Environmental health and preventive medicine · 2016
Sasa veitchii extract suppresses carbon tetrachloride-induced hepato- and nephrotoxicity in mice.
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Yoshioka Hiroki, Tanaka Miki, Fujii Hirohisa, Nonogaki Tsunemasa
Аннотация
OBJECTIVE: The aim of this study was to investigate the therapeutic effects of a Sasa veitchii leaf extract (SE) on carbon tetrachloride (CCl4)-induced hepato- and nephrotoxicity.
METHODS: Seven-week-old male ddy mice were orally administered SE or saline for seven days. Twenty-four hours after the last SE or saline administration, the mice were intraperitoneally injected with 3 g/kg CCl4 or olive oil. The mice from each group were euthanized and bled for plasma analysis 24 h after the CCl4/olive oil injection.
RESULTS: We found that pretreatment with SE completely abolished the CCl4-induced mortality in the mice after 24 h. The mice pretreated with SE exhibited significantly decreased levels of functional markers, and reduced histological damage in both the liver and the kidney. Furthermore, we found that the SE pretreatment decreased lipid peroxidation and calcium levels in the liver. Although SE could not induce the free radical-scavenging metallothioneins, the plasma biological antioxidant power was significantly increased in the mice pretreated with SE.
CONCLUSION: Our findings demonstrate that prophylactic treatment with SE protects mice from CCl4-induced lethal toxicity by decreasing oxidative stress in the liver and kidney, presumably by increasing biological antioxidant power.
METHODS: Seven-week-old male ddy mice were orally administered SE or saline for seven days. Twenty-four hours after the last SE or saline administration, the mice were intraperitoneally injected with 3 g/kg CCl4 or olive oil. The mice from each group were euthanized and bled for plasma analysis 24 h after the CCl4/olive oil injection.
RESULTS: We found that pretreatment with SE completely abolished the CCl4-induced mortality in the mice after 24 h. The mice pretreated with SE exhibited significantly decreased levels of functional markers, and reduced histological damage in both the liver and the kidney. Furthermore, we found that the SE pretreatment decreased lipid peroxidation and calcium levels in the liver. Although SE could not induce the free radical-scavenging metallothioneins, the plasma biological antioxidant power was significantly increased in the mice pretreated with SE.
CONCLUSION: Our findings demonstrate that prophylactic treatment with SE protects mice from CCl4-induced lethal toxicity by decreasing oxidative stress in the liver and kidney, presumably by increasing biological antioxidant power.