Abstract
Inflammation and oxidative stress contribute to liver injury. Amla (Emblica officinalis Gaertn.) is rich in vitamin C, gallic acid, flavonoids, and tannins, which may protect against hepatoxicity-induced liver injury. We elucidated the effects of supplementary Amla (100 mg/kg of body weight) on N-nitrosodiethylamine-induced injury by evaluating reactive oxygen species (ROS) responses in the liver and bile, the degree of accumulated leukocytes and Kupffer cell infiltration, 3-nitrotyrosine and 4-hydroxynonenal stains, apoptosis and autophagy, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (γ-GT) levels, and antioxidant/oxidant enzymes in rats. Amla was more potent than vitamin C in scavenging O 2 -•, hydrogen peroxide, and nitric oxide. N-Nitrosodiethylamine increased ROS production in liver and bile, hepatic Kupffer cell and leukocyte infiltration, 3-nitrotyrosine and 4-hydroxynonenal accumulations, apoptosis and autophagy, and plasma ALT, AST, and γ-GT levels in the rats, decreased hepatic manganese superoxide dismutase (MnSOD) and catalase protein expressions, and enhanced inducible nitric oxide synthase (iNOS) and cytochrome P450 2E1 (CYP2E1) protein expressions. Amla significantly preserved MnSOD and catalase expressions and decreased iNOS and CYP2E1 protein expressions in N-nitrosodiethylamine-treated livers. Amla decreased N-nitrosodiethylamine-enhanced hepatic apoptosis and autophagy appearances via down-regulation of the Bax/Bcl-2 ratio and Beclin-1 expression. Thus Amla supplementation counteracts N-nitrosodiethylamine-induced liver injury via its antioxidant, anti-inflammation, anti-apoptosis, and anti-autophagy properties.
| Original language | English |
|---|---|
| Pages (from-to) | 746-755 |
| Number of pages | 10 |
| Journal | Journal of Medicinal Food |
| Volume | 14 |
| Issue number | 7-8 |
| DOIs | |
| Publication status | Published - 2011 Jul 1 |
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Keywords
- antioxidant
- apoptosis
- autophagy
- inflammation
- liver injury
- reactive oxygen species
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Nutrition and Dietetics
Cite this
Emblica officinalis gaertn. attentuates N-nitrosodiethylamine-induced apoptosis, autophagy, and inflammation in rat livers. / Chen, Kuo Hsin; Lin, Bor Ru; Chien, Chiang-Ting; Ho, Chien Hsin.
In: Journal of Medicinal Food, Vol. 14, No. 7-8, 01.07.2011, p. 746-755.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Emblica officinalis gaertn. attentuates N-nitrosodiethylamine-induced apoptosis, autophagy, and inflammation in rat livers
AU - Chen, Kuo Hsin
AU - Lin, Bor Ru
AU - Chien, Chiang-Ting
AU - Ho, Chien Hsin
PY - 2011/7/1
Y1 - 2011/7/1
N2 - Inflammation and oxidative stress contribute to liver injury. Amla (Emblica officinalis Gaertn.) is rich in vitamin C, gallic acid, flavonoids, and tannins, which may protect against hepatoxicity-induced liver injury. We elucidated the effects of supplementary Amla (100 mg/kg of body weight) on N-nitrosodiethylamine-induced injury by evaluating reactive oxygen species (ROS) responses in the liver and bile, the degree of accumulated leukocytes and Kupffer cell infiltration, 3-nitrotyrosine and 4-hydroxynonenal stains, apoptosis and autophagy, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (γ-GT) levels, and antioxidant/oxidant enzymes in rats. Amla was more potent than vitamin C in scavenging O 2 -•, hydrogen peroxide, and nitric oxide. N-Nitrosodiethylamine increased ROS production in liver and bile, hepatic Kupffer cell and leukocyte infiltration, 3-nitrotyrosine and 4-hydroxynonenal accumulations, apoptosis and autophagy, and plasma ALT, AST, and γ-GT levels in the rats, decreased hepatic manganese superoxide dismutase (MnSOD) and catalase protein expressions, and enhanced inducible nitric oxide synthase (iNOS) and cytochrome P450 2E1 (CYP2E1) protein expressions. Amla significantly preserved MnSOD and catalase expressions and decreased iNOS and CYP2E1 protein expressions in N-nitrosodiethylamine-treated livers. Amla decreased N-nitrosodiethylamine-enhanced hepatic apoptosis and autophagy appearances via down-regulation of the Bax/Bcl-2 ratio and Beclin-1 expression. Thus Amla supplementation counteracts N-nitrosodiethylamine-induced liver injury via its antioxidant, anti-inflammation, anti-apoptosis, and anti-autophagy properties.
AB - Inflammation and oxidative stress contribute to liver injury. Amla (Emblica officinalis Gaertn.) is rich in vitamin C, gallic acid, flavonoids, and tannins, which may protect against hepatoxicity-induced liver injury. We elucidated the effects of supplementary Amla (100 mg/kg of body weight) on N-nitrosodiethylamine-induced injury by evaluating reactive oxygen species (ROS) responses in the liver and bile, the degree of accumulated leukocytes and Kupffer cell infiltration, 3-nitrotyrosine and 4-hydroxynonenal stains, apoptosis and autophagy, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (γ-GT) levels, and antioxidant/oxidant enzymes in rats. Amla was more potent than vitamin C in scavenging O 2 -•, hydrogen peroxide, and nitric oxide. N-Nitrosodiethylamine increased ROS production in liver and bile, hepatic Kupffer cell and leukocyte infiltration, 3-nitrotyrosine and 4-hydroxynonenal accumulations, apoptosis and autophagy, and plasma ALT, AST, and γ-GT levels in the rats, decreased hepatic manganese superoxide dismutase (MnSOD) and catalase protein expressions, and enhanced inducible nitric oxide synthase (iNOS) and cytochrome P450 2E1 (CYP2E1) protein expressions. Amla significantly preserved MnSOD and catalase expressions and decreased iNOS and CYP2E1 protein expressions in N-nitrosodiethylamine-treated livers. Amla decreased N-nitrosodiethylamine-enhanced hepatic apoptosis and autophagy appearances via down-regulation of the Bax/Bcl-2 ratio and Beclin-1 expression. Thus Amla supplementation counteracts N-nitrosodiethylamine-induced liver injury via its antioxidant, anti-inflammation, anti-apoptosis, and anti-autophagy properties.
KW - antioxidant
KW - apoptosis
KW - autophagy
KW - inflammation
KW - liver injury
KW - reactive oxygen species
UR - http://www.scopus.com/inward/record.url?scp=79960458862&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79960458862&partnerID=8YFLogxK
U2 - 10.1089/jmf.2010.1459
DO - 10.1089/jmf.2010.1459
M3 - Article
C2 - 21761987
AN - SCOPUS:79960458862
VL - 14
SP - 746
EP - 755
JO - Journal of Medicinal Food
JF - Journal of Medicinal Food
SN - 1096-620X
IS - 7-8
ER -