Hepatoprotective effect of fermented black radish (Raphanus sativus L. var niger) in CCl4 induced liver injury in rats

서지정보

ㆍ발행기관 : 한국예방수의학회(구 한국수의공중보건학회) ㆍ수록지정보 : 예방수의학회지 / 41권 / 4호
ㆍ저자명 : Jeongtae Kim, Meejung Ahn, Seong-Eun Kim, Hak Sung Lee, Hyun Kyu Kim, Gi Ok Kim, Taekyun Shin

목차

INTRODUCTION
MATERIALS AND METHODS
Animals
Fermentation of black radish
Total phenolic content
DPPH radical scavenging activity
Experimental groups
CCl4 -induced hepatotoxicity
Histopathological examination
Serum chemistry
Measurement of liver superoxide dismutase and catalase activities
Measurement of lipid peroxidation in the liver
Immunohistochemistry
Statistical analysis
RESULTS
Black radish fermentation
Serum chemistry
FBR ameliorates the down-regulation of radical-scavenging enzymes
Histopathology
FBR reduces lipid peroxidation
FBR reduces Kupffer cells/macrophages activation
DISCUSSION
ACKNOWLEDGEMENTS
REFERENCES

영어 초록

Oxidative stress is one of common cause of fatty changes in the liver. Antioxidant capacity was confirmed in various vegetables including black radish (Raphanus sativus L. var niger). Fermentation of vegetables using Lactobacillus plantarum has been known to generate bioactive components. This study was conducted to determine if fermented black radish (FBR) ameliorates oxidative liver injury induced by CCl4 in rats. To accomplish this, FBR (250 and 500 mg/ kg) was orally administered to rats for 7 consecutive days, single CCl4 (1.5 mL/kg) treatment or no treatment orally. Serum chemistry at 24 hours after CCl4 injury showed that FBR (500 mg/kg) significantly reduced the level of both alanine aminotransferase and aspartate aminotransferase in CCl4 exposed rats. Moreover, FBR treatment significantly increased radical-scavenging effects in livers with the reduction of lipid peroxidation in CCl4 exposed rats. Histopathologic findings including Kupffer cell activation in the liver of each group matched those of serum chemistry. Collectively, black radish, through fermentation, exerts hepatoprotective capacity in CCl4 induced liver injury in rats through anti-oxidation.

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