Sasa veitchii extract protects against carbon tetrachloride-induced hepatic fibrosis in mice.
10.1186/s12199-018-0739-7
- Author:
Hiroki YOSHIOKA
1
;
Tsunemasa NONOGAKI
2
;
Shiori FUKAYA
2
;
Yoshimi ICHIMARU
2
;
Akito NAGATSU
2
;
Masae YOSHIKAWA
2
;
Hirohisa FUJII
2
;
Makoto NAKAO
2
Author Information
1. College of Pharmacy, Kinjo Gakuin University, 2-1723 Omori, Moriyamaku, Nagoya, Aichi, 463-8521, Japan. h-yoshioka@kinjo-u.ac.jp.
2. College of Pharmacy, Kinjo Gakuin University, 2-1723 Omori, Moriyamaku, Nagoya, Aichi, 463-8521, Japan.
- Publication Type:Journal Article
- Keywords:
Carbon tetrachloride;
Liver fibrosis;
Mitogen-activated protein kinase;
Nuclear factor kappa B;
Sasa veitchii
- MeSH:
Animals;
Carbon Tetrachloride;
toxicity;
Liver Cirrhosis;
chemically induced;
drug therapy;
Male;
Mice;
Mice, Inbred C57BL;
Plant Extracts;
pharmacology;
Protective Agents;
pharmacology;
Random Allocation;
Sasa;
chemistry
- From:Environmental Health and Preventive Medicine
2018;23(1):49-49
- CountryJapan
- Language:English
-
Abstract:
BACKGROUND:The current study aimed to investigate the hepatoprotective effects of Sasa veitchii extract (SE) on carbon tetrachloride (CCl)-induced liver fibrosis in mice.
METHODS:Male C57BL/6J mice were intraperitoneally injected with CCl dissolved in olive oil (1 g/kg) twice per week for 8 weeks. SE (0.1 mL) was administered orally once per day throughout the study, and body weight was measured weekly. Seventy-two hours after the final CCl injection, mice were euthanized and plasma samples were collected. The liver and kidneys were collected and weighed.
RESULTS:CCl administration increased liver weight, decreased body weight, elevated plasma alanine aminotransferase, and aspartate aminotransferase and increased liver oxidative stress (malondialdehyde and glutathione). These increases were attenuated by SE treatment. Overexpression of tumor necrosis factor-α was also reversed following SE treatment. Furthermore, CCl-induced increases in α-smooth muscle actin, a marker for hepatic fibrosis, were attenuated in mice treated with SE. Moreover, SE inhibited CCl-induced nuclear translocation of hepatic nuclear factor kappa B (NF-κB) p65 and phosphorylation of mitogen-activated protein kinase (MAPK).
CONCLUSION:These results suggested that SE prevented CCl-induced hepatic fibrosis by inhibiting the MAPK and NF-κB signaling pathways.
