treatment · Food Quality and Safety Studies
- Palabras clave
- Malondialdehyde, Hepatic fibrosis, Internal medicine, Fibrosis, Superoxide dismutase, Endocrinology, Chemistry, H&E stain, Hyaluronic acid, Glutathione, Medicine, Oxidative stress, Immunohistochemistry, Biochemistry, Enzyme
- MeSH
- animals, humans, rats, rats, sprague-dawley, liver cirrhosis, malondialdehyde, carbon tetrachloride, nad(p)h dehydrogenase (quinone), superoxide dismutase, glutathione transferase, alanine transaminase, hyaluronic acid, plant preparations, drugs, chinese herbal, phytotherapy, random allocation, male, nf-e2-related factor 2, blueberry plants
1 autor
- Yuping Wang · autor de correspondencia
Resumen
El texto original del estudio, en el idioma en que se publicó.
Aim
To investigate the effects of blueberry on hepatic fibrosis and NF-E2-related factor 2 (Nrf2) transcription factor in rats.
Methods
Forty-five male Sprague-Dawley rats were randomly divided into control group (A); CCl(4)-induced hepatic fibrosis group (B); blueberry prevention group (C); Dan-shao-hua-xian capsule (DSHX) prevention group (D); and blueberry + DSHX prevention group (E). Liver fibrosis was induced in rats by subcutaneous injection of CCl(4) and a high-lipid/low-protein diet for 8 wk (except the control group). The level of hyaluronic acid (HA) and alanine aminotransferase (ALT) in serum was examined. The activity of superoxide dismutase (SOD), glutathione-S-transferase (GST) and malondialdehyde (MDA) in liver homogenates was determined. The degree of hepatic fibrosis was evaluated by hematoxylin and eosin and Masson staining. Expression of Nrf2 and NADPH quinone oxidoreductase 1 (Nqo1) was detected by real-time reversed transcribed-polymerase chain reaction, immunohistochemical techniques, and western blotting.
Results
Compared with group B, liver indices, levels of serum HA and ALT of groups C, D and E were reduced (liver indices: 0.038 +/- 0.008, 0.036 +/- 0.007, 0.036 +/- 0.005 vs 0.054 +/- 0.009, P < 0.05; HA: 502.33 +/- 110.57 ng/mL, 524.25 +/- 255.42 ng/mL, 499.25 +/- 198.10 ng/mL vs 828.50 +/- 237.83 ng/mL, P < 0.05; ALT: 149.44 +/- 16.51 U/L, 136.88 +/- 10.07 U/L, 127.38 +/- 11.03 U/L vs 203.25 +/- 31.62 U/L, P < 0.05), and SOD level was significantly higher, but MDA level was lower, in liver homogenates (SOD: 1.36 +/- 0.09 U/mg, 1.42 +/- 0.13 U/mg, 1.50 +/- 0.15 U/mg vs 1.08 +/- 0.19 U/mg, P < 0.05; MDA: 0.294 +/- 0.026 nmol/mg, 0.285 +/- 0.025 nmol/mg, 0.284 +/- 0.028 nmol/mg vs 0.335 +/- 0.056 nmol/mg, P < 0.05). Meanwhile, the stage of hepatic fibrosis was significantly weakened (P < 0.05). Compared with group A, the activity of GST liver homogenates and expression levels of Nrf2 and Nqo1 in group B were elevated (P < 0.05). The expression level of Nrf2 and Nqo1 in groups C, D, and E were increased as compared with group B, but the difference was not significant.
Conclusion
Blueberry has preventive and protective effects on CCl(4)-induced hepatic fibrosis by reducing hepatocyte injury and lipid peroxidation. However, these effects may not be related to the activation of Nrf2 during long-term of CCl(4).
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
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